The effects of nitroprusside-induced hypotension on cerebral blood flow and cerebral oxygen consumption were investigated in nine patients scheduled for cerebral arterial aneurysm surgery. Anesthesia was maintained with nitrous oxide/oxygen and fentanyl; muscle relaxation was achieved with pancuronium; PaCO2 was maintained at 4.79-5.32 kPa. Mean arterial pressure was reduced to 50 mmHg by nitroprusside infusion after opening of the dura. Measurements were recorded and blood samples were taken 15 min before induction of hypotension, during stable hypotension and 15 min after termination of nitroprusside infusion. Measurements included: cerebral blood flow, using the argon-washin technique, cardiac output (thermodilution), mean arterial pressure and heart rate. Cerebral blood flow averaged 56 +/- 6 min . 100 g before hypotension. Nitroprusside produced hypotension but did not significantly alter cerebral blood flow (61 +/- 7 ml/min . 100 g). Cerebral blood flow remained virtually at preinfusion values upon cessation of infusion (53 +/- 6 ml/min . 100 g). Cerebral oxygen uptake averaged 3 +/- 0.2 ml/min . 100 g before hypotension and did not change significantly during hypotension (3.3 +/- 0.3 ml/min . 100 g) and after termination of hypotension (2.7 +/- -0.3 ml/min . 100 g). In two patients nitroprusside produced a 17 and 20% increase, respectively, in cerebral blood flow with no change in cerebral oxygen consumption, together with a marked increase in cardiac output and heart rate.
The effects of halothane on myocardial blood flow and myocardial oxygen balance were studied in seven male patients with stable angina and normal left ventricular function. Patients were receiving maintenance doses of beta-receptor antagonists and underwent coronary artery bypass surgery. Anaesthesia consisted of halothane and 50% nitrous oxide in oxygen. Halothane decreased myocardial blood flow and myocardial oxygen consumption by 29% and 32%, respectively, after induction of anaesthesia, and during sternotomy. Myocardial lactate production was not observed at any time. Cardiac index, stroke volume index, mean arterial pressure and mean diastolic arterial pressure were decreased significantly after induction of anaesthesia and during sternotomy. Heart rate remained unchanged. The global myocardial oxygen supply and demand relationship was maintained. The results suggest that halothane is a safe anaesthetic for coronary revascularization in patients with unimpaired left ventricular function.
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