Canine systemic and cerebral effects of hypotension induced by hemorrhage, trimethaphan, halothane, or nitroprusside.
In 62 dogs, hypotension to a mean arterial pressure of either 40 or 50 torr (equivalent to a cerebral perfusion pressure of 30 or 40 torr, respectively) for one hour was induced by hemorrhage (oligemia), trimethaphan, halothane, or sodium nitroprusside. Before and during the period of hypotension, the following were measured: mean arterial blood pressure, cardiac output, whole-body O2 consumption, cerebral blood flow, cerebral O2 consumption, arterial blood gases, blood O2 content, and lactate, pyruvate, glucose, epinephrine, and norepinephrine concentrations. At the end of the period of hypotension, brain biopsies were taken for determination of adenosine triphosphate, phosphocreatine, lactate, and pyruvate concentrations. In an additional eight dogs following one hour of hypotension (at 40 torr) induced by one of the four techniques, the brains were perfused with carbon black, removed, and examined. In another ten dogs following hypotension (at 40 torr) induced with either halothane or trimethaphan, the animals were observed for three days and then killed for examination of the brain. Dogs maintained at a mean arterial pressure of 40 torr, despite differences in cerebral blood flow, demonstrated metabolic disturbances compatible with systemic and cerebral hypoxia. These were greatest in those dogs given nitroprusside in excess of 1.0 mg/kg, presumably due to cyanide toxicity. In dogs maintained at 50 torr, metabolic disturbances were minimal or absent in the halothane- and nitroprusside-treated dogs but were still apparent in the oligemic and trimethaphan-treated dogs. Carbon black infusions revealed no evidence of non-homogeneous flow. Three of the ten dogs observed for three days had persistent post-hypotension neurologic dysfunction. Two of these were given trimethaphan. The results suggest that the systemic and cerebral effects of halothane and nitroprusside (at doses less than 1.0 mg/kg) are similar and at a mean arterial pressure of 50 torr are of little consequence. By contrast, hypotension induced by trimethaphan or oligemia results in detectable metabolic alterations even at a pressure of 50 torr.
D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D004285:Dogs; D005292:Ferricyanides / Q000494:pharmacology*; D006221:Halothane / Q000494:pharmacology*; D006439:Hemodynamics / Q000187:drug effects; D006454:Hemoglobins / Q000378:metabolism; D006470:Hemorrhage / Q000150:complications*; D007022:Hypotension / Q000139:chemically induced / Q000209:etiology / Q000503:physiopathology*; D007773:Lactates / Q000378:metabolism; D009599:Nitroprusside / Q000494:pharmacology*; D010725:Phosphocreatine / Q000032:analysis; D014294:Trimethaphan / Q000494:pharmacology*
D005292:Ferricyanides; D006454:Hemoglobins; D007773:Lactates; D010725:Phosphocreatine; D009599:Nitroprusside; D014294:Trimethaphan; D000255:Adenosine Triphosphate; D006221:Halothane