• P M Patel and W A Mutch.
• Department of Anaesthesia, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
• Anesthesiology. 1990 Jan 1; 72 (1): 118-24.

AbstractThe influence of different vasopressors on the cerebral pressure-flow relationship during 1.0 MAC isoflurane anesthesia has been studied. Mean arterial pressure (MAP) was increased by one of three vasopressors [angiotensin II (AT), norepinephrine (NE), or phenylephrine (PE)] in three groups of New Zealand white rabbits (n = 11, 10, and 9, respectively). Regional cerebral blood flow (CBF) was measured at five intervals by the injection of radioactive microspheres at a stable 2.05% (1.0 MAC) end-tidal isoflurane concentration (baseline) and following elevation of mean arterial pressure (MAP) by 20%, 40%, 60%, and 80% above baseline MAP with either AT, NE, or PE. Baseline MAP was the same in all groups. No differences in MAP were seen between groups when MAP was elevated from 20% to 80% above baseline. Normocapnia (PaCO2 35.8-38.2 mmHg) was maintained throughout. Total cerebral blood flow (tCBF), hemispheric CBF (hCBF), and posterior fossa (cerebellum and brain stem) CBF (pCBF) were determined. Baseline tCBF, hCBF, and pCBF was similar in all groups. For each experiment a pressure-flow curve was generated by curvilinear regression analysis. Mean slopes and intercepts were derived for each group. For all regions examined, the slope of the pressure-flow curve was significantly less steep when MAP was elevated with AT versus NE or PE (P less than 0.05 Tukey's studentized range test). There was no difference in slope between the NE and PE groups for any region. These results indicate that either NE and PE result in indirect cerebral vasodilation or that AT has intrinsic cerebral vasoconstrictive effects during 1.0 MAC isoflurane anesthesia in the rabbit.(ABSTRACT TRUNCATED AT 250 WORDS)

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