RESUMEN
BACKGROUND: Gastro-oesophageal reflux disease (GERD) and gastric acid hypersecretion respond well to suppression of gastric acid secretion. However, clinical management and research in diseases of acid secretion have been hindered by the lack of a non-invasive, accurate and reproducible tool to measure gastric acid output (GAO). Thus, symptoms or, in refractory cases, invasive testing may guide acid suppression therapy. AIM: To present and validate a novel, non-invasive method of GAO analysis in healthy subjects using a wireless pH sensor, SmartPill (SP) (SmartPill Corporation, Buffalo, NY, USA). METHODS: Twenty healthy subjects underwent conventional GAO studies with a nasogastric tube. Variables impacting liquid meal-stimulated GAO analysis were assessed by modelling and in vitro verification. Buffering capacity of Ensure Plus was empirically determined. SP GAO was calculated using the rate of acidification of the Ensure Plus meal. Gastric emptying scintigraphy and GAO studies with radiolabelled Ensure Plus and SP assessed emptying time, acidification rate and mixing. Twelve subjects had a second SP GAO study to assess reproducibility. RESULTS: Meal-stimulated SP GAO analysis was dependent on acid secretion rate and meal-buffering capacity, but not on gastric emptying time. On repeated studies, SP GAO strongly correlated with conventional basal acid output (BAO) (r = 0.51, P = 0.02), maximal acid output (MAO) (r = 0.72, P = 0.0004) and peak acid output (PAO) (r = 0.60, P = 0.006). The SP sampled the stomach well during meal acidification. CONCLUSIONS: SP GAO analysis is a non-invasive, accurate and reproducible method for the quantitative measurement of GAO in healthy subjects. SP GAO analysis could facilitate research and clinical management of GERD and other disorders of gastric acid secretion.
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Endoscopía Capsular/métodos , Ácido Gástrico/metabolismo , Modelos Teóricos , Adulto , Femenino , Ácido Gástrico/fisiología , Determinación de la Acidez Gástrica , Humanos , Concentración de Iones de Hidrógeno , Masculino , Persona de Mediana Edad , Reproducibilidad de los Resultados , Adulto JovenRESUMEN
A method is described for freezing thin strips of smooth muscle by replacing physiological saline in the muscle chamber with cold organic solvent in <100 ms. Calculations suggest that, with a perfectly stirred boundary at the tissue surface, freezing could occur within approximately 15 ms at the center of a 200-microm-thick piece of tissue by use of acetone coolant at -78.5 degrees C and in approximately half the time with either isopentane at its freezing point (-160 degrees C) or aluminum chilled with liquid nitrogen. Myosin light chain phosphorylation in muscles frozen with cold acetone began to rise approximately 200 ms earlier than force and increased at a much more rapid rate. The difference in onsets of the two processes reflects the delay in arresting phosphorylation plus two lags associated with force generation, attachment of phosphorylated bridges followed by force generating movements of the attached bridges. The much more rapid rise of phosphorylation, once it began, suggests that most of this delay is due to physiological lags and not to slow arrest of metabolism.
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Congelación , Músculo Liso/metabolismo , Músculo Liso/fisiología , Animales , Perros , Técnicas In Vitro , Bombas de Infusión , Cinética , Cadenas Ligeras de Miosina/metabolismo , Miosinas/metabolismo , Miosinas/fisiología , Fosforilación , SolucionesRESUMEN
To better understand excitation-contraction coupling in smooth muscle, myosin phosphorylation and force-velocity properties of canine tracheal muscle were compared during the rise and early plateau of force in electrically stimulated tetani. Velocity reached a peak of approximately 1.5 times plateau value when force had risen to approximately 45% of its maximum value and then declined progressively. Except early in the tetanus, when phosphorylation rose rapidly, maximum power and phosphorylation had nearly parallel time courses, reaching peaks of 1.2-1.3 times reference at 6-8 s before declining to the plateau level at approximately 12 s. Force, velocity, maximum power, and phosphorylation fell somewhat during the plateau, with the closest correlation between phosphorylation and power. These results suggest that 1) early velocity slowing is not associated with light chain dephosphorylation and 2) maximum power, which we use to signal changes in activation, is closely correlated with the degree of light chain phosphorylation, at least when phosphorylation level is not changing rapidly. Dissociation of these two properties would be expected early in the tetanus if phosphorylation precedes mechanical activity.
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Músculo Liso/fisiología , Miosinas/metabolismo , Tráquea/fisiología , Animales , Western Blotting , Perros , Estimulación Eléctrica , Técnicas In Vitro , Contracción Isométrica/fisiología , Contracción Muscular/fisiología , Músculo Liso/metabolismo , Cadenas Ligeras de Miosina/química , Cadenas Ligeras de Miosina/metabolismo , Miosinas/química , Fosforilación , Tráquea/metabolismoRESUMEN
Vasoconstrictor agents may induce a decrease in hepatic vascular volume passively, by decreasing distending pressure, or actively, by stimulating contractile elements of capacitance vessels. Hepatic venular resistance was estimated in anesthetized rabbits from hepatic venular pressure (P(mu hv); by servo-null micropipette), inferior vena cava pressure, and total hepatic blood flow (F(hv); by ultrasound flow probe). Changes in liver volume were estimated from measures of liver lobe thickness. Angiotensin (ANG) II, endothelin (ET)-1, norepinephrine (NE), and vasopressin (VP) were infused into the portal vein at a constant rate for 5 min. We conclude that ANG II and NE induced active constriction of hepatic capacitance vessels, because the liver lobe thickness decreased significantly even though P(mu hv) and portal venous distending pressure (P(pv)) increased. All four agents increased splanchnic and hepatic venous resistances in similar proportions. With VP, P(mu hv) and P(pv) decreased, but with ET-1, P(mu hv) and P(pv) increased. However, lobe thickness was not significantly changed by either drug during the infusion compared with the 2-min control period. Thus VP and ET-1 have only minor effects on hepatic capacitance vessels. ET-1, at 0.04 microg. min(-1). kg body wt(-1), caused an increase in systemic arterial blood pressure, but erythrocyte movement through the sinusoids in some animals stopped.
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Angiotensina II/metabolismo , Endotelina-1/metabolismo , Hígado/irrigación sanguínea , Hígado/metabolismo , Norepinefrina/metabolismo , Vasopresinas/metabolismo , Angiotensina II/administración & dosificación , Animales , Relación Dosis-Respuesta a Droga , Endotelina-1/administración & dosificación , Femenino , Infusiones Intravenosas , Hígado/diagnóstico por imagen , Hígado/efectos de los fármacos , Circulación Hepática/efectos de los fármacos , Circulación Hepática/fisiología , Masculino , Microcirculación/diagnóstico por imagen , Microcirculación/efectos de los fármacos , Microcirculación/metabolismo , Norepinefrina/administración & dosificación , Vena Porta , Conejos , Ultrasonografía , Resistencia Vascular/efectos de los fármacos , Resistencia Vascular/fisiología , Vasopresinas/administración & dosificaciónRESUMEN
A force transducer with variable sensitivity and speed is described. Its moving element is a cantilever beam that projects vertically into a muscle bath. A brace constrains bending of the beam to a short, proximal "hinge." Rotation of the beam about the hinge is amplified 30-fold by an optical lever consisting of a laser diode beam reflected from a mirror on the cantilever to a photodiode pair. This design places the electrical components at a distance from the damp environment of the muscle bath. Large changes in sensitivity and speed can be obtained by substituting different cantilevers. Smaller changes can be made by varying the length of the hinge. A transducer with a 6-mm cantilever optimized for the study of single, skinned skeletal muscle fibers is described in detail. This device had a resonant frequency of 22 kHz and sensitivity such that the total root-mean-square noise in the circuit was more than 500-fold smaller than the expected maximum force. Variations of this device with orders of magnitude different sensitivities are also described.
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Rayos Láser , Contracción Muscular/fisiología , Transductores , Amplificadores Electrónicos , Animales , Diseño de Equipo , Contracción Isométrica/fisiología , Contracción Isotónica/fisiología , Cinética , Movimiento , Fibras Musculares Esqueléticas/fisiología , Músculo Esquelético/fisiología , Músculo Liso/fisiología , Rotación , Sensibilidad y Especificidad , Tráquea , AguaRESUMEN
Changes in hepatic venous resistance were estimated in rabbits from the hepatic venular-inferior vena caval pressure gradient [servo-null micropipettes in 49 +/- 15 (SD) microns vessels] and the total hepatic blood flow (ultrasound probe encircling the hepatic artery and the portal vein). Changes in liver volume, and thus vascular capacitance, were estimated from measures of the liver lobe thickness. Norepinephrine (NE), isoproterenol (Iso), adenosine (Ado), histamine (Hist), or acetylcholine (ACh) was infused into the portal vein at a constant rate for 5 min. NE, Hist, and Ado increased hepatic venular pressure, but only NE and Hist significantly increased hepatic venular resistance. NE reduced the liver thickness, but Hist and Ado caused engorgement. Hepatic blood flow was increased by NE and Ado and decreased by ACh. The influence of intraportal vein infusion of Iso on the liver vasculature, at doses similar to that of NE, was insignificant. We conclude that NE acted on all the hepatic microvasculature, increasing resistance and actively decreasing vascular volume. Hist passively induced engorgement by increasing outflow resistance, whereas the liver engorgement seen with Ado was passively related to the increased blood flow. ACh constricted the portal venules but did not change the liver volume.
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Acetilcolina/farmacología , Adenosina/farmacología , Histamina/farmacología , Isoproterenol/farmacología , Hígado/irrigación sanguínea , Norepinefrina/farmacología , Vénulas/efectos de los fármacos , Animales , Presión Sanguínea/efectos de los fármacos , Volumen Sanguíneo/efectos de los fármacos , Sistema Porta , Conejos , Flujo Sanguíneo Regional/efectos de los fármacos , Resistencia Vascular/efectos de los fármacosRESUMEN
The effect of temperature and thermal dose (equivalent minutes at 43 degrees C) on ultrasonic attenuation in fresh dog muscle, liver, and kidney in vitro, was studied over a temperature range from room temperature to 70 degrees C. The effect of temperature on ultrasonic absorption in muscle was also studied. The attenuation experiments were performed at 4.32 MHz, and the absorption experiments at 4 MHz. Attenuation and absorption increased at temperatures higher than 50 degrees C, and eventually reached a maximum at 65 degrees C. The rate of change of tissue attenuation as a function of temperature was between 0.239 and 0.291 Np m-1 MHz-1 degree C-1 over the temperature range 50-65 degrees C. A change in attenuation and absorption was observed at thermal doses of 100-1000 min, where a doubling of these loss coefficients was observed over that measured at 37 degrees C, presumably the result of changes in tissue composition. The maximum attenuation or absorption was reached at thermal dosages on the order of 10(7) min. It was found that the rate at which the thermal dose was applied (i.e., thermal dose per min) plays a very important role in the total attenuation absorption. Lower thermal dose rates resulted in larger attenuation coefficients. Estimation of temperature-dependent absorption using a bioheat equation based thermal model predicted the experimental temperature within 2 degrees C.
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Regulación de la Temperatura Corporal , Temperatura Corporal , Ultrasonido , Animales , PerrosRESUMEN
To test the hypothesis that the hepatic sinusoidal pressure is virtually identical to the portal venous pressure (Ppv) or the abdominal vena caval pressure (Pave), microvascular pressures were measured in liver vascular networks supplied by a single portal venule near the liver surface of alpha-chloralose-urethan-anesthetized rabbits. With the use of a servo-null pressure-measuring system, the pressures in terminal portal venules, sinusoids, and initial hepatic venules averaged 5.7 +/- 0.8 (SD), 5.4 +/- 0.7, and 4.7 +/- 0.6 mmHg, respectively, relative to the middle of the right atrium. The mean Ppv was 7.7 +/- 1.1 mmHg and the Pave was 3.9 +/- 0.7 mmHg. The sinusoidal pressure (Psinu) averaged 2.33 +/- 1.04 mmHg lower than the Ppv, and 1.54 +/- 0.63 mmHg higher than the Pave. The pressure gradient across the sinusoids averaged < 1 mmHg. The fractional pressure gradient from the sinusoids to the vena cava averaged 41 +/- 15% of the total Ppv to Pave gradient. We conclude that most of the transhepatic resistance cannot be attributed to a specific vascular segment or vessel type and that sinusoidal pressures are not closely similar to either the Ppv or the Pave, as is often assumed.
Asunto(s)
Presión Sanguínea , Circulación Hepática , Animales , Vasos Sanguíneos/fisiología , Microcirculación , Vena Porta/fisiología , Conejos , Resistencia Vascular , Venas Cavas/fisiología , Presión VenosaRESUMEN
Temperature changes in tissue, caused by high-intensity focused ultrasound, cause time shifts in the echoes that traverse the heated tissue. These time shifts are caused by thermally induced changes in the distribution of the velocity of sound and by thermal expansion within the tissue. Our analytical model relates these shifts to changes in temperature distribution. It is proposed that these relationships can be used as a method for the noninvasive estimation of temperature within the tissue. The model shows that the echo shifts depend mostly on changes in the mean velocity along the acoustical path of the echoes and that no explicit information about the shape of the velocity distribution is required. The effects of the tissue thermal expansion are small in comparison, but may be significant under certain conditions. The theory, as well as numerical simulations, also predicts that the time shifts have an approximately linear behavior as a function of temperature. This suggests that an empirical linear delay-temperature relationship can be determined for temperature prediction. It is also shown that, alternatively, the distribution of temperature in the tissue can be estimated from the distribution of echo delays along the acoustical path. In the proposed system, low-level pulse echoes are sampled during brief periods when the high-intensity ultrasonic irradiation is off, and thus linear acoustic behavior is assumed. The possibility of nonlinear aftereffects and other disturbances limiting this approach is discussed.
Asunto(s)
Temperatura Corporal , Ultrasonido , Acústica , Humanos , Modelos BiológicosRESUMEN
Time shifts in echo signals returning from a heated volume of tissue correlate well with the temperature changes. In this study the relationship between these time shifts (or delays) and the tissue temperature was investigated in excised muscle tissue (turkey breast) as a possible dosimetric method. Heat was induced by the repeated activation of a sharply focused high-intensity ultrasound beam. Pulse echoes were sent and received with a confocal diagnostic transducer during the brief periods when the high-intensity ultrasonic beam was inactive. The change in transit time between echoes collected at different temperatures was estimated using cross-correlation techniques. With spatial-peak temporal-peak intensities (ISPTP) of less than 950W/cm2, the delay versus temperature relationship was fit to a linear equation with highly reproducible coefficients. The results confirmed that for spatial-peak temperature increases of approximately 10 degrees C, temperature-dependent changes in velocity were the single most important factor determining the observed delay, and a linear approximation could produce accurate temperature estimations. Nonlinear phenomena that occurred during the high-intensity irradiation had no significant effect on the measured delay. At ISPTP of 1115-2698 W/cm2, the delay-temperature relationship showed a similar monotonically decreasing pattern, but as the temperature peaked its slope gradually increased. This may reflect the curvilinear nature of the velocity-temperature relationship, but it may also be related to irreversible tissue modifications and to the use of the spatial-peak temperature to experimentally characterize the temperature changes. Overall, the results were consistent with theoretical predictions and encourage further experimental work to validate other aspects of the technique.
Asunto(s)
Acústica , Temperatura Corporal , Ultrasonido , Humanos , Técnicas In Vitro , Modelos BiológicosRESUMEN
The liver provides a reservoir available for mobilizing large amounts of blood, but if a change in downstream (outflow) pressure below a certain magnitude (break pressure) does not change upstream pressures, blood volume redistribution may be limited. For downstream pressures larger than the break pressure, the upstream pressures change proportionately. We tested the hypothesis that this nonlinear mode of pressure transmission could be found from the abdominal vena cava to the hepatic microcirculation and from the hepatic microcirculation to the portal vein. Using a servo-null micropipette technique, we measured microvascular pressures at the liver surface of rabbits. In 16 of 30 measurements, increasing the pressure at the liver outflow, by partially occluding the caudal thoracic vena cava, caused an increase in hepatic venular pressure only after the abdominal vena caval pressure exceeded a break pressure of 2.85 +/- 0.92 mmHg. In 13 of 31 measurements, portal venous pressure was not changed until the hepatic venular pressure exceeded a break pressure of 3.36 +/- 0.54 mmHg. Similar behavior and values were obtained for sinusoids and portal venules. When present, the sharp inflection in the upstream-downstream pressure plots suggests that this may be caused by a Starling resistor-type mechanism. When the break was absent, the downstream pressure may have been larger than the break pressure. We conclude that significant hepatic resistances with nonlinear characteristics exist upstream and downstream to the central venules, sinusoids, and portal venules.
Asunto(s)
Circulación Hepática , Resistencia Vascular , Abdomen , Animales , Presión Sanguínea , Microcirculación , Modelos Cardiovasculares , Vena Porta/fisiología , Conejos , Tórax , Venas Cavas/fisiologíaRESUMEN
To quantify the degree of autonomic reflex control of the gastrointestinal vasculature, we studied the responses to a 10-ml/kg hemorrhage or transfusion and autonomic blockade in fentanyl- and pentobarbital-anesthetized dogs. The active total blood volume was estimated by indocyanine green dilution. Transfusion and hemorrhage did not significantly change gastrointestinal vascular compliance [1.82 +/- 0.68 (SD) ml/mmHg], but autonomic blockade with hexamethonium and atropine increased it by 0.57 +/- 0.37 ml/mmHg. Neither hemorrhage nor autonomic blockade significantly changed gastrointestinal vascular resistance from its control value of 10.8 +/- 4 mmHg.ml-1.min.kg body wt, but transfusion reduced it by 3.0 +/- 1.2 mmHg.ml-1.min.kg body wt. The ratio of gastrointestinal vascular resistance to total peripheral resistance was not significantly changed, however. We conclude that vascular compliance and resistance of the gastrointestinal bed are minimally influenced by the autonomic nervous system under the conditions studied. Portal pressure and flow measurements (transit-time ultrasound) during the above maneuvers were also combined with estimations of mean circulatory filling pressure (Pmcf) to test the hypothesis that, when the heart is stopped to measure Pmcf, portal pressure equals central venous pressure (Pcv) and hence that portal flow is zero. Seven seconds after the heart was stopped, portal venous pressure (Ppv) remained 0.83 +/- 0.78 mmHg higher than Pcv and portal flow decreased to only 25% of its control value. However, gastrointestinal compliance times (Ppv-Pcv), an estimate of the extra distending volume, was only 0.07 +/- 0.07 ml/kg body wt. Thus we conclude that the error in estimating Pmcf, given this (Ppv-Pcv) difference, is physiologically insignificant.
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Adaptación Fisiológica , Sistema Digestivo/irrigación sanguínea , Hemorragia Gastrointestinal/fisiopatología , Animales , Sistema Nervioso Autónomo/fisiología , Vasos Sanguíneos/fisiopatología , Volumen Sanguíneo , Gasto Cardíaco , Adaptabilidad , Perros , Hemodinámica , Vena Porta/fisiopatología , Reflejo/fisiología , Resistencia VascularRESUMEN
We tested the hypothesis that the larger (greater than 2 mm ID) hepatic veins are the primary site of the portal-to-caval venous pressure gradient in the dog. Double-lumen catheters were inserted through the caval wall into hepatic veins of pentobarbital sodium-anesthetized dogs. One lumen opened at the end, and the other to the side. Each catheter was advanced until stopped and then it was withdrawn. The pressure at either port dropped from 87 +/- 31 to 13 +/- 11% of the portal-to-caval pressure difference as each moved past a transition point (TP). The location of the TP depended on the catheter diameter. Intraportal histamine or norepinephrine, 4 and 2.6 micrograms.min-1.kg body wt-1 respectively, augmented only the pressure measured upstream to the TP. A mathematical model of flow through a vessel with a catheter inside predicted a marked increase in resistance when the ratio of catheter OD to vessel ID exceeded approximately 0.6. Autopsy revealed ratios greater than 0.6 upstream to the TP. A hydraulic model confirmed that this effect caused the appearance of the TP. Given the depth (11.7 cm) at which near caval pressures could be found, even during histamine administration, we conclude that the major pressure gradients in the canine liver must lie upstream to the large hepatic veins.
Asunto(s)
Venas Hepáticas/fisiología , Circulación Hepática , Resistencia Vascular , Animales , Cateterismo , Perros , Venas Hepáticas/anatomía & histología , Histamina/farmacología , Modelos Cardiovasculares , Norepinefrina/farmacología , Presión Venosa/efectos de los fármacosRESUMEN
We tested the hypotheses that the hepatic venule pressures (Phv), just downstream from the hepatic sinusoids, are closely similar (less than 2 mmHg) either to the portal venous pressure (Ppv), indicating a high hepatic venous resistance, or to the inferior vena cava (Pivc) pressure, indicating a high portal-sinusoidal venous resistance, as reported by previous investigators. A micropipette servo-null pressure measurement technique was used with rats, dogs, and rabbits. Phv, referred to the anatomic level of the vena cava, averaged 5.1 +/- 1.0, 6.4 +/- 1.1, and 5.4 +/- 1.0 (SD) mmHg in the rats, puppies, and rabbits, respectively. Ppv averaged 8.0 +/- 1.4, 10.8 +/- 2.2, and 7.4 +/- 1.5 mmHg, respectively. Norepinephrine infusion into the portal vein (1-5 micrograms.min-1.kg-1) caused Ppv to increase and the portal venous flow to decrease but did not significantly affect Phv. The hepatic venous circuit contributed 44 +/- 17% (rats) and 31 +/- 26% (dogs) of the total liver venous vascular resistance under control conditions. We conclude that the portal and sinusoidal vasculatures are the dominant, but not exclusive, resistance sites of the liver venous vasculature both at rest and during norepinephrine-induced vasoconstriction.
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Presión Sanguínea , Circulación Hepática , Vena Porta/fisiología , Resistencia Vascular , Vénulas/fisiología , Animales , Presión Sanguínea/efectos de los fármacos , Perros , Circulación Hepática/efectos de los fármacos , Masculino , Modelos Cardiovasculares , Músculo Liso Vascular/efectos de los fármacos , Músculo Liso Vascular/fisiología , Norepinefrina/farmacología , Conejos , Ratas , Ratas Endogámicas , Especificidad de la Especie , Vénulas/efectos de los fármacosRESUMEN
We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.
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Seno Carotídeo/fisiología , Hígado/fisiología , Presorreceptores/fisiología , Bazo/fisiología , Animales , Presión Sanguínea/fisiología , Volumen Sanguíneo/fisiología , Gasto Cardíaco/fisiología , Seno Carotídeo/ultraestructura , Gatos , Frecuencia Cardíaca/fisiología , Hígado/anatomía & histología , Hígado/diagnóstico por imagen , Tamaño de los Órganos/fisiología , Bazo/anatomía & histología , Bazo/diagnóstico por imagen , Ultrasonografía , Resistencia Vascular/fisiologíaRESUMEN
Aortic chemoreceptor influences on vascular capacitance after changes in blood carbon dioxide and oxygen were studied in mongrel dogs anesthetized with methoxyflurane and nitrous oxide. The mean circulatory filling pressure (Pmcf), measured during transient cardiac fibrillation, provided a measure of capacitance vessel tone. Hypercapnia, hypoxia, and hypoxic hypercapnia significantly increased most variables, except that hypercapnia caused the total peripheral resistance (TPR) to decrease. Hypocapnia caused a significant decrease in mean systemic (Psa) and pulmonary (Ppa) arterial blood pressures, cardiac output (CO), and central blood volume and an increase in TPR and heart rate. The changes in Pmcf on changing blood gas tensions could be described by the equation delta Pmcf = -1.60 + 0.036 (arterial PCO2) + 50.8/arterial PO2. Thus a 10 mmHg increase in arterial PCO2 caused a 0.36 mmHg increase in Pmcf with receptors intact. Cold block (2 degrees C) of the cervical vagosympathetic trunks did not significantly influence the measured variables at control. During severe hypercapnia, vagal cooling caused a small but significant decrease in Pmcf, Psa, Ppa, and CO but not TPR. During hypoxia, vagal cooling caused the Pmcf, Psa, and TPR to decrease. We conclude that although hypercapnia or hypoxia acts reflexly to increase the capacitance vessel tone (an increase in Pmcf), the aortic and cardiopulmonary chemoreceptors with afferents in the vagi have only a small influence on the capacitance system, accounting for only approximately 25% of the total body response.
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Aorta/fisiopatología , Sistema Cardiovascular/fisiopatología , Células Quimiorreceptoras/fisiopatología , Hipercapnia/fisiopatología , Hipoxia/fisiopatología , Resistencia Vascular , Animales , Aorta/inervación , Presión Sanguínea , Frío , Circulación Coronaria , Perros , Bloqueo Nervioso , Análisis de Regresión , Nervio Vago/fisiopatologíaRESUMEN
The role of beta-adrenergic agonists, such as isoproterenol, on vascular capacitance is unclear. Some investigators have suggested that isoproterenol causes a net transfer of blood to the chest from the splanchnic bed. We tested this hypothesis in dogs by measuring liver thickness, cardiac output, cardiopulmonary blood volume, mean circulatory filling pressure, portal venous, central venous, pulmonary arterial, and systemic arterial pressures while infusing norepinephrine (2.6 micrograms.min-1.kg-1), or isoproterenol (2.0 micrograms.min-1.kg-1), or histamine (4 micrograms.min-1.kg-1), or a combination of histamine and isoproterenol. Norepinephrine (an alpha- and beta 1-adrenergic agonist) decreased hepatic thickness and increased mean circulatory filling pressure, cardiac output, cardiopulmonary blood volume, total peripheral resistance, and systemic arterial and portal pressures. Isoproterenol increased cardiac output and decreased total peripheral resistance, but it had little effect on liver thickness or mean circulatory filling pressure and did not increase the cardiopulmonary blood volume or central venous pressure. Histamine caused a marked increase in portal pressure and liver thickness and decreased cardiac output, but it had little effect on the estimated mean circulatory filling pressure. Isoproterenol during histamine infusions reduced histamine-induced portal hypertension, reduced liver size, and increased cardiac output. We conclude that the beta-adrenergic agonist, isoproterenol, has little influence on vascular capacitance or liver volume of dogs, unless the hepatic outflow resistance is elevated by agents such as histamine.
Asunto(s)
Agonistas Adrenérgicos beta/farmacología , Hemodinámica/efectos de los fármacos , Resistencia Vascular/efectos de los fármacos , Animales , Presión Sanguínea/efectos de los fármacos , Volumen Sanguíneo/efectos de los fármacos , Gasto Cardíaco/efectos de los fármacos , Perros , Histamina/farmacología , Isoproterenol/farmacología , Hígado/efectos de los fármacos , Circulación Hepática/efectos de los fármacos , Norepinefrina/farmacología , Tamaño de los Órganos/efectos de los fármacos , Vasoconstricción/efectos de los fármacosRESUMEN
We tested the hypothesis that the changes in venous tone induced by changes in arterial blood oxygen or carbon dioxide require intact cardiovascular reflexes. Mongrel dogs were anesthetized with sodium pentobarbital and paralyzed with veruronium bromide. Cardiac output and central blood volume were measured by indocyanine green dilution. Mean circulatory filling pressure, an index of venous tone at constant blood volume, was estimated from the central venous pressure during transient electrical fibrillation of the heart. With intact reflexes, hypoxia (arterial PaO2 = 38 mmHg), hypercapnia (PaCO2 = 72 mmHg), or hypoxic hypercapnia (PaO2 = 41; PaCO2 = 69 mmHg) (1 mmHg = 133.32 Pa) significantly increased the mean circulatory filling pressure and cardiac output. Hypoxia, but not normoxic hypercapnia, increased the mean systemic arterial pressure and maintained the control level of total peripheral resistance. With reflexes blocked with hexamethonium and atropine, systemic arterial pressure supported with a constant infusion of norepinephrine, and the mean circulatory filling pressure restored toward control with 5 mL/kg blood, each experimental gas mixture caused a decrease in total peripheral resistance and arterial pressure, while the mean circulatory filling pressure and cardiac output were unchanged or increased slightly. We conclude that hypoxia, hypercapnia, and hypoxic hypercapnia have little direct influence on vascular capacitance, but with reflexes intact, there is a significant reflex increase in mean circulatory filling pressure.
Asunto(s)
Hipercapnia/fisiopatología , Hipoxia/fisiopatología , Reflejo/fisiología , Resistencia Vascular , Animales , Análisis de los Gases de la Sangre , Volumen Sanguíneo , Gasto Cardíaco/efectos de los fármacos , Perros , Compuestos de Hexametonio/farmacología , Técnicas In Vitro , Músculo Liso Vascular/fisiopatología , Norepinefrina/farmacologíaRESUMEN
Reflex respiratory responses to brief carotid baroreceptor stimuli in vagotomized pentobarbital-anesthetized cats were characterized and compared with those reported previously for chloralose-anesthetized dogs. To eliminate effects due to the anesthetic choice, dogs were reexamined under pentobarbital. Stimuli were applied to the isolated carotid sinus (CS) of both animals within a single respiratory phase. The stimuli were either steps triggered after one of four delays (5, 25, 50, and 75% of the control phase duration) and terminated at the end of the phase or pulses lasting 300-500 ms. In cats, 80-mmHg steps during inspiration shortened inspiratory duration by 23.2*, 25.0*, 20.4*, and 4.1% (*P less than 0.01) at the above four delays, respectively; inspired volume decreased by 21.4*, 18.0*, 8.0*, and 2.2%. Steps during expiration lengthened expiration by 38.4*, 37.1*, 21.9*, and 3.4%; expired volume changed less than 4%. Qualitatively, similar responses were obtained with steps 40 mmHg in amplitude. In dogs, 40-mmHg stimuli lengthened both inspiration (by 12.8*, 8.9*, -1.2, and -2.5%) and expiration (by 75.2*, 57.9*, 54.0*, and 61.4*%) but tidal volume did not change. Similar differences were observed when pulses were used. Selective baroreceptor denervation in the cat and occipital arterial occlusion in the dog confirmed that the responses were not chemoreceptor mediated. We conclude that although CS baroreceptor activity inhibits ventilation in both cats and dogs, the pattern of the responses is strongly species dependent.