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Cirugía Bariátrica , Progresión de la Enfermedad , Obesidad Mórbida , Pérdida de Peso , Humanos , Pérdida de Peso/fisiología , Cirugía Bariátrica/métodos , Cirugía Bariátrica/efectos adversos , Obesidad Mórbida/cirugía , Obesidad Mórbida/fisiopatología , Circulación Renal/fisiología , Insuficiencia Renal Crónica/fisiopatología , Riñón/irrigación sanguínea , Riñón/fisiopatologíaRESUMEN
Background: Increased intra-abdominal pressure resulting from pneumoperitoneum can cause renal physiological changes, such as oliguria and anuria, in mammals. Although videolaparoscopic operations are common, the occurrence of renal lesions due to these procedures has not been precisely documented in the literature. The aim of this study was to evaluate the impact of pneumoperitoneum on renal blood flow using renal scintigraphy in a rabbit model. Methods: Six New Zealand male rabbits weighing 3 kg, previously anesthetized, were mechanically ventilated and underwent pneumoperitoneum. Each animal served as its own control and was analyzed in two different moments: [99mTc] diethylenetriaminepentaacetic acid (DTPA) renal blood flow evaluation in baseline conditions (T0) and 30 minutes after installation of 15 mmHg-pneumoperitoneum (T1). The animals were monitored throughout the study by capnography, oximetry, and arterial pressure median, and were euthanized at the end of the experiment. Results: The quantitative analysis of the scintigraphic images of renal uptake of the radiopharmaceutical evidence reduced renal arterial blood flow during pneumoperitoneum. Compared with baseline conditions, all animals presented a reduction of renal blood flow varying from 16% to 82%, with mean [±standard deviation] of 53% [±24%]. Conclusions: Pneumoperitoneum induces a significant reduction of the renal blood flow, as determined in this experimental method in rabbits and dynamic renal scintigraphy with [99mTc] DTPA is an adequate method to investigate this event in the experimental setting.
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Riñón/diagnóstico por imagen , Neumoperitoneo Artificial/efectos adversos , Circulación Renal/fisiología , Animales , Riñón/irrigación sanguínea , Pruebas de Función Renal , Masculino , Conejos , Cintigrafía , Radiofármacos , Pentetato de Tecnecio Tc 99mRESUMEN
Tissue nonspecific alkaline phosphatase (TNAP) contributes to the production of adenosine by the kidney, and A1-receptor activation enhances renovascular responses to norepinephrine. Therefore, we hypothesized that TNAP regulates renovascular responsiveness to norepinephrine. In isolated, perfused rat kidneys, the TNAP inhibitor l-p-bromotetramisole (0.1 mmol/L) decreased renal venous levels of 5'-AMP (adenosine precursor) and adenosine by 61% (P<0.0384) and 62% (P=0.0013), respectively, at 1 hour into treatment and caused a 10-fold rightward shift of the concentration-response relationship to exogenous norepinephrine (P<0.0001). Similarly, 2 other TNAP inhibitors, levamisole (1 mmol/L) and 2,5-dimethoxy-N-(quinolin-3-yl)benzenesulfonamide (0.02 mmol/L), also right shifted the concentration-response relationship to norepinephrine. The ability of TNAP inhibition to blunt renovascular responses to norepinephrine was mostly prevented or reversed by restoring A1-adenosinergic tone with the A1-receptor agonist 2-chloro-N6-cyclopentyladenosine (100 nmol/L). All 3 TNAP inhibitors also attenuated renovascular responses to renal sympathetic nerve stimulation, suggesting that TNAP inhibition attenuates renovascular responses to endogenous norepinephrine. In control propranolol-pretreated rats, acute infusions of norepinephrine (10 µg/kg/min) increased mean arterial blood pressure from 95±5 mm Hg to a peak of 169±4 mm Hg and renovascular resistance from 12±2 mm Hg/mL/min to a peak of 55±12 mm Hg/mL/min; however, in rats also treated with intravenous l-p-bromotetramisole (30 mg/kg), the pressor and renovascular effects of norepinephrine were significantly attenuated (blood pressure: basal and peak, 93±7 and 146±6 mm Hg, respectively; renovascular resistance: basal and peak, 13±2 and 29±5 mm Hg/mL/min, respectively). TNAP inhibitors attenuate renovascular and blood pressure responses to norepinephrine, suggesting that TNAP participates in the regulation of renal function and blood pressure.
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Fosfatasa Alcalina/antagonistas & inhibidores , Presión Sanguínea/efectos de los fármacos , Levamisol/farmacología , Norepinefrina/farmacología , Arteria Renal/efectos de los fármacos , Circulación Renal/efectos de los fármacos , Sistema Nervioso Simpático/efectos de los fármacos , Animales , Riñón/irrigación sanguínea , Riñón/inervación , Masculino , Modelos Animales , Ratas , Ratas Sprague-Dawley , Circulación Renal/fisiología , Resistencia VascularRESUMEN
We evaluated the effects of K+ channel blockers in the vascular reactivity of in vitro perfused kidneys, as well as on the influence of vasoactive agents in the renal blood flow of rats subjected to the cecal ligation and puncture (CLP) model of sepsis. Both norepinephrine and phenylephrine had the ability to increase the vascular perfusion pressure reduced in kidneys of rats subjected to CLP at 18 h and 36 h before the experiments. The non-selective K+ channel blocker tetraethylammonium, but not the Kir6.1 blocker glibenclamide, normalized the effects of phenylephrine in kidneys from the CLP 18 h group. Systemic administration of tetraethylammonium, glibenclamide, or the KCa1.1 blocker iberiotoxin, did not change the renal blood flow in control or septic rats. Norepinephrine or phenylephrine also had no influence on the renal blood flow of septic animals, but its injection in rats from the CLP 18 h group previously treated with either glibenclamide or iberiotoxin resulted in an exacerbated reduction in the renal blood flow. These results suggest an abnormal functionality of K+ channels in the renal vascular bed in sepsis, and that the blockage of different subtypes of K+ channels may be deleterious for blood perfusion in kidneys, mainly when associated with vasoactive drugs.
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Canales KATP/antagonistas & inhibidores , Subunidades alfa de los Canales de Potasio de Gran Conductancia Activados por Calcio/antagonistas & inhibidores , Norepinefrina/farmacología , Fenilefrina/farmacología , Bloqueadores de los Canales de Potasio/farmacología , Circulación Renal/efectos de los fármacos , Sepsis/tratamiento farmacológico , Animales , Velocidad del Flujo Sanguíneo/efectos de los fármacos , Velocidad del Flujo Sanguíneo/fisiología , Canales KATP/fisiología , Subunidades alfa de los Canales de Potasio de Gran Conductancia Activados por Calcio/fisiología , Masculino , Bloqueadores de los Canales de Potasio/uso terapéutico , Ratas , Ratas Wistar , Circulación Renal/fisiología , Sepsis/fisiopatologíaRESUMEN
NEW FINDINGS: What is the topic of this review? This review describes the role of renal nerves as the key carrier of signals from the kidneys to the CNS and vice versa; the brain and kidneys communicate through this carrier to maintain homeostasis in the body. What advances does it highlight? Whether renal or autonomic dysfunction is the predominant contributor to systemic hypertension is still debated. In this review, we focus on the role of the renal nerves in a model of renovascular hypertension. The sympathetic nervous system influences the renal regulation of arterial pressure and body fluid composition. Anatomical and physiological evidence has shown that sympathetic nerves mediate changes in urinary sodium and water excretion by regulating the renal tubular water and sodium reabsorption throughout the nephron, changes in the renal blood flow and the glomerular filtration rate by regulating the constriction of renal vasculature, and changes in the activity of the renin-angiotensin system by regulating the renin release from juxtaglomerular cells. Additionally, renal sensory afferent fibres project to the autonomic central nuclei that regulate blood pressure. Hence, renal nerves play a key role in the crosstalk between the kidneys and the CNS to maintain homeostasis in the body. Therefore, the increased sympathetic nerve activity to the kidney and the renal afferent nerve activity to the CNS may contribute to the outcome of diseases, such as hypertension.
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Presión Sanguínea/fisiología , Sistema Nervioso Central/fisiología , Hipertensión/fisiopatología , Riñón/inervación , Circulación Renal/fisiología , Animales , Humanos , Riñón/irrigación sanguínea , Sistema Renina-Angiotensina/fisiologíaRESUMEN
BACKGROUND: Sepsis-induced acute kidney injury (AKI) is an early and frequent organ dysfunction, associated with increased mortality. AIM: To evaluate the impact of macrohemodynamic and microcirculatory changes on renal function and histology during an experimental model of intra-abdominal sepsis. MATERIAL AND METHODS: In 18 anaesthetized pigs, catheters were installed to measure hemodynamic parameters in the carotid, right renal and pulmonary arteries. After baseline assessment and stabilization, animals were randomly divided to receive and intra-abdominal infusion of autologous feces or saline. Animals were observed for 18 hours thereafter. RESULTS: In all septic animals, serum lactate levels increased, but only eight developed AKI (66%). These animals had higher creatinine and interleukin-6 levels, lower inulin and para-aminohippurate clearance (decreased glomerular filtration and renal plasma flow), and a negative lactate uptake. Septic animals with AKI had lower values of mean end arterial pressure, renal blood flow and kidney perfusion pressure, with an associated increase in kidney oxygen extraction. No tubular necrosis was observed in kidney histology. CONCLUSIONS: The reduction in renal blood flow and renal perfusion pressure were the main mechanisms associated with AKI, but were not associated with necrosis. Probably other mechanisms, such as microcirculatory vasoconstriction and inflammation also contributes to AKI development.
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Lesión Renal Aguda , Sepsis , Lesión Renal Aguda/sangre , Lesión Renal Aguda/patología , Lesión Renal Aguda/fisiopatología , Animales , Biomarcadores/sangre , Creatinina/sangre , Modelos Animales de Enfermedad , Femenino , Tasa de Filtración Glomerular/fisiología , Hemodinámica/fisiología , Interleucina-6/sangre , Microcirculación/fisiología , Circulación Renal/fisiología , Sepsis/sangre , Sepsis/patología , Sepsis/fisiopatología , Porcinos , Factores de TiempoRESUMEN
Background: Sepsis-induced acute kidney injury (AKI) is an early and frequent organ dysfunction, associated with increased mortality. Aim: To evaluate the impact of macrohemodynamic and microcirculatory changes on renal function and histology during an experimental model of intra-abdominal sepsis. Material and Methods: In 18 anaesthetized pigs, catheters were installed to measure hemodynamic parameters in the carotid, right renal and pulmonary arteries. After baseline assessment and stabilization, animals were randomly divided to receive and intra-abdominal infusion of autologous feces or saline. Animals were observed for 18 hours thereafter. Results: In all septic animals, serum lactate levels increased, but only eight developed AKI (66%). These animals had higher creatinine and interleukin-6 levels, lower inulin and para-aminohippurate clearance (decreased glomerular filtration and renal plasma flow), and a negative lactate uptake. Septic animals with AKI had lower values of mean end arterial pressure, renal blood flow and kidney perfusion pressure, with an associated increase in kidney oxygen extraction. No tubular necrosis was observed in kidney histology. Conclusions: The reduction in renal blood flow and renal perfusion pressure were the main mechanisms associated with AKI, but were not associated with necrosis. Probably other mechanisms, such as microcirculatory vasoconstriction and inflammation also contributes to AKI development.
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Animales , Femenino , Lesión Renal Aguda , Sepsis , Lesión Renal Aguda/sangre , Lesión Renal Aguda/patología , Lesión Renal Aguda/fisiopatología , Biomarcadores/sangre , Creatinina/sangre , Modelos Animales de Enfermedad , Tasa de Filtración Glomerular/fisiología , Hemodinámica/fisiología , /sangre , Microcirculación/fisiología , Circulación Renal/fisiología , Sepsis/sangre , Sepsis/patología , Sepsis/fisiopatología , Porcinos , Factores de TiempoRESUMEN
This paper presents the design, experimental modeling, and control of a pump-driven renal perfusion pressure (RPP)-regulatory system to implement precise and relatively fast RPP regulation in rats. The mechatronic system is a simple, low-cost, and reliable device to automate the RPP regulation process based on flow-mediated occlusion. Hence, the regulated signal is the RPP measured in the left femoral artery of the rat, and the manipulated variable is the voltage applied to a dc motor that controls the occlusion of the aorta. The control system is implemented in a PC through the LabView software, and a data acquisition board NI USB-6210. A simple first-order linear system is proposed to approximate the dynamics in the experiment. The parameters of the model are chosen to minimize the error between the predicted and experimental output averaged from eight input/output datasets at different RPP operating conditions. A closed-loop servocontrol system based on a pole-placement PD controller plus dead-zone compensation was proposed for this purpose. First, the feedback structure was validated in simulation by considering parameter uncertainty, and constant and time-varying references. Several experimental tests were also conducted to validate in real time the closed-loop performance for stepwise and fast switching references, and the results show the effectiveness of the proposed automatic system to regulate the RPP in the rat, in a precise, accurate (mean error less than 2 mmHg) and relatively fast mode (10-15 s of response time).
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Algoritmos , Biorretroalimentación Psicológica/instrumentación , Determinación de la Presión Sanguínea/instrumentación , Bombas de Infusión , Perfusión/instrumentación , Circulación Renal/fisiología , Terapia Asistida por Computador/instrumentación , Animales , Presión Sanguínea/fisiología , Electrónica Médica/instrumentación , Diseño de Equipo , Análisis de Falla de Equipo , RatasRESUMEN
PURPOSE: To investigate the effect of lovastatin on renal ischemia followed by reperfusion. METHODS: Thirty one Wistar rats submitted to left renal ischemia for 60 minutes followed by contralateral nephrectomy were divided into two groups: A (n =17, control, no treatment), and B (n=14, lovastatin 15 mg/kg/day p.o. ten days before ischemia). The animals were sacrificed at the end of ischemia, after 24 hours and at seven days after reperfusion. Survival, serum urea and creatinine levels and renal mitochondrial function were evaluated. RESULTS: Mortality was 29.4% in group A and 0.7% in group B. Urea and creatinine levels were increased in both groups, but the values were significantly lower in group B. Mitochondrial function showed decoupling in 83.4% of group A, as opposed to 38.4/% of group B. CONCLUSIONS: The result shows a protective action of renal function by lovastatin administered before ischemia/reperfusion. Since most of the mitochondrial fraction presented membranes with the ability to maintain ATP production in group B, stabilization of the mitochondrial membrane should be considered as part of the protective action of lovastatin on renal function in ischemia/reperfusion.
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Hipolipemiantes/farmacología , Riñón/efectos de los fármacos , Lovastatina/farmacología , Mitocondrias Hepáticas/efectos de los fármacos , Daño por Reperfusión/tratamiento farmacológico , Animales , Creatinina/sangre , Riñón/irrigación sanguínea , Riñón/fisiopatología , Masculino , Mitocondrias Hepáticas/fisiología , Nefrectomía , Ratas , Ratas Wistar , Circulación Renal/efectos de los fármacos , Circulación Renal/fisiología , Daño por Reperfusión/sangre , Daño por Reperfusión/fisiopatología , Factores de Tiempo , Urea/sangreRESUMEN
PURPOSE: To investigate the effect of lovastatin on renal ischemia followed by reperfusion. METHODS: Thirty one Wistar rats submitted to left renal ischemia for 60 minutes followed by contralateral nephrectomy were divided into two groups: A (n =17, control, no treatment), and B (n=14, lovastatin 15 mg/kg/day p.o. ten days before ischemia). The animals were sacrificed at the end of ischemia, after 24 hours and at seven days after reperfusion. Survival, serum urea and creatinine levels and renal mitochondrial function were evaluated. RESULTS: Mortality was 29.4% in group A and 0.7% in group B. Urea and creatinine levels were increased in both groups, but the values were significantly lower in group B. Mitochondrial function showed decoupling in 83.4% of group A, as opposed to 38.4/% of group B. CONCLUSIONS: The result shows a protective action of renal function by lovastatin administered before ischemia/reperfusion. Since most of the mitochondrial fraction presented membranes with the ability to maintain ATP production in group B, stabilization of the mitochondrial membrane should be considered as part of the protective action of lovastatin on renal function in ischemia/reperfusion.
OBJETIVO: Investigar a ação da lovastatina na isquemia renal seguida de reperfusão. MÉTODOS: Trinta e um ratos Wistar submetidos à isquemia renal esquerda durante 60 minutos, seguida da nefrectomia contralateral, foram distribuídos em dois grupos: A (n=17, controle, sem tratamento) e B (n=14, recebendo 15 mg/Kg/dia de lovastatina via oral), durante os dez dias que antecederam a isquemia. Os animais foram mortos ao final da isquemia, e com 24 horas e sete dias após a reperfusão. Foram avaliadas a sobrevida, os valores séricos de uréia e creatinina e a função mitocondrial renal. RESULTADOS: A mortalidade foi 29,4% no grupo A e 0,7% no grupo B. Os níveis de uréia e creatinina elevaram-se nos dois grupos, mas foram significativamente menores no grupo B. No grupo A a função mitocondrial renal ficou desacoplada em 83,4% dos ensaios, enquanto que no grupo B isto ocorreu em apenas 38,4% dos ensaios. CONCLUSÕES: Os resultados mostram que a administração de lovastatina antes do episódio de isquemia protege a função renal. No grupo B, como a maior parte da fração mitocondrial isolada apresentou função acoplada à produção de ATP, deve-se também considerar a estabilização da membrana mitocondrial como parte da ação protetora da lovastatina na função renal durante isquemia e reperfusão.
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Animales , Masculino , Ratas , Hipolipemiantes/farmacología , Riñón/efectos de los fármacos , Lovastatina/farmacología , Mitocondrias Hepáticas/efectos de los fármacos , Daño por Reperfusión/tratamiento farmacológico , Creatinina/sangre , Riñón/irrigación sanguínea , Riñón/fisiopatología , Mitocondrias Hepáticas/fisiología , Nefrectomía , Ratas Wistar , Circulación Renal/efectos de los fármacos , Circulación Renal/fisiología , Daño por Reperfusión/sangre , Daño por Reperfusión/fisiopatología , Factores de Tiempo , Urea/sangreRESUMEN
Renal vasodilation and sympathoinhibition are recognized responses induced by hypernatremia, but the central neural pathways underlying such responses are not yet entirely understood. Several findings suggest that A2 noradrenergic neurons, which are found in the nucleus of the solitary tract (NTS), play a role in the pathways that contribute to body fluid homeostasis and cardiovascular regulation. The purpose of this study was to determine the effects of selective lesions of A2 neurons on the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Male Wistar rats (280-350 g) received an injection into the NTS of anti-dopamine-beta-hydroxylase-saporin (A2 lesion; 6.3 ng in 60 nl; nâ=â6) or free saporin (sham; 1.3 ng in 60 nl; nâ=â7). Two weeks later, the rats were anesthetized (urethane 1.2 gâ kg(-1) b.wt., i.v.) and the blood pressure, renal blood flow (RBF), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA) were recorded. In sham rats, the HS infusion (3 M NaCl, 1.8 mlâ kg(-1) b.wt., i.v.) induced transient hypertension (peak at 10 min after HS; 9±2.7 mmHg) and increases in the RBF and RVC (141±7.9% and 140±7.9% of baseline at 60 min after HS, respectively). HS infusion also decreased the RSNA (-45±5.0% at 10 min after HS) throughout the experimental period. In the A2-lesioned rats, the HS infusion induced transient hypertension (6±1.4 mmHg at 10 min after HS), as well as increased RBF and RVC (133±5.2% and 134±6.9% of baseline at 60 min after HS, respectively). However, in these rats, the HS failed to reduce the RSNA (115±3.1% at 10 min after HS). The extent of the catecholaminergic lesions was confirmed by immunocytochemistry. These results suggest that A2 noradrenergic neurons are components of the neural pathways regulating the composition of the extracellular fluid compartment and are selectively involved in hypernatremia-induced sympathoinhibition.
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Hipernatremia/fisiopatología , Riñón/fisiopatología , Neuronas/metabolismo , Norepinefrina/metabolismo , Núcleo Solitario/fisiopatología , Sistema Nervioso Simpático/fisiopatología , Animales , Presión Sanguínea/efectos de los fármacos , Frecuencia Cardíaca/efectos de los fármacos , Frecuencia Cardíaca/fisiología , Hipernatremia/inducido químicamente , Hipernatremia/metabolismo , Riñón/efectos de los fármacos , Masculino , Neuronas/efectos de los fármacos , Ratas , Ratas Wistar , Circulación Renal/efectos de los fármacos , Circulación Renal/fisiología , Proteínas Inactivadoras de Ribosomas Tipo 1/farmacología , Solución Salina Hipertónica/farmacología , Saporinas , Núcleo Solitario/efectos de los fármacos , Núcleo Solitario/metabolismo , Sistema Nervioso Simpático/efectos de los fármacos , Sistema Nervioso Simpático/metabolismo , Tirosina 3-Monooxigenasa/metabolismoRESUMEN
To test the effect of insulin on renal perfusion and the participation of NO and PG as mediators of this response, renal blood flow (RBF) was measured in sheep (n = 8) implanted with ultrasonic flow probes around renal arteries and with a systemic arterial pressure (SAP, n = 4) telemetry device. Three protocols were performed: 1) RBF and SAP were recorded (0800 to 1800 h) in fed and fasted sheep, with the latter receiving intravenous (i.v.) infusions (0.5 mL/min) of insulin at 2 or 6 mU/(kg·min); 2) fasted sheep received i.v. infusions of either an inhibitor of NO synthesis (N(G)-nitro-L-arginine methyl ester, L-NAME) alone [0.22 mg/(kg·min), 1000 to 1200 h] or L-NAME (1000 to 1200 h) + insulin during the second hour (6 mU/(kg·min), 1100 to 1200 h); and 3) the same protocol was followed as in protocol 2, substituting L-NAME with ketoprofen [0.2 mg/(kg·min)], a cyclooxygenase inhibitor. In all protocols, plasma insulin and glucose were determined. During insulin administration, euglycemia was maintained and hypokalemia was prevented by infusing glucose and KCl solutions. After the onset of meals, a long-lasting 18% increase in RBF and a 48% insulin increase were observed (P < 0.05), without changes in SAP. Low- and high-dose insulin infusions increased RBF by 19 and 40%, respectively (P < 0.05). As after meals, the increases in RBF lasted longer than the insulin increase (P < 0.05). The L-NAME infusion decreased RBF by 15% (P < 0.05); when insulin was added, RBF increased to preinfusion values. Ketoprofen decreased RBF by 9% (P < 0.05); when insulin was added, RBF increased to 13% above preinfusion values (P < 0.05). In no case was a modification in SAP or glucose noted during the RBF changes. In conclusion, insulin infusion mimics the meal-dependent increase in RBF, independent of SAP, and lasts longer than the blood insulin plateau. The RBF increase induced by insulin was only partially prevented by L-NAME. Ketoprofen failed to prevent the insulin-dependent RBF increase. Both facts suggested that complementary vasodilatatory agents accounted for the insulin effect on sheep renal hemodynamics.
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Insulina/farmacología , Óxido Nítrico/fisiología , Prostaglandinas/fisiología , Circulación Renal/efectos de los fármacos , Animales , Glucemia/análisis , Presión Sanguínea/efectos de los fármacos , Inhibidores de la Ciclooxigenasa/farmacología , Relación Dosis-Respuesta a Droga , Femenino , Infusiones Intravenosas/veterinaria , Insulina/administración & dosificación , Insulina/sangre , Cetoprofeno/farmacología , Monitoreo Fisiológico/veterinaria , NG-Nitroarginina Metil Éster/farmacología , Óxido Nítrico/antagonistas & inhibidores , Circulación Renal/fisiología , Ovinos/fisiologíaRESUMEN
Renal diseases are common in older cats. Decreased renal blood flow may be the first sign of dysfunction and can be evaluated by Doppler ultrasound. But previous studies suggest that the resistive index (RI) has a low sensitivity for detecting renal disease. Doppler waveforms of renal and intrarenal arteries demonstrate decreased blood flow before there are any changes in the RI. The purpose of this study was to evaluate the normal Doppler flowmetrics parameters of renal arteries (RAs), interlobar arteries (IAs) and abdominal aorta (AO) in adult healthy, Persian cats. Twenty-five Persian cats (13 females and 12 males with mean age of 30 months and an age range 12-60 months) with normal clinical examinations and biochemical tests and normal systemic blood pressure were given B-mode ultrasonographies in order to exclude all nephropathies, including polycystic kidney disease. All measurements were performed on both kidneys. Both kidneys (n=50) were examined by color mapping of the renal vasculature. Pulsed Doppler was used to examine both RAs, the IAs at cranial, middle and caudal sites, and the AO. The RI was calculated for all of the vessels. Early systolic acceleration (ESA) of RA and IA was obtained with Doppler spectral analysis. Furthermore, the ratio indices between RA/AO, and IA/RA velocities were calculated. The mean values of peak systolic velocity (PSV) and the diameter for AO were 53.17±13.46 cm/s and 0.38±0.08 cm, respectively. The mean RA diameter for all 50 kidneys was 0.15±0.02 cm. Considering the velocimetric values in both RAs, the mean PSV and RI that were obtained were 41.17±9.40 cm/s and 0.54±0.07. The RA had a mean ESA of 1.12±1.14 m/s(2) and the calculated upper limit of the reference value was 3.40 m/s(2). The mean renal-aortic ratio was 0.828±0.296. The IA showed PSV and RI values of 32.16±9.33 cm/s and 0.52±0.06, respectively. The mean ESA of all IAs was 0.73±0.61 m/s(2). The calculated upper limit of the reference value was 2.0m/s(2). The mean renal-interlobar artery ratio was 1.45±0.57. The RI values obtained in this study were similar to values reported in the literature. Some conditions that lead to a decrease in compliance and to an increase in vascular resistance can affect the Doppler spectral waveforms without changes in RI. To our knowledge, there are no studies that were directed toward to the normal ESA values of the renal vasculature in Persian cats. This study introduced a new ratio between the PSV of the RA and the IA. This index was developed based on the well-known effects of Doppler on the detection of stenosis, regardless of the cause. Further studies are necessary to verify the hemodynamic behavior of this index under pathological conditions in cats as well as the effect of aging, nephropathies and systemic pressure on Doppler velocimetric parameters.
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Aorta Abdominal/fisiología , Riñón/irrigación sanguínea , Arteria Renal/fisiología , Circulación Renal/fisiología , Ultrasonografía Doppler en Color/veterinaria , Animales , Aorta Abdominal/diagnóstico por imagen , Velocidad del Flujo Sanguíneo , Gatos , Femenino , Riñón/diagnóstico por imagen , Masculino , Valores de Referencia , Arteria Renal/diagnóstico por imagen , Resistencia VascularRESUMEN
INTRODUCTION: Decline in glomerular filtration rate (GFR) is one of several changes in renal physiology in the elderly. Renal reserve (RR) is the kidney's capacity to increase its basal GFR by at least 20% after a protein overload. Even though it has already been reported that RR is preserved in healthy old people, there is no information whether RR is also preserved in the healthy very old one (older than 74 of age), which we decided to study and report our findings in this paper. MATERIAL AND METHOD: We studied RR in 16 healthy persons divided into three age groups: young: 20-40 years old (n: 5): 64-74 years old (n: 6) and oldest old: >74 years old (n: 5). Renal reserve test was performed by assessing creatinine clearance with cimetidine before and after an oral protein load. Statistical analysis was performed using ANOVA test. RESULTS: Even though renal reserve response was present in all age groups, its magnitude (delta GFR) was significantly higher in the healthy young group (103.6 ± 53 ml/min) compared to the old one (34.1 ± 40 ml/min) (P = 0.002), while it was significantly lower in the healthy oldest old (20.7 ± 0.7 ml/min) group compared to the other two groups (P = 0.002). CONCLUSION: Renal reserve is preserved in healthy very old people, but its magnitude decreases significantly with age.
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Envejecimiento , Tasa de Filtración Glomerular/fisiología , Riñón/fisiología , Circulación Renal/fisiología , Adulto , Anciano , Femenino , Humanos , Pruebas de Función Renal , Masculino , Persona de Mediana Edad , Valores de Referencia , Adulto JovenRESUMEN
BACKGROUND: Cyclosporine A (CsA)-induced chronic nephrotoxicity is characterized by renal dysfunction and interstitial fibrosis. Early and progressive renal macrophage influx, correlating with latter interstitial fibrotic areas, has been associated with CsA treatment. This study investigated the role of macrophages, the nitric oxide (NO) pathway, and the oxidative stress on chronic CsA nephrotoxicity. METHODS: The macrophages were depleted by clodronate liposomes. Animals were distributed into four groups: vehicle (olive oil for 21 days), CsA 7.5 mg/kg per day (21 days), CsA plus clodronate (5 mg/mL intraperitoneally on days -4, 1, 4, 11, and 18 of CsA treatment), or vehicle plus clodronate. On day 22, glomerular filtration rate, renal blood flow, renal tubulointerstitial fibrosis, CsA blood levels, serum malondialdehyde and renal tissue immunohistochemistry for macrophages, inducible NO synthase, transforming growth factor-beta, nuclear factor-kbeta, alpha-smooth muscle actin, vimentin, and nitrotyrosine were assessed. RESULTS: CsA-induced increase in the macrophage was prevented by clodronate. Macrophage depletion attenuated the reductions in the glomerular filtration rate and renal blood flow, the development of tubulointerstitial fibrosis, malondialdehyde increase and increases in nuclear factor-kbeta, transforming growth factor-beta, vimentin, inducible NO synthase, and nitrotyrosine expression provoked by CsA. Clodronate did not affect alpha-smooth muscle actin expression and CsA blood levels. CONCLUSIONS: Renal macrophage influx plays an important role in CsA-induced chronic nephrotoxicity. The NO pathway and oxidative stress are likely mechanisms involved in the genesis of this form of renal injury.
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Ácido Clodrónico/farmacología , Ciclosporina/farmacología , Tasa de Filtración Glomerular/fisiología , Inmunosupresores/farmacología , Macrófagos/fisiología , Animales , Anticuerpos/farmacología , Ciclosporina/sangre , Diuresis/efectos de los fármacos , Diuresis/fisiología , Tasa de Filtración Glomerular/efectos de los fármacos , Hemodinámica/efectos de los fármacos , Hemodinámica/fisiología , Riñón/efectos de los fármacos , Riñón/fisiología , Pruebas de Función Renal , Macrófagos/efectos de los fármacos , Masculino , FN-kappa B/inmunología , Óxido Nítrico/fisiología , Ratas , Ratas Wistar , Circulación Renal/efectos de los fármacos , Circulación Renal/fisiología , Tirosina/inmunología , Resistencia Vascular/efectos de los fármacos , Vimentina/inmunologíaRESUMEN
INTRODUCTION: Halogenated anesthetics can cause changes in the variables that modify the cardiac output necessary to maintain renal hemodynamic during hemorrhagic shock and resuscitation. However, halogenated anesthetics seem to protect against renal ischemia-reperfusion injury. In a model of pressure-guided hemorrhagic shock in dogs, we studied the comparative effects of three halogenated anesthetics-halothane, sevoflurane, and isoflurane-at equipotent concentrations on renal responses after resuscitation. METHODS: Thirty dogs were anesthetized with 1.0 minimum alveolar anesthetic concentration (MAC) of halothane, sevoflurane, or isoflurane. The dogs were splenectomized and hemorrhaged to hold mean arterial pressure at 40-50 mm Hg over 45 min and then resuscitated with the shed blood volume. Hemodynamic variables were measured at baseline, after 45 min of hemorrhage, and 15 and 60 min after resuscitation. Renal variables were measured at baseline and 15 and 60 min after resuscitation. RESULTS: Hemorrhage induced reductions of mean arterial pressure, filling pressures, and cardiac index (p < 0.05), without significant differences among groups (p > 0.05). After 60 min of shed blood replacement, all groups restored hemodynamic and renal variables to the prehemorrhage levels (p > 0.05), without significant differences among groups (p > 0.05), with the exception of sodium fractional excretion, the values for which were significantly higher in isoflurane group, in relation to the other groups after 15 min of re-transfusion (p < 0.05), and renal vascular resistance, the values for which remain lower than baseline in halothane group (p < 0.05). CONCLUSIONS: We conclude that no difference could be detected between choosing equipotent doses of halothane, sevoflurane, or isoflurane in relation to renal variables in dogs submitted to pressure-adjusted hemorrhagic shock and resuscitation.
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Anestésicos por Inhalación/uso terapéutico , Halotano/uso terapéutico , Isoflurano/uso terapéutico , Éteres Metílicos/uso terapéutico , Circulación Renal/fisiología , Choque Hemorrágico/terapia , Animales , Presión Sanguínea , Gasto Cardíaco , Creatinina/metabolismo , Modelos Animales de Enfermedad , Perros , Femenino , Tasa de Filtración Glomerular/fisiología , Masculino , Resucitación , Sevoflurano , Choque Hemorrágico/complicaciones , Choque Hemorrágico/fisiopatologíaRESUMEN
To assess the roles of feeding behavior (eating and rumination) and systemic arterial pressure (SAP) on determination of the circadian rhythm of renal blood flow (RBF), 20 sheep fitted with ultrasonic flow-metering probes around both renal arteries and a submandibular balloon to monitor jaw movements (6 of them with a telemetry measurement system into the carotid artery for SAP recording), were successively assigned to 6 feeding patterns: once daily in the morning (0900 to 1100 h), afternoon (1700 to 1900 h), or evening (1900 to 2100 h); twice daily at 0900 to 1100 h and 1700 to 1900 h; ad libitum (food renewed each 2 h); and fasting (40 h). All protocols were carried out in autumn-winter, and the fasting pattern was repeated in spring-summer to evaluate the effect of the daylight length on RBF. In the once-daily feeding patterns, a rapid increase in RBF (P < 0.05 vs. 1-h prefeeding mean values) subsequent to the onset of meals was observed, followed by a progressive increase (P < 0.05), reaching a maximum 4 to 6 h after the beginning of eating, and a subsequent gradual decline until the next meal [differences vs. prefeeding values were no longer significant after 11 h (morning pattern), 13 h (afternoon pattern), and 15 h (evening pattern) from the beginning of eating]. In the twice-daily feeding pattern, each meal was also followed by an increase in RBF (P < 0.05 vs. prefeeding values), reaching a maximum 3 to 5 h after the onset of meals, and a posterior decline [differences vs. prefeeding values were no longer significant after 8 h (morning meal) and 5 h (afternoon meal) from the beginning of eating]. In the ad libitum feeding, no apparent rhythm in RBF was found. During fasting, a progressive reduction of RBF was observed from 2 h after the beginning of fasting (P < 0.05 vs. the mean value of the first fasting hour), with a slight rebound (P < 0.05) lasting several hours from approximately 0700 h in autumn-winter and approximately 0500 h in spring-summer. No change in the RBF profile was observed in association with rumination. Except during meals, no correlation was found between RBF and SAP. A detailed description of RBF and SAP recordings is presented. In conclusion, results showed a circadian rhythm of RBF determined by eating behavior, but not by rumination, that was independent of blood pressure and that seemed superimposed on a primary lighting-cycle-dependent RBF rhythm.
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Presión Sanguínea/fisiología , Ritmo Circadiano/fisiología , Digestión/fisiología , Ingestión de Alimentos/fisiología , Circulación Renal/fisiología , Ovinos/fisiología , Animales , Femenino , Frecuencia Cardíaca , Distribución Aleatoria , Análisis de Regresión , Estaciones del Año , Ovinos/metabolismoRESUMEN
PURPOSE OF THE REVIEW: The adenosine-angiotensin II (ADO-AngII) interaction plays an important role in the regulation of glomerular filtration rate, vascular resistance and tubuloglomerular feedback. Although the interaction was described more than 30 years ago, the intrinsic mechanisms of the synergism between both autacoids remains incompletely understood. RECENT FINDINGS: Current evidence suggests that ADO-metabolizing enzymes such as ecto-5'-nucleotidase or ADO deaminase, as well as enzymes that degrade ATP to adenosine, play an important role in the vasoconstrictor signals sent from the macula densa to the afferent arterioles when tubuloglomerular feedback is activated; increased ADO concentration induced by temporal infusion of AngII results in downregulation of A2 ADO receptors, leading to a predominant effect of A1 receptors; the alteration in the ADO receptors balance further contributes to the synergic interaction between ADO and AngII. SUMMARY: The ADO-metabolizing enzymes have become important regulators of the effects of ADO on the tone of the afferent and efferent arterioles. As AngII is able to increase de-novo renal ADO content through decrease of ADO-metabolizing enzymes, accumulation of ADO induces downregulation of ADO A2 receptor population without modifying ADO A1 receptor, thereby enhancing the constrictive effects of AngII in the renal vasculature.