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Changes in plasma potassium concentration after administration of depolarizing neuromuscular blockers were measured in patients during halothane-nitrous oxide anaesthesia. Suxamethonium 100 mg intravenously caused a peak rise of 0.55 m.equiv/1. and decamethonium 4 mg produced an elevation of similar magnitude. Injured patients had increases in potassium averaging 1.80 m.equiv/1. there being a direct correlation between degree of rise and time since injury. By giving tubocurarine 0.1 mg/kg body weight 5 minutes beforehand, the elevation in potassium caused by suxamethonium, though not by decamethonium, could be halved.

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Some effects of the /3-adrenergic receptor blocker, propranolol, were studied in 20 normal, fasting, conscious men. The measurements made included cardiac output, splanchnic blood flow and oxygen consumption, arterial and hepatic venous blood pressure, and heart rate. The intravenous administration of propranolol (0.13 mg/kg) was followed by significant reductions in splanchnic blood flow and oxygen consumption, in cardiac output and in heart rate. Splanchnic perfusion pressure was unchanged; the splanchnic vascular resistance was significantly elevated. Previous treatment with glucose did not alter these findings. Phenoxybenzamine prerreatment lessened the increase in splanchnic vascular resistance which propranolol ordinarily caused. Ganglionic blockade with hexamethonium prevented all of the changes which propranolol produced in untreated individuals. These results may best be explained by assuming that the splanchnic circulation in man is influenced both by a receptors, which cause vasoconstriction when activated, and by /9 receptors, which when activated cause vasodilatation and increase oxygen consumption.ADDITIONAL KEY WORDS alpha-adrenergic receptor blockade splanchnic vascular resistance beta-adrenergic receptor blockade propranolol hexamethonium splanchnic oxygen consumption phenoxybenzamine• One of us has reported (1) that the administration of propranolol (a /3-adrenergic receptor blocking drug of high specificity) to human subjects anesthetized with cyclopropane caused a marked reduction in splanchnic blood flow. This reduction resulted from increased vascular resistance and was usually accompanied by a diminution in local oxygen consumption. Since cyclopropane is believed to increase the impulse frequency in sympathetic nerves supplying the abdominal viscera (2), these observations raised the question whether some of the activity