The cerebral response to sodium nitroprusside and trimethaphan controlled hypotension.

THE EFFECTS of altered arterial blood pressure on cerebral blood flow ( CBF ) have been well documented by Lassen 1'2 and Olesen 3 in man, and by Rapela, 4 Waltz ~ and Yashon 6 in dogs. The critical determinants of cerebral blood flow are the cerebral perfusion pressure (CPP) and the cerebrovascular resistance (CVR). The CPP is the difference between the driving force of the mean arterial pressure and the intracranial pressure, or the intracranial venous pressure. It has been shown that CBF remains constant over the range from 60 to more than 150 mm Hg 2. This ability to keep CBF constant in the face of altered perfusion pressure has been termed auto-regulation. Below 60 mm Hg, cessation of autoregulation has been shown by Lassen, 2 Finnerty, 7 and Sokoloff. s It is assumed that this is due to the loss of change in vascular resistance when maximal vasodilatation is present. As an adjunct to neurosurgical anaesthesia, pharmacological agents have been used to lower perfusion pressure while maintaining CBF and autoregulation. Sodium nitroprusside and trimethaphan are two agents used to produce controlled hypotension by alterations in vascular resistance. The purpose of this study was to compare the changes in CBF, cerebral metabolic oxygen consumption (CMRO,~), CVR, and cardiac output (CO) with sodium nitroprusside and trimethaphan. Based on these results, a delineation of the safe limits for controlled hypotension would be made.