Key words: Anesthetics, intravenous: etomidate; ketamine; midazolam; propofol; thiopental. Heart, atria: human; isometric contraction; inotropic effect.
INTRAVENOUS induction of general anesthesia often is associated with hypotension. [1-4] Several mechanisms have been thought responsible for the decreased blood pressure, including a direct effect on the contractility of the myocardium. Indirect factors, such as concomitant changes in preload and afterload of the heart, sympathetic activity, baroreflex activity, and central nervous system activity make the direct effects of anesthetics on contractility difficult to measure in vivo, although relative heart rate and load-independent indexes of contractility can be derived from a series of pressure-volume diagrams of the left ventricle.
Measurement of the intrinsic myocardial contractility is more accurately performed in an in vitro model. In different animal species, the in vitro effects of propofol, [5-8] thiopental, [5,9-12] etomidate [13,14] and ketamine [15-17] on the contractility of isolated cardiac tissue have been determined. The results of these studies show a variable degree of negative inotropic action in papillary or left atrial muscle. In contrast, etomidate did not induce a significant inotropic effect in papillary muscle of hamster, [18] whereas positive inotropy was demonstrated in rats [19] and ferrets [20] after ketamine administration. Midazolam has not yet been studied in isolated myocardium. To the best of