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The effect of metabolic and hypercapnic acidosis on myocardial blood flow was studied during intravenous infusions of hydrochloric acid solutions (n = 12) and during passive ventilation with 5% CO2 (n = 5) in anaesthetized, closed chest dogs. Below a pH of 7.2 metabolic acidosis at normal arterial CO2-tensions caused an increase of coronary blood flow and a decrease of coronary vascular resistance associated with a narrowed myocardial arteriovenous O2-difference, indicating vasodilation at unchanged myocardial oxygen consumption. In propranolol-pretreated dogs myocardial blood flow and coronary oxygen AV difference remained unaffected, suggesting that the coronary dilatory effect of metabolic acidemia involves beta adrenergic stimulation. Coronary vasodilation induced by increasing arterial pCO2 was found to the significantly greater as compared with the dilatory effect of metabolic acidosis at the same blood pH level. Blocking of beta receptors did not reduce the coronary response to increased arterial CO2-tensions. It is concluded that the coronary vasodilation observed during hypercapnic acidosis is neither mediated by a beta adrenergic stimulation nor dependent of the concomitant change in blood pH. The possible sites of the coronary dilatory actions of increased arterial CO2-tensions are discussed.

Glaxo CT 1341 (Althesin) is a new steroid anaesthetic agent dissolved in Cremophor EL. Its influence on hemodynamics was studied in dogs, especially regarding the myocardial contractility, coronary perfusion and myocardial oxygen consumption.The unpremedicated experimental animals were induced 'with 3 mg/kg piritramide intravenously and normoventilated with a mixture of 70% N20 and 30% 0 2 . All animals were pretreated with a powerful antihistaminic agent (Tavegil") in order to block reactions to histamine released by Cremophor EL. Five hours later the animals received single intravenous doses of Althesin (1.0 and 2.0 mg/kg).Significant hemodynamic changes (P< 0.025-0.0005) were caused by 2.0 mg/kg. Heart rate, cardiac output and mean pulmonary pressure increased, total peripheral resistance decreased; while central venous pressure, mean aortic pressure and renal blood flow remained unchanged. The resulting increased cardiac work caused a rise in coronary blood flow of 88%, an increased myocardial oxygen consumption of 66% and a decreased coronary resistance of 48%. As coronary arteriovenous difference in oxygen decreased slightly, Althesin has coronary dilatory properties. Myocardial depression was seen in a marked fall of dp/dtm.= (the rate of change of the left ventricular pressure) (30%), in a decreased stroke volume and in an increased left ventricular end-diastolic pressure. Maximal hemodynamic responses occurred within the first minute after injection and returned to their preinjection levels after approximately 20 min.A recommended dose in man is 2 mg/kg Althesin Myocardial depression and increased oxygen consumption suggest a cautious use of Althesin in cases of heart and coronary insufficiency.