Acute aortic regurgitation was produced under anesthesia in 11 closed-chest dogs previously instrumented with ultrasound transducers. The immediate responses included increases in end-diastolic diameter (EDD), fractional shortening (FS), heart rate, left ventricular end-diastolic pressure (LVEDP), and pulmonary capillary wedge pressure (PCWP), the latter being transient as was a decrease in left ventricular peak systolic pressure (LVSP). End-systolic diameter (ESD) did not change. The grouped data suggest that no further changes occurred following the initial responses except in PCWP and LVSP. The data from individual dogs showed that there was a tendency for EDP, LVEDP, and PCWP to return toward control values after the initial increases in those dogs in which the heart rate increased after valve damage. This suggests that there were ongoing compensatory adjustments after the initial responses in this subgroup. Twelve dogs were followed chronically in the intact conscious state with echocardiographic measurements after acute aortic valve damage. EDD and ESD increased rapidly for about 80 days after which EDD increased slowly, whereas ESD showed no further change. Wall thickness and FS did not change throughout the period of study, suggesting that increasing wall thickness may be a relatively late change and that it may be related to the level of myocardial compensation.
|Original language||English (US)|
|Journal||The American journal of physiology|
|State||Published - Jul 1 1981|
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