Journal of anesthesia
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Journal of anesthesia · Sep 1994
Therapy with antibody to tumor necrosis factor against endotoxin shock in rabbits.
The purpose of this study was to determine the efficacy of treatment with anti-tumor necrosis factor (TNF) antibody in preventing the deleterious effects of endotoxin. Polyclonal anti-TNF antibody was produced by immunizing rabbits. Experiments were carried out on 16 rabbits intravenously infused with the lethal dose of lipopolysaccharide (LPS). ⋯ Prominent histopathological changes in the liver and kidney were evident in the LPS group. In contrast, pathologic changes in the tissue from the anti-TNF antibody group were considerably less prominent. These results support the idea that TNF plays a central role in mediating the pathophysiologic changes during endotoxin shock.
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Journal of anesthesia · Sep 1994
The effect of pentobarbital sodium on the dorsal horn of the spinal cord.
The effect of intravenously administered pentobarbital sodium on the activity of single unit in Rexed lamina V of the transected feline lumbar spinal cord was studied using an extracellular microelectrode recording technique. Pentobarbital sodium 1.0 mg·kg(-1), 2.5 mg·kg(-1), and 5.0 mg·kg(-1) administered intravenously suppressed both the spontaneous and the evoked activity in Rexed lamina V cells, known to respond principally to noxious stimuli, in a dose-dependent manner. ⋯ We conclude that pentobarbital sodium intravenously administered has a suppressive effect on single unit activity of cells in Rexed lamina V and probably has an analgesic effect. Its suppressive effect is dose-dependent.
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Journal of anesthesia · Sep 1994
Nitrous oxide does not depress left ventricular contractility in ischemic rat heart.
The direct effects of nitrous oxide on left ventricular contractility and myocardial oxygen consumption (MVO2) in the ischemic isolated rat heart were studied. The rat heart was isolated and perfused by a Langendorf technique. The aortic stump was cannulated and the heart was perfused with Kumpeis solution bubbled with 95% O2 and 5% CO2 (control phase). ⋯ After 15 min of ischemic phase, the perfusion pressure was increased and the gas mixture was changed to the standard gas mixture (reperfusion phase). Nitrous oxide did not further depress myocardial contractility compared with nitrogen in the ischemic phase, and did not alter MVO2 in the ischemic phase compared with nitrogen. Halothane significantly depressed myocardial contractility and decreased MVO2 in the ischemic phase compared with the control.