Why the study?
Do halothane and isoflurane differentially depress contractility and action potentials in isolated human ventricular myocardium?
Do halothane and isoflurane differentially depress contractility and action potentials in isolated human ventricular myocardium?
Halothane causes greater frequency-dependent contractile and electrophysiological depression than isoflurane in isolated human ventricular myocardium, consistent with prior animal models.
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May warrant caution with halothane in impaired myocardium; leaves open translation from isolated tissue to clinical practice.
Segments of viable human left ventricular trabeculae were obtained at the time of endocardial resection for intractable ventricular ectopy. Muscle segments which showed suitable and reproducible contractions in 26 mM K Tyrode solution with 1 microM isoproterenol were electrically stimulated after rest, and at frequencies of 0.1, 0.25, 0.5, and 1 Hz. Effects of 0.75% halothane and 1.3% isoflurane on peak tension, maximum rate of tension development (dT/dt-max), and on slow (calcium dependent) action potential (AP) characteristics were studied. Halothane depressed peak tension, dT/dt-max, and slow AP maximum rate of depolarization (Vmax) at all frequencies, and caused a significantly greater depression of peak tension and dT/dt-max at 0.5-1 Hz than after rest and at 0.1-0.25 Hz. Isoflurane did not significantly depress slow AP Vmax, showed no frequency dependent contractile depression, and depressed dT/dt-max less than halothane at 0.5 and 1 Hz. Halothane and isoflurane caused differing depression in the pattern of developed tension. The differential depression by halothane and isoflurane of human ventricular myocardium was similar to that previously observed in isolated animal ventricular tissue.
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A 1988 study studied this question.
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