Regional distribution of brain and myocardial perfusion in swine while awake and during 1.0 and 1.5 MAC isoflurane anaesthesia produced without or with 50% nitrous oxide.

Abstract

Isoflurane has been hailed as the anaesthetic of the eighties. We examined the effects of isoflurane anaesthesia on regional distribution of brain and myocardial blood flow in 11 healthy isocapnic pigs using 15 micron diameter radionuclide labelled microspheres that were injected into the left atrium. Each animal was studied during five of the following six conditions: (i) unanaesthetised (control; n = 8); (ii) 1.45% end-tidal (ET; 1.0 MAC) isoflurane anaesthesia (n = 10); (iii) 2.18% ET (1.5 MAC) isoflurane anaesthesia (n = 9); (iv) 0.95% ET isoflurane + 50% N2O anaesthesia (equivalent to 1 MAC; n = 8); (v) 1.68% ET isoflurane + 50% N2O anaesthesia (equivalent to 1.5 MAC; n = 8); and (vi) 50% N2O alone (n = 8). The order of anaesthetised steps was randomised for each pig. At every step 50 to 55 min were allowed for equilibration with isoflurane, and for N2O 35 to 40 min were allowed for equilibration. Recovery periods of 60 min each were interposed between anaesthetised steps to allow pigs to recover towards control values. Control values of blood flow in the cerebrum, cerebellum, and brain-stem were 81 +/- 5, 87 +/- 8, and 64 +/- 6 ml X min-1 X 100 g-1, respectively. During 1.45% isoflurane anaesthesia, cerebral, cerebellar and brainstem blood flows were 120%, 152%, and 145% of respective control values. With 2.18% isoflurane, perfusion in these regions of the brain was 140%, 200%, and 226% of respective control values. Substitution of 50% N2O to maintain equipotent anaesthesia markedly exaggerated the increment in cerebral blood flow, while changes in cerebellar and brain-stem blood flow were similar. Cerebral blood flow during 0.95% isoflurane + 50% N2O and 1.68% isoflurane + 50% N2O anaesthesia was 137% and 210% of the control value, respectively. Regional brain blood flow was only insignificantly altered by 50% N2O alone. It is concluded that isoflurane caused dose-dependent vasodilatation in all regions of the brain, the magnitude being greater in the cerebellum and the brain-stem. The administration of N2O with isoflurane to maintain equipotent anaesthesia exaggerated cerebral vasodilatation, especially at deeper level of anaesthesia. Myocardial blood flow in isoflurane anaesthetised pigs decreased, especially in the inner layers, in a dose-related manner. The use of 50% N2O with isoflurane permitted higher heart rate, perfusion pressure, rate-pressure product, and transmural myocardial blood flow.