Effects of halothane on left ventricular function and distribution of regional blood flow in dogs and primates.

Left ventricular and regional vascular effects of halothane were assessed in dogs and primates in which coronary, mesenteric, renal, and iliac blood flows, arterial blood pressure, left ventricular diameter and pressure, dD/dt (i.e., the velocity of myocardial fiber shortening), and dP/dt were continuously measured in the control resting state, while the conscious animals were breathing O2, and during halothane-O2 anesthesia maintained at 1% or at 2% for 90 minutes (separate experimental days). Halothane caused a concentration-dependent depression of myocardial contractility: (dP/dt)/P fell 68 ± 5% during 2% halothane anesthesia and left ventricular end-diastolic diameter rose. Halothane also caused a redistribution of regional blood flows. At a concentration of 1% halothane, the most intense vasodilatation occurred in the renal bed (renal resistance fell 46 ± 5%), but mesenteric resistance rose (42 ± 15%). With 1% halothane regional vascular resistances tended to rise with time, but with 2% halothane regional blood flows rose with time. A direct vasodilating action of halothane was observed following direct intra-arterial injection of the drug. Probably this action was responsible for the renal and iliac vasodilatations and for the opposition to the metabolically induced vasoconstriction in the coronary bed. Thus, the administration of the most commonly employed potent inhalation anesthetic, halothane, substantially alters myocardial contractility and regional blood flows and resistances. These effects are, in many instances, a function of the concentration of the anesthetic and the duration of its administration.