Importance of Myocardial Loading Conditions in Determining the Effects of Enflurane on Left Ventricular Function in the Intact and Isolated Canine Heart

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Abstract
The effects of enflurane (2% and 4% inspired) on left ventricular (LV) function were examined in chronically instrumented dogs, both intact and after isolation of their hearts and lungs from the systemic circulation. Enflurane in the intact dogs increased heart rate (32 .+-. 5% with 2% and 41 .+-. 4% with 4%) and elicited striking, dose-dependent decreases in LV stroke shortening (-30 .+-. 3% and -41 .+-. 4%), the maximum velocity of LV fiber shortening, dD/dt [change in diameter/change in time] (-23 .+-. 2% and -40 .+-. 2%), LV systolic pressure (-25 .+-. 3% and -33 .+-. 2%), the maximum rise of LV-pressure, dP/dt (-33 .+-. 5% and -55 .+-. 3%), and mean aortic pressure (-27 .+-. 2% and -37 .+-. 1%). The LV diastolic performance was impaired little, i.e., even with the higher concentration the LV end-diastolic pressure rose only moderately (32 .+-. 4%), while the LV end-diastolic dimensions failed to change significantly; both LV end-diastolic pressure and LV end-diastolic diameter were decreased with the low concentration. Enflurane, after .beta.-adrenergic blockade alone or after combined .beta.-adrenergic and cholinergic blockades, or with spontaneous ventilation instead of controlled ventilation, had similar effects. In the hearts that were isolated from the systemic circulation and the complex neurohumoral environments, enflurane increased both LV end-diastolic pressure (116 .+-. 32% and 492 .+-. 58%) and LV end-diastolic diameter (13 .+-. 3% and 28 .+-. 7%). In intact dogs with aortic pressure artificially increased to conscious control levels, enflurane likewise caused a distinct depression of the LV diastolic performance. LV systolic unloading appears to be mandatory to prevent acute myocardial failure from higher doses of enflurane. The observed changes in LV function with enflurane are largely independent of cardiac rate, adrenergic and cholinergic influences, and the hemodynamic consequences of intermittent positive-pressure ventilation.