The interaction of sodium nitroprusside, hypotension, and isoflurane in determining cerebral vasculature effects.

Eighteen mongrel dogs were anesthetized with isoflurane and prepared for determining cerebral blood flow (CBF, sagittal sinus outflow), cerebral metabolic rate (CMRO2), and ICP. Dogs were divided into three groups of six each. Group 1 dogs were maintained on 1 MAC isoflurane and, following control measurements (step 1), sodium nitroprusside (SNP) was infused to decrease mean arterial pressure (MAP) to 60 mmHg (step 2). After 20 min SNP was discontinued and a second control period of 20 min followed (step 3). Thereafter, SNP was repeated for 20 min as in step 2, but MAP was maintained by inflating a balloon in the descending aorta (step 4). SNP was again discontinued followed by a final 20 min control period (step 5). During SNP with hypotension (step 2) there was a significant 21% decrease in CBF and no change in ICP. During SNP with normotension (step 4) both CBF and ICP increased (16 and 39%, respectively). In group 2 dogs isoflurane was discontinued and a spinal anesthetic was administered. Thereafter, these dogs were studied as in group 1. The only significant change in these dogs was a 35% increase in ICP during SNP with normotension. Group 3 dogs were studied identically to group 2, but hypotension was induced with trimethaphan (TMP). There were no significant changes in these dogs. The authors conclude that SNP, in the absence of isoflurane, dilates capacitance vessels because ICP increased without a concomitant increase in CBF at normotension. In the presence of isoflurane, SNP dilates both capacitance and resistance vessels because ICP and CBF increased concomitantly at normotension.(ABSTRACT TRUNCATED AT 250 WORDS)