Arrhythmic doses of epinephrine and dopamine during halothane, enflurane, methoxyflurane, and fluroxene anesthesia in goats.

The cardiac arrhythmicity of epinephrine and dopamine was compared in awake goats and during approximate equivalent levels of halothane, enflurane, methoxyflurane, and fluroxene anesthesia. The arrhythmic threshold dose for epinephrine and dopamine was significantly (p less than 0.05) reduced during halothane anesthesia when compared to values determined in awake animals. Enflurane anesthesia had no significant affect on the arrhythmic threshold dose for either catecholamine. However, methoxyflurane and fluroxene anesthesia significantly (p less than 0.05) elevated the arrhythmic threshold dose for dopamine. Epinephrine produced greater elevations in mean arterial pressure than dopamine with all anesthetics except enflurane, and dopamine produced significantly (p less than 0.05) higher heart rates in the awake animals and those anesthetized with halothane and enflurane. The authors conclude that, in terms of arrhythmic potential, there is no advantage in the use of dopamine rather than epinephrine for the reversal of halothane-induced myocardial depression during halothane or enflurane anesthesia.

Sodium nitroprusside and cerebral blood flow in the anesthetized and unanesthetized goat.

The effects of dodium nitroprusside (SNP) on total, ipsilateral cerebral blood flow (CBF) in the unanesthetized and anesthetized goat was evaluated under four conditions: 1) bolus injection of SNP into the cerebral circulation via the temporal artery; 2) continuous infusion of SNP into the temporal artery in amounts too small to affect the peripheral circulation (0.57-1.14 mug/kg/min); 3) intravenous infusion of SNP; 4) continuous intravenous infusion of SNP with a bolus injection af angiotensin. Small doses (20, 40, and 80 mug) of SNP injected directly in the cerebral circulation of the awake goat produced immediate increases of 21 +/- 8, 36 +/- 8, and 48+/- 10 per cent, respectively, in CBF lasting 1 to 3 min without causing peripheral cardiovascular changes. The effects of SNP were attenuated by 1.5 per cent halothane anesthesia. Continuous infusion of SNP into the temporal artery in amounts too small to cause peripheral cardiovascular effects produced sustained increases in CBF averaging 31+/- 8 percent; CBF returned to preinfusion values upon cessation of infusion. Intravenous infusion of SNP in both anesthetized and unanesthetized animals in recommended clinical dosages (3-8 mug/kg/min) produced hypotension but did not significantly alter CBF. However, upon injection of angiotensin (1.43 mug/kg), both peripheral blood pressure and CBF increased sharply, suggesting that SNP may impair autoregulation of CBF. The results of this study indicate that SNP dilates the cerebral vascular system in a way that is probably similar to its effects on other vascular beds.

The effect of pancuronium on myocardial contraction and catecholamine metabolism.

The effects of pancuronium bromide infusion on the uptake and release of [14C] noradrenaline (14C-NA) by the isolated, perfused rat heart and on the chronotropic and inotropic activity of the isolated heart were evaluated. Hearts were removed from animals under light ether anaesthesia, transferred to a modified Langendorff perfusing apparatus and perfused with Krebs-Ringer bicarbonate solution at a rate of 5 ml min-1. The effect of pancuronium on the uptake of noradrenaline was determined by perfusing hearts for 5 min with perfusate containing various concentrations of pancuronium and 200 ng ml-1 of 14C-NA. After 5 min pancuronium-treated hearts contained less 14C-NA. The degree of reduced uptake increased with increasing concentrations of pancuronium. In addition, the combination of pancuronium perfusion and electrical stimulation (15 mA for 10 ms at 4 Hz) blocked the 50 min uptake of 14C-NA by the heart to a greater degree than either factor separately. The release of noradrenaline was determined after perfusing hearts with 14C-NA followed by perfusion with solution containing pancuronium but no 14C-NA for 1 h. Pancuronium infusion did not significantly alter the release of 14C-NA from the heart after 1 h of perfusion. The infusion of pancuronium caused a reduction in both the rate and strength of myocardial contraction of the isolated heart which was reversed by perfusion with perfusate free of pancuronium. Following perfusion with pancurnium the rate and strength of contraction of the heart was seen to "rebound" above pre-pancuronium values for a short period. The rebound of myocardial rate and contraction may have been due to the presence of myocardial noradrenaline previously blocked from reuptake by pancuronium since hearts removed from reserpinized animals did not demonstrate "rebound."