Anesthesiology
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The effect of hypocapnia on autoregulation of cerebral blood flow (CBF) and the lower limit of autoregulation (LLA) was determined in dogs anesthetized with nitrous oxide (66%) and halothane (0.2%, end-expired concentration). CBF and cerebral vascular resistance (CVR) were determined during both normocapnia and hypocapnia (PaCO2 21-22 mmHg) at control cerebral perfusion pressure (CPP) and after reducing CPP (by hemorrhage) to 80%, 60%, 50%, and 40% of control. At control CPP hypocapnia decreased CBF from 75 +/- 5 to 48 +/- 3 ml.100 g-1.min-1 (mean +/- SEM, P less than 0.05). ⋯ Below the LLA the CBF-CPP slopes differed from zero but did not differ between hypocapnia and normocapnia. Hypocapnia does not produce a substantial shift of the LLA, and over the range of CPP values studied here, autoregulatory cerebral vasodilation only partially abolishes hypocapnia-induced cerebral vasoconstriction. The results suggest that when cerebral autoregulation is intact and in the absence of cerebrovascular disease, hypocapnia does not reduce global CBF to a level that is likely to produce ischemia and remains a useful therapeutic treatment so long as CPP remains above the LLA.
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Hypocapnia and induced hypotension have been claimed by some to cause cerebral hypoxia because of insufficient perfusion. Regional cerebral blood flow (rCBF) and regional cerebral glucose utilization (rCMRglc) were measured simultaneously in the same animal subjected to hypocapnia or hypocapnia combined with induced arterial hypotension. The rCMRglc was measured with (3H) deoxyglucose and the rCBF with (14C) iodoantipyrine with the use of tissue biopsy methods and scintillation counting. ⋯ Although hypocapnia alone did not cause a statistically significant decrease of rCBF except in hippocampus, hypocapnia combined with hypotension resulted in a significant reduction of rCBF in four of seven regions when compared with hypocapnia alone; rCMRglc values were unchanged during hypocapnia. However, the addition of hypotension induced by adenosine led to a significant decline of glucose utilization in five of seven brain regions. In the present study the authors observed no increase of regional glucose utilization and hence no signs of cerebral ischemia during hypocapnia alone or combined with hypotension induced by adenosine.
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Comparative Study
The dose-response relationship of mivacurium chloride in humans during nitrous oxide-fentanyl or nitrous oxide-enflurane anesthesia.
The dose-response relationships of mivacurium chloride during N2O/fentanyl or N2O/enflurane anesthesia were compared in 70 patients intraoperatively. Responses were defined in terms of percentage changes in the evoked twitch tension of the adductor pollicis muscle, and dose-response curves were constructed following probit transformation of the responses. End-tidal concentrations of enflurane during the were study were 0.9-1.2%. ⋯ Regression lines describing the relationship between the maximum depression of twitch tension (response) and the time interval between the injection of mivacurium and the return of twitch tension to 90% of the control value (duration) were constructed. The response-duration line for N2O/enflurane anesthesia was displaced significantly to the left of the line for N2O/fentanyl (P less than 0.05), indicating that enflurane anesthesia was associated with a prolongation of mivacurium-induced neuromuscular blockade. The neuromuscular blocking effect of mivacurium is both enhanced by and prolonged during N2O/enflurane compared with that during N2O/fentanyl anesthesia.