摘要:

ABSTRACT—The present study compared hemodynamic response to hypertonic saline (HTS; NaCI 8.0%) treatment of uncontrolled hemorrhage from a stab injury in the abdominal aorta (A) or vena cava (V), respectively. The hypothesis was challenged that adverse effects of HTS treatment is dependent on the pressure load in the lesioned vessel. Uncontrolled hemorrhage was produced in anesthetized rats by vessel puncture with a syringe needle. After 10 min of hemorrhage, subjects were randomized to HTS infusion, 2.0 mL/Kg i.v. given at .4 mL/min (AHTS, n = 10 and VHTS, n = 10), or to no treatment (AC, n = 12 and VC, n = 7). Mean arterial pressure (MAP), heart rate, plasma electrolytes, protein, and hematocrit were recorded continuously for 240 min. HTS treatment produced MAP elevation but did not influence the final outcome in either A or V lesions. Thus, evidence of worsened outcome related to HTS treatment was not confirmed. However, one-half of all subjects with arterial hemorrhage died, compared to only 1 of 17 subjects with venous hemorrhage. Spontaneous MAP recovery during hemorrhage, and MAP response to HTS treatment, were shown to have predictive value for survival.

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ABSTRACT-The objective of this study was to demonstrate nitric oxide (NO) production and determine its role in the rat small intestine following endotoxin treatment. By using electron paramagnetic resonance (EPR) spectroscopy, we were able to detect high concentrations of nitrosylated proteins in the small intestines of rats administered 1 mg/kg lipopolysaccharide (LPS) and sacrificed 6 h later. EPR spectra of non-heme and heme nitrosyl complexes were detected in the epithelium layer and intestinal wall. Only EPR spectra characteristic of nitrosyl hemoprotein complexes were detected in the luminal contents of these rats. LPS administration elevated the concentrations of intestinal lipid peroxidation biomarkers, thiobarbi-turic acid-reactive substances, and conjugated dienes. These changes were attenuated by NO synthase inhibitor treatment. We conclude that oxidants associated with NO formation were at least in part involved in the oxidation of tissue lipids. This process may be one of the mechanisms of intestinal injury induced by LPS.

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ABSTRACT—Dichloroacetate (DCA), an activator of pyruvate dehydrogenase (PDHC), enhances postischemic mechanical recovery of isolated hearts. It is not known whether this is secondary to reduced infarction or preservation of contractile function in viable cardiomyocytes. This study investigated the effect of DCA on myocardial infarct size. Anesthetized open chest rabbits underwent regional coronary occlusion and reperfusion. DCA (300 mg/kg plus 150 mg/kg 1 h later) was administered intravenously either before occlusion (DCA-O; n = 8) or at reperfusion (DCA-R; n = 7). Control rabbits (n = 8) received saline vehicle. Myocardial PDHC activity was measured after administration of 300 mg/kg i.v. DCA in 10 separate rabbits. DCA reduced plasma lactate levels and increased PDHC activity by 76%, from 2.79 ± .30 μmol/min-g-1to 4.92 ± .44 μmol/min-g-1(p< .005). However, infarct size in DCA-treated animals was not significantly different from Control (60 ± 5% DCA-O, 57 ± 6% DCA-R, 58 ± 7% Control). We conclude that stimulation of pyruvate dehydrogenase does not limit infarct size.

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ABSTRACT—The functional capacity of the hepatic reticuloendothelial system (RES) was studied under conditions of intestinal shock. Wistar rats underwent intestinal ischemia (60 min)-reperfusion or a sham procedure. One-half of each group received intravenous infusion of 2.6 x 10-6g/kg lipopolysaccharide B. Phagocytic clearance and phagocytic killing by the hepatic RES were quanitited using a double label bacteria clearance assay. Hepatic phagocytosis was unchanged 3 h after reperfusion of the ischemic intestine but hepatic killing was significantly decreased compared with the sham situation. The results were not different in animals who had received LPS B infusion. The plasma endotoxin levels correlated inversely to the hepatic killing efficiency (r = -.081) in the shocked animals given exogenous endotoxin. The decreased capacity of the hepatic RES to degrade bacteria present in the portal circulation could be an important pathophysiologic mechanism in the development of bacterial translocation.

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID