Impaired systolic thickening associated with halothane in the presence of a coronary stenosis is mediated by changes in hemodynamics.

Myocardial ischemia results when halothane is administered to animals with severe coronary stenosis. This study was done to separate the effect of halothane, per se, on myocardial ischemia from indirect cardiovascular effects, primarily hypotension, that might cause ischemia by altering the oxygen supply-demand balance. Eight dogs underwent sterile surgery for implantation of sonomicrometer crystals and atrioventricular (A-V) heart block. One week later, each dog was anesthetized with morphine and chloralose. Heart rate was controlled by ventricular pacing and altered in five steps from 50 to 150 beats/min. Arterial blood pressure was controlled by blood withdrawal or phenylephrine infusion at four levels of arterial pressure (60 to 120 mmHg). Regional myocardial contraction was measured at each of the resulting 20 points as an indicator of myocardial ischemia. Twenty points were collected under each of four conditions in each animal: control, halothane (1% inspired), stenosis, halothane plus stenosis. Systolic thickening in the presence of stenosis was divided, on a point-by-point basis, by values obtained in the absence of stenosis to obviate the direct effects of blood pressure and heart rate on thickening. A separate normalization was done for data obtained in the presence of halothane. The normalized data demonstrate impaired systolic contraction at low arterial pressures and high heart rates. Multiple regression analysis failed to demonstrate a significant effect of halothane on systolic contraction once the effects of blood pressure, heart rate, and the negative inotropic effect of halothane were taken into account. Thus, the contraction failure that occurred during halothane and severe stenosis was mediated by changes in hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)