This review covers three main aspects of adrenergic pharmacology, the role of α-adrenergic activity in cardiac inotropy and coronary vasoconstriction, β-adrenoceptors in heart failure, and α2-adrenoceptor agonists in relation to their anaesthetic effects. Myocardial ischaemia causes a reflex increase in sympathetic activity, largely mediated by α-adrenergic mechanisms, which may cause coronary constriction. There is controversy as to whether this is beneficial in terms of preventing transmural steal, or detrimental in that it can cause distal arteriolar constriction and further ischaemia. The role of α-adrenoceptor antagonists in preventing the latter is discussed. Highly selective α2-adrenoceptor agonists such as dexmedetomidine exert anaesthetic actions in both experimental animals and in man, and can decrease requirements for other anaesthetics. New applications for clonidine, a less selective α2-adrenoceptor agonist, are reviewed together with their mechanisms of action.
Plasma serotonin concentrations, assayed as plasma 5-hydroxyindoles (5-HI) and platelet 5-hydroxytryptamine (5-HT), were measured in 12 patients undergoing coronary artery graft surgery (group 1) and five patients undergoing valve replacement (group 2). Mean values of plasma 5-HI before cardiopulmonary bypass (CPB) were 29.8 +/- 2.0 ng ml-1 in group 1 and 30.6 +/- 2.8 ng ml-1 in group 2. No significant changes of plasma 5-HI occurred during or after CPB in either group. Although postoperative hypertension occurred in 75% of group 1 patients, no significant correlation was found between plasma 5-HI concentration and systolic blood pressure. A significant increase of platelet 5-HT occurred during bypass (327 ng/2 X 10(8) platelets increasing to 488 ng/2 X 10(8) platelets, p less than 0.01) but returned to baseline values postoperatively. We conclude that plasma 5-HI concentrations are not involved in the pathophysiology of postoperative hypertension following myocardial revascularization.
Cardiovascular effects of nitrous oxide during enflurane anesthesia were studied in 12 healthy, young volunteer subjects ventilated to maintain normal PaC0]. Twelve circulatory variables were measured and 13 more calculated. When nitrogen, 70 per cent, was added to enflurane, 1.86 per cent (1 MAC), or enflurane, 2.93 per cent end-tidal, no change was observed. When nitrous oxide, 70 per cent, was added, only minimal changes were observed. In a second part of the study, enflurane was compared with enflurane-nitrous oxide, 70 per cent, at equipotent levels. The following three variables (in percentages) decreased less in relation to awake control values at 1 MAC enflurane-nitrous oxide-oxygen than at 1 MAC enflurane-oxygen: left ventricular stroke work, -47.2 vs. -55.9; aortic dP/dt, -44.0 vs. -57.1; pressure- pulse product, -26.6 ns. -39.4. Forearm venous compliance decreased more: -26.0 vs. 2.9. The difference between the anesthetic mixtures was much more noticeable at 1.5 MAC, where eight variables (in percentages) decreased less with enfluranenitrous oxide-oxygen than with enflurane-oxygen: cardiac output, -6.9 vs. -22.1; stroke volume, -31.4 ns. -46.0; left ventricular minute work, -32.6 vs. —49.6; left ventricular stroke work, -50.8 vs. -65.8; left ventricular stroke power, -48.2 us. -63.1; ballistocardiogram, -34.5ns. -49.1; aortic dP/dt, -49.7ns. -65.8; pressure-pulse product, -32.3 vs. -42.3. Heart rate increased less when nitrous oxide was included in the mixture: 34.5 ns. 43.6. The lack of response during the addition of nitrous oxide to enflurane-oxygen is contrary to the significant sympathomimetic response seen when nitrous oxide is added to halothane, fluroxene, or diethyl ether. The apparent protection afforded by nitrous oxide at equipotent anesthetic levels is small enough that the main consideration in choosing between the two mixtures should be the concentration of oxygen needed by the patient.
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