• W E Hoffman, G Edelman, R Ripper, and H M Koenig.
• Department of Anesthesiology, University of Illinois at Chicago, 60612, USA. whoffman@uic.edu
• Anesth. Analg. 2001 Jul 1; 93 (1): 166-70.

UnlabelledWe compared sodium nitroprusside (SNP)-induced hypotension with 3% isoflurane-induced hypotension with regard to brain tissue oxygen pressure (PtO(2)), middle cerebral artery (MCA) blood flow, and cerebral arteriovenous shunting. Eight dogs were anesthetized with 1.5% isoflurane. After a craniotomy, a probe was inserted into the left frontoparietal brain cortex to mea-sure tissue gases and pH. Blood flow was measured in a secondary branch of the MCA by a flowprobe. Measurements were made during baseline 1.5% isoflurane, during 1.5% isoflurane and SNP-induced hypotension or 3% isoflurane-induced hypotension to a mean pressure of 60-65 mm Hg, and during continued treatment with SNP or 3% isoflurane with blood pressure support to baseline levels with phenylephrine. Shunting was calculated from arterial, sagittal sinus, and tissue (indicating capillary) oxygen content. During hypotension with SNP, PtO(2) decreased 50%, and shunting increased 50%. During hypotension with 3% isoflurane, PtO(2) and shunting did not change. Blood pressure support increased PtO(2) and MCA flow during both SNP and 3% isoflurane treatment. These results show that SNP is a cerebrovasodilator but that hypotension will decrease PtO(2), probably because of an increase in arteriovenous shunting and a decrease in capillary perfusion.ImplicationsWe measured brain arteriovenous shunting and tissue oxygen pressure(PtO(2))during a 40% decrease in blood pressure induced by sodium nitroprusside (SNP)or 3% isoflurane. Large-dose isoflurane maintainedPtO(2) with no change in shunting. SNP infusion decreasedPtO(2) 50%and increased shunting 50%. This suggests that SNP-induced hypotension decreases PtO(2) because of a decrease in capillary perfusion.

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