We have studied the effects of i.v. bolus doses of magnesium sulphate (MgSO4) 60, 90 and 120 mg kg-1 on haemodynamic state, the coronary circulation and myocardial metabolism in nine dogs anaesthetized with pentobarbitone and fentanyl. MgSO4 produced dose-dependent decreases in arterial pressure, heart rate, left ventricular dP/dtmax and left ventricular minute work index (LVMWI) and an increase in the time constant of left ventricular isovolumic relaxation. Stroke volume increased, systemic vascular resistance decreased and cardiac output did not change significantly. MgSO4 produced decreases in coronary perfusion pressure, coronary vascular resistance and myocardial oxygen consumption (MVO2). Coronary sinus blood flow, lactate extraction ratio and the ratio of LVMWI to myocardial MVO2, that is an index of cardiac efficiency, did not change significantly. This study indicated that the depressant effect of MgSO4 on cardiac function was offset by lowering of peripheral vascular resistance, so that cardiac pump function remained effective, and the almost constant coronary sinus blood flow resulted from the decrease in coronary vascular resistance even at higher doses.

We studied the responses of plasma epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH), cortisol, and antidiuretic hormone (ADH) during and immediately after sevoflurane-nitrous oxide anaesthesia supplemented with vecuronium in seven elderly patients (mean 76.6 408.6 • 135.5 pg" ml -t, 635.7 • 167.8 pg" ml -J, 222.6 • 48.0 pg" m1-1, and 113.6 • 67.5 #g" d1-1, respectively 408,6 + 135,5 pg" d1-1, 635,7 • 167,8 pg" ml -~, 222,6 + 48,0 pg' ml -j, et de 113,6 + 67,5 t~g' dl -t imm~diatement aprbs l~ntubation (P < 0,05

It is not known how sevoflurane affects the cardiac conduction system. We compared the effects of halothane, isoflurance, and sevoflurane on specialized atrioventricular (AV) conduction times in eight pentobarbital-anesthetized dogs. AV conduction times with three inhaled anesthetics at end-tidal concentrations of 1 and 2 minimum alveolar anesthetic concentration (MAC), were measured by His-bundle electrocardiography during both sinus rhythm and right atrial pacing at a slightly higher rate than sinus one. Heart rate and arterial pressure were simultaneously recorded. Halothane prolonged AV nodal conduction time during sinus rhythm (A-H interval) at 2 MAC compared with the control value, whereas isoflurane and sevoflurane did not alter the A-H interval, His-Purkinje conduction time (H-V interval), and ventricular conduction time (H-S interval) during sinus rhythm at 1 and 2 MAC. All three inhaled anesthetics did not change AV conduction times during right atrial pacing. No significant difference in AV conduction times was observed between isoflurane and sevoflurane. Heart rate during sinus rhythm remained unchanged despite a decrease in arterial pressure with three inhaled anesthetics. The property of sevoflurane and isoflurane which does not affect the cardiac conduction system may be important in the stability of the cardiac rhythm during anesthesia with these drugs.

We have studied the effects of a 30-min infusion of propofol 6, 9, 12, 15, 18 and 21 mg kg-1 h-1 on cardiovascular haemodynamics, coronary circulation and myocardial metabolism in 12 mongrel dogs. Mean plasma concentrations of propofol after infusion of 6 and 21 mg kg-1 h-1 increased from 2.9 (SEM 0.3) to 11.5 (0.1) micrograms ml-1. Propofol produced a progressive decrease in arterial pressure. Heart rate tended to decrease at 15, 18 and 21 mg kg-1 h-1 and cardiac index decreased significantly at infusion rates > or = 9 mg kg-1 h-1. Systemic vascular resistance tended to increase except at 21 mg kg-1 h-1 and left ventricular systolic and diastolic function were depressed. Both coronary sinus blood flow and myocardial oxygen consumption decreased in parallel with a decrease in left ventricular minute work index without producing lactate. Propofol produced progressive decreases in coronary blood flow and myocardial oxygen consumption but did not exert adverse effects on the coronary circulation.

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