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INTRODUCTION: Although the use of ultrasound for the insertion of central catheters has proven to be cost-effective in adults, it is not known if this is the case in the neonatal population. This study compared the cost-effectiveness of ultrasound-guided umbilical venous catheterisation with conventional catheterisation in a neonatal intensive care unit of a Public University Hospital. PATIENTS AND METHODS: A retrospective observational study was conducted on newborns that required an umbilical venous catheter before completing their first 24hours of extra-uterine life. Two retrospective cohorts were formed, including one with ultrasound-guided catheterisation and the other with conventional catheterisation. The effectiveness was measured using 2 variables: placement of ideal position and insertion without complications. The cost of human and material resources (consumable and non-consumable), the cost-effectiveness ratio, and the incremental cost-effectiveness ratio were estimated, as well as carrying out a sensitivity analysis. RESULTS: Catheter obstruction was more frequent in guided catheterisation than in conventional catheterisation (7.7% vs. 0%, p=.04) and catheter dysfunction was higher in the latter (79% vs. 3.8%, p<.0001). The cost-effectiveness ratio of the guided catheterisation was 153.9, and 484.6 for the conventional one. The incremental cost-effectiveness ratio was 45.5. The sensitivity analysis showed a 2.6 increase in the cost-effectiveness ratio of the guided catheterisation and 47 in the conventional one. CONCLUSIONS: The use of ultrasound to guide umbilical catheterisation is more efficient than conventional catheterisation since, despite using more economic resources, it offers greater effectiveness.
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Cateterismo Venoso Central/métodos , Custos de Cuidados de Saúde/estatística & dados numéricos , Ultrassonografia de Intervenção/economia , Veias Umbilicais , Cateterismo Venoso Central/economia , Análise Custo-Benefício , Feminino , Humanos , Recém-Nascido , Masculino , México , Estudos RetrospectivosRESUMO
Sepsis is a serious condition characterized by an infectious process that induces a severe systemic inflammatory response. In this study, the effects of gemfibrozil (GFZ) on the inflammatory response associated with abdominal sepsis were investigated using a rat model of cecal-ligation and puncture (CLP). Male Wistar rats were randomly divided into three groups: Sham-operated group (sham), where laparotomy was performed, the intestines were manipulated, and the cecum was ligated but not punctured; control group, subjected to CLP; and GFZ group, which received GFZ prior to undergoing CLP. The groups were then subdivided into three different time-points: 2, 4 and 24 h, indicating the time at which blood samples were obtained for analysis. Serum concentrations of tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), malondialdehyde (MDA), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) were determined. The LDH, AST and ALT values were significantly elevated following CLP compared with those in the sham group, and GFZ treatment was able to reduce these elevations. GFZ also reduced the sepsis-induced elevations of TNF-α and IL-1. In conclusion, GFZ treatment was able to attenuate the inflammatory response associated with CLP-induced sepsis, by diminishing the release of inflammatory cytokines, thereby reducing tissue injury and oxidative stress.
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OBJECTIVE: It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate. We used Chiús classification to grade the histopathological damage. METHODS: We studied 35 Wistar rats divided into groups according to reperfusion time. The superior mesenteric artery was clamped for 30 minutes, and blood and biopsies were collected at 1, 3, 6, 12, 24, and 48 hours after reperfusion. We plotted the mean ± standard deviation and compared the baseline and maximum values for each marker using Student's t-test. RESULTS: The maximum values of interleukin-1 beta and lactic dehydrogenase were present before the maximal histopathological damage. The maximum tumor necrosis factor alpha and D-lactate expressions coincided with histopathological damage. Alanine aminotransaminase and aspartate aminotransferase had a maximum expression level that increased following the histopathological damage. The maximum expressions of interluken-6 and intestinal fatty acid binding protein were not significantly different from the Sham treated group. CONCLUSION: For the evaluation of injury secondary to acute intestinal ischemia reperfusion with a 30 minute ischemia period, we recommend performing histopathological grading, quantification of D-lactate, which is synthesized by intestinal bacteria and is considered an indicator of mucosal injury, and quantification of tumor necrosis factor alpha as indicators of acute inflammation three hours after reperfusion.
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Biomarcadores/sangue , Intestinos/irrigação sanguínea , Traumatismo por Reperfusão/sangue , Animais , Aspartato Aminotransferases/sangue , Biópsia , Citocinas/sangue , Modelos Animais de Doenças , Proteínas de Ligação a Ácido Graxo/sangue , Feminino , Intestinos/patologia , Lactato Desidrogenases/sangue , Ratos , Ratos Wistar , Valores de Referência , Fatores de TempoRESUMO
OBJECTIVE: It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate. We used Chiús classification to grade the histopathological damage. METHODS: We studied 35 Wistar rats divided into groups according to reperfusion time. The superior mesenteric artery was clamped for 30 minutes, and blood and biopsies were collected at 1, 3, 6, 12, 24, and 48 hours after reperfusion. We plotted the mean ± standard deviation and compared the baseline and maximum values for each marker using Student's t-test. RESULTS: The maximum values of interleukin-1 beta and lactic dehydrogenase were present before the maximal histopathological damage. The maximum tumor necrosis factor alpha and D-lactate expressions coincided with histopathological damage. Alanine aminotransaminase and aspartate aminotransferase had a maximum expression level that increased following the histopathological damage. The maximum expressions of interluken-6 and intestinal fatty acid binding protein were not significantly different from the Sham treated group. CONCLUSION: For the evaluation of injury secondary to acute intestinal ischemia reperfusion with a 30 minute ischemia period, we recommend performing histopathological grading, quantification of D-lactate, which is synthesized by intestinal bacteria and is considered an indicator of mucosal injury, and quantification of tumor necrosis ...
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Animais , Feminino , Ratos , Biomarcadores/sangue , Intestinos/irrigação sanguínea , Traumatismo por Reperfusão/sangue , Aspartato Aminotransferases/sangue , Biópsia , Citocinas/sangue , Modelos Animais de Doenças , Proteínas de Ligação a Ácido Graxo/sangue , Intestinos/patologia , Lactato Desidrogenases/sangue , Ratos Wistar , Valores de Referência , Fatores de TempoRESUMO
After peripheral nerve injury, a process of axonal degradation, debris clearance, and subsequent regeneration is initiated by complex local signaling, called Wallerian degeneration (WD). This process is in part mediated by neuroglia as well as infiltrating inflammatory cells and regulated by inflammatory mediators such as cytokines, chemokines, and the activation of transcription factors also related to the inflammatory response. Part of this neuroimmune signaling is mediated by the innate immune system, including arachidonic acid (AA) derivatives such as prostaglandins and leukotrienes. The enzymes responsible for their production, cyclooxygenases and lipooxygenases, also participate in nerve degeneration and regeneration. The interactions between signals for nerve regeneration and neuroinflammation go all the way down to the molecular level. In this paper, we discuss the role that AA derivatives might play during WD and nerve regeneration, and the therapeutic possibilities that arise.
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Ácido Araquidônico/farmacologia , Ciclo-Oxigenase 2/metabolismo , Regeneração Nervosa , Nervos Periféricos/efeitos dos fármacos , Degeneração Walleriana/metabolismo , Ácido Araquidônico/metabolismo , Inibidores de Ciclo-Oxigenase/farmacologia , Eicosanoides/metabolismo , Humanos , Inflamação/metabolismo , Mediadores da Inflamação/metabolismo , Leucotrienos/metabolismo , Traumatismos dos Nervos Periféricos/tratamento farmacológico , Traumatismos dos Nervos Periféricos/metabolismo , Nervos Periféricos/metabolismo , Fosfolipases/metabolismo , Prostaglandinas/metabolismo , Transdução de Sinais , Degeneração Walleriana/tratamento farmacológicoRESUMO
Ischemia/reperfusion (I/R) is a condition that stimulates an intense inflammatory response. No ideal treatment exists. Triflusal is an antiplatelet salicylate derivative with anti-inflammatory effects. S-adenosylmethionine is a metabolic precursor for glutathione, an endogenous antioxidant. Dextromethorphan is a low-affinity N-methyl-D-aspartate receptor inhibitor. There is evidence that these agents modulate some of the pathways involved in I/R physiopathology. Intestinal I/R was induced in rats by clamping the superior mesenteric artery for 60 minutes, followed by 60 minutes of reperfusion. Rats either received saline or the drugs studied. At the end of the procedure, serum concentrations of tumor necrosis factor-alpha (TNF-alpha), malonaldehyde (MDA), and total antioxidant capacity (TAC) were determined and intestinal morphology analyzed. I/R resulted in tissue damage, serum TNF-alpha and MDA elevations, and depletion of TAC. All drugs showed tissue protection. Only triflusal reduced TNF-alpha levels. All drugs lowered MDA levels, but only triflusal and S-adenosylmethionine maintained the serum TAC.
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Dextrometorfano/uso terapêutico , Intestinos/irrigação sanguínea , Inibidores da Agregação Plaquetária/uso terapêutico , Traumatismo por Reperfusão/tratamento farmacológico , S-Adenosilmetionina/uso terapêutico , Salicilatos/uso terapêutico , Animais , Antioxidantes/metabolismo , Masculino , Malondialdeído/metabolismo , Ratos , Ratos Wistar , Fator de Necrose Tumoral alfa/sangueRESUMO
PURPOSE: Intestinal ischemia reperfusion (I/R) induces severe injury and significant mortality. New therapeutic interventions are needed; ketamine is an anesthetic with anti-inflammatory properties, which has shown protective effects on I/R in various organs. This study investigated effects of ketamine on intestinal I/R injury. METHODS: Male Wistar rats underwent either sham surgery or 30 min of intestinal ischemia followed by 60 min reperfusion. Ketamine pretreatment was administered by intraperitoneal injections at doses of 100, 50, 12.5, or 6.25 mg/kg. The intestinal morphology, mucosal damage, leukocyte infiltration, serum P-selectin, serum intracellular adhesion molecule-1 (ICAM-1), serum antithrombin-III (ATIII), and myenteric ganglion cell structure were evaluated. RESULTS: Intestinal I/R led to severe mucosal damage, leukocyte (especially neutrophil) infiltration, P-selectin and ICAM-1 elevations, ATIII depletion, and myenteric ganglion cell morphological alterations. The ketamine dose dependently diminished these alterations (except for ICAM-1 serum levels), reaching statistical significance at 100, 50, and 12.5 mg/kg. CONCLUSIONS: Ketamine protects the intestine against I/R injury. Ketamine anesthesia has been recommended for clinical situations of sepsis and hemodynamic instability, both frequent during intestinal I/R. The clinical application of ketamine in situations of intestinal I/R warrants consideration.
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Antagonistas de Aminoácidos Excitatórios/uso terapêutico , Inflamação/prevenção & controle , Intestinos/irrigação sanguínea , Isquemia/tratamento farmacológico , Ketamina/uso terapêutico , Traumatismo por Reperfusão/prevenção & controle , Análise de Variância , Animais , Antitrombina III/análise , Modelos Animais de Doenças , Antagonistas de Aminoácidos Excitatórios/administração & dosagem , Antagonistas de Aminoácidos Excitatórios/farmacologia , Injeções Intraperitoneais , Molécula 1 de Adesão Intercelular/sangue , Intestinos/efeitos dos fármacos , Intestinos/patologia , Isquemia/complicações , Ketamina/administração & dosagem , Ketamina/farmacologia , Masculino , Plexo Mientérico/patologia , Selectina-P/sangue , Ratos , Ratos Wistar , Receptores de N-Metil-D-Aspartato/antagonistas & inibidoresRESUMO
Wallerian degeneration, the self-destructive set of cellular and molecular processes by which degenerating axons and myelin are cleared after injury, is initiated by macrophages and Schwann cells. Molecular inflammatory mediators such as cytokines (IL-1, IL-6, IL-10, and TNF-alpha, among others), transcription factors (NF-kappaB, c-Jun), the complement system and arachidonic acid metabolites have been shown to modulate these processes in various studies. However, the exact role that each of these mediators plays during axonal degeneration and regeneration has not been fully established. Understanding the molecular basis of these interactions between the immune system and peripheral nerve injury would open the possibility of targeting these inflammatory mediators as therapeutic interventions. In this review we attempt to integrate the current evidence generated around this issue, and to explore the therapeutic possibilities that arise.
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Mediadores da Inflamação/fisiologia , Inflamação/fisiopatologia , Regeneração Nervosa/fisiologia , Nervos Periféricos/fisiopatologia , Degeneração Walleriana/fisiopatologia , Animais , Humanos , Inflamação/imunologia , Inflamação/metabolismo , Nervos Periféricos/imunologia , Nervos Periféricos/metabolismo , Degeneração Walleriana/imunologia , Degeneração Walleriana/metabolismoRESUMO
BACKGROUND AND AIMS: Intestinal ischemia/reperfusion (I/R) is a common clinical entity with severe consequences. We studied the effects of ketamine and the participation of the myenteric plexus in I/R injury. METHODS: Rats were divided into six groups: sham, IR (30 min ischemia/60 min reperfusion), KET+IR (50 mg/kg i.p. ketamine injection before I/R), DEN (myenteric plexus ablated with benzalkonium chloride (BAC) and sham operation performed), DEN+IR (BAC treated and I/R induced), and DEN+KET+IR (BAC treated, ketamine administered, and I/R induced). Serum concentrations of p-selectin, intracellular adhesion molecule-1 (ICAM-1), and antithrombin III (ATIII) were measured, and tissue samples were obtained for histological analysis. RESULTS: IR group had higher intestinal mucosa injury and elevated serum concentrations of ICAM-1 and p-selectin, as well as ATIII depletion, compared with sham group (P < 0.05). In KET+IR group these alterations were significantly reduced (P < 0.05). DEN group showed ICAM-1 elevations when compared with sham group (P < 0.05), and DEN+IR group showed no difference in any parameter compared with IR group. However, ketamine administration in group DEN+KET+IR had no effect on any parameter when compared with DEN+IR group. CONCLUSIONS: Ketamine was able to diminish alterations induced by I/R. Myenteric plexus ablation with BAC treatment alone had no effects on intestinal I/R injury. However, this procedure abolished ketamine's protective effects. Ketamine seems to require an intact enteric nervous system to exert its protective action.
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Compostos de Benzalcônio/farmacologia , Intestinos/irrigação sanguínea , Ketamina/farmacologia , Plexo Mientérico/efeitos dos fármacos , Traumatismo por Reperfusão/tratamento farmacológico , Animais , Antitrombina III/metabolismo , Biomarcadores/sangue , Modelos Animais de Doenças , Imuno-Histoquímica , Molécula 1 de Adesão Intercelular/sangue , Molécula 1 de Adesão Intercelular/metabolismo , Mucosa Intestinal/irrigação sanguínea , Mucosa Intestinal/efeitos dos fármacos , Mucosa Intestinal/patologia , Precondicionamento Isquêmico/métodos , Masculino , Selectina-P/sangue , Selectina-P/metabolismo , Distribuição Aleatória , Ratos , Ratos Wistar , Valores de Referência , Traumatismo por Reperfusão/sangue , Traumatismo por Reperfusão/patologia , Sensibilidade e EspecificidadeRESUMO
Intestinal ischemia/reperfusion causes severe injury and alters motility. N-methyl-D-aspartate (NMDA) receptor antagonists have been shown to reduce ischemia/reperfusion injury in the nervous system, and in other organs. In this study, we set out to investigate the effects of NMDA receptor antagonists over intestinal ischemia/reperfusion injury. Male Wistar rats were randomly divided into four groups: (1) a control, sham-operated group; (2) an intestinal ischemia/reperfusion group subjected to 45 min ischemia and 1h reperfusion; (3) a group treated with 10 mg/kg ketamine before ischemia/reperfusion; and (4) a group treated with 10 mg/kg memantine before ischemia/reperfusion. Intestinal samples were taken for histological evaluation. Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), malondialdehyde (MDA), total antioxidant capacity, tumor necrosis factor alpha (TNF-alpha), P-selectin and antithrombin III (ATIII) were measured. Intestinal transit time was determined to evaluate intestinal motility. Fecal pellet output and animal weight were also registered daily for 7 days post-ischemia. After reperfusion, AST, LDH, TNF-alpha and P-selectin levels were elevated, ATIII levels were depleted, and ALT levels were unchanged in serum. Additionally, levels of MDA were increased and total antioxidant capacity was reduced in serum, indicating oxidative stress. Intestinal mucosa showed severe injury. Ketamine, but not memantine, diminished these alterations. Intestinal motility and fecal pellet output were also altered after ischemia/reperfusion. Both drugs abolished the alterations in motility. In conclusion, ketamine's protective effects over ischemia/reperfusion do not appear to be NMDA mediated, but they could be playing a role in protecting the intestine against ischemia-induced functional changes.
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Intestinos/efeitos dos fármacos , Intestinos/patologia , Ketamina/farmacologia , Memantina/farmacologia , Receptores de N-Metil-D-Aspartato/antagonistas & inibidores , Traumatismo por Reperfusão/prevenção & controle , Alanina Transaminase/sangue , Animais , Antioxidantes/metabolismo , Antitrombina III/metabolismo , Aspartato Aminotransferases/sangue , Biomarcadores/sangue , Peso Corporal/efeitos dos fármacos , Fezes , Motilidade Gastrointestinal/efeitos dos fármacos , Mucosa Intestinal/efeitos dos fármacos , Mucosa Intestinal/metabolismo , Mucosa Intestinal/patologia , Intestinos/fisiopatologia , L-Lactato Desidrogenase/sangue , Masculino , Malondialdeído/sangue , Estresse Oxidativo/efeitos dos fármacos , Selectina-P/sangue , Ratos , Ratos Wistar , Traumatismo por Reperfusão/sangue , Traumatismo por Reperfusão/patologia , Traumatismo por Reperfusão/fisiopatologia , Fatores de Tempo , Fator de Necrose Tumoral alfa/sangueRESUMO
The inflammatory response appears to be essential in the modulation of the degeneration and regeneration process after peripheral nerve injury. In injured nerves, cyclooxygenase-2 (COX-2) is strongly upregulated around the injury site, possibly playing a role in the regulation of the inflammatory response. In this study we investigated the effect of celecoxib, a COX-2 inhibitor, on functional recovery after sciatic nerve crush in rats. Unilateral sciatic nerve crush injury was performed on 10 male Wistar rats. Animals on the experimental group (n = 5) received celecoxib (10 mg/kg ip) immediately before the crush injury and daily for 7 days after the injury. Control group (n = 5) received normal saline at equal regimen. A sham group (n = 5), where sciatic nerve was exposed but not crushed, was also evaluated. Functional recovery was then assessed by calculating the sciatic functional index (SFI) on days 0,1,7,14 and 21 in all groups, and registering the day of motor and walking onset. In comparison with control group, celecoxib treatment (experimental group) had significant beneficial effects on SFI, with a significantly better score on day 7. Anti-inflammatory drug celecoxib should be considered in the treatment of peripheral nerve injuries, but further studies are needed to explain the mechanism of its neuroprotective effects.
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A series of seven patients with severe hypertriglyceridemia (triglyceride levels > 1000 mg/dL) is presented. Four of the patients were diabetics, two of them were in treatment with anti-retroviral drugs, and three of them presented acute pancreatitis. In all patients intravenous infusion of insulin was initiated at a rate of 0.05-2 U/kg/day. Two and a half days after this treatment, the serum triglyceride level remained lower than 400 mg/dL. There were no complications during the treatment. The long treatment included basal insulin, fibrates and avoidance of pharmacotherapy. Insulin therapy for diabetic and non-diabetic patients with severe hypertriglyceridemia is an effective and safe treatment.