ANESTHETIC EFFECTS ON CARDIAC AND SMOOTH MUSCLE

Almost all drugs used in the practice of anesthesiology and critical care medicine exert significant hemodynamic effects by virtue of actions on the peripheral vasculature or on the myocardium. Of great clinical concern are the concentration-dependent myocardial depressant effects of intravenous and of inhalational anesthetics. Some anesthetic actions are direct on myocardial cells, some anesthetic actions are indirect through interactions with neurohumoral mechanisms that regulate myocardial contractility.
Volatile anesthetics also act to relax airway smooth muscle in a concentration-dependent fashion. We are investigating the cellular mechanisms of myocardial and smooth muscle contractile depression by drugs used in clinical anesthesia. There is evidence that anesthetics depress contractility by directly decreasing the availability of intracellular Ca²⁺ and (for some anesthetics) by altering myofibrillar Ca²⁺ sensitivity, i.e., the amount of force developed at a given [Ca²⁺].