Splanchnic Circulation During Halothane Anesthesia and Hypercapnia in Normal Man

Abstract

In 9 normal adult men the administration of halothane caused significant alterations in splanchnic hemodynamics which could not be attributed to hypoxia, hypercapnia, hypothermia or surgical stimulation. Halothane caused a reduction of splanchnic perfusion pressure with a parallel fall in splanchnic blood flow. There was no significant change in splanchnic vascular resistance. Intermittent positive pressure respiration was required in only 3 subjects and did not appear to contribute importantly to the results. Administration of carbon dioxide produced striking increases in the splanchnic blood flow associated with a significant fall in the splanchnic vascular resistance. The perfusion pressure was unchanged. The data suggest that halothane interferes with the expected splanchnic vasoconstriction normally seen when hypotension or hypercapnia would be expected to produce sympathetic activation. The degree of vasodilatation produced by carbon dioxide and the resulting increase in average blood flow suggest that hepatic ischemia is not an important cause of hepatic dys-function following halothane anesthesia complicated by hypercapnia.