To determine the time course of changes in left ventricular diastolic properties after a large myocardial infarction, we serially measured left ventricular relaxation, chamber stiffness, and the ratio of left ventricular cavity to wall volume (V/Vw) after coronary artery ligation in rats. Left ventricular relaxation was measured during the occlusion and then both relaxation and chamber stiffness were measured at 3 hr, 24 hr, and 3, 5, and more than 22 days after infarction. Left ventricular pressures and left ventricular dP/dt were recorded with micromanometer-tipped catheters. Left ventricular relaxation was measured by computer digitization of the left ventricular pressure tracings and averaged over 100 to 150 cardiac cycles. Five chamber stiffness constants were calculated from pressure-volume curves that were obtained ex vivo. We found ventricular relaxation prolonged for the first hour after coronary occlusion; relaxation was maximally prolonged at 10 to 15 min after onset of occlusion. After 1 hr relaxation returned to normal. However, by 5 days ventricular relaxation was again prolonged. Left ventricular stiffness constants were increased at 3 and 24 hr, resulting in a shift of the left ventricular pressure-volume relation to the left. At 3 days after coronary artery ligation, all stiffness constants and the pressure-volume relation returned to normal. At more than 22 days the pressure-volume relation was shifted to the right and the stiffness constant for low filling pressures was decreased. V/Vw was significantly decreased from 0.603 + 0.021 at 3 and 24 hr to 0.379 ± 0.024 and 0.362 ± 0.032, respectively. V/Vw was significantly increased at more than 22 days (0.921 ± 0.094).We conclude that left ventricular diastolic function in rats is dynamic during the acute and healing phases of myocardial infarction. Left ventricular relaxation is prolonged at 10 to 15 min after coronary occlusion, then returns to normal, and by 5 days is again prolonged. Changes in left ventricular chamber stiffness are biphasic, first increasing then decreasing. These observed changes in chamber stiffness are related in part to changes in V/Vw. Circulation 77, No. 6, 1424No. 6, -1431No. 6, , 1988 TRANSIENT PERIODS of myocardial ischemia that are relatively brief and do not result in infarction prolong left ventricular relaxation and shift the diastolic pressure-volume relation leftward toward the pressure axis.1-5 When diastolic function has been examined after myocardial ischemia of sufficient duration to produce infarction, conflicting results have been reported. For example, early after acute infarction in dogs, left ventricular compliance has been found to be both increased6 and decreased.7-9From In rats studied 3 weeks or longer after myocardial infarction, left ventricular chamber stiffness is decreased and the pressure-volume relation is shifted to the right for that portion of pressure-volume relation that is linear, i.e., over the range of low distending pressures'0 and higher filling pressures." The reason fo...

The cardiovascular system of hypothyroid, normal, and hyperthyroid rats was studied by evaluation of the peripheral venous circulation and left ventricular (LV) systolic and diastolic performance in rats. Cardiac index (CI) and CI during a volume load were measured in open-chest rats. When compared with control, hypothyroid rats showed a decrease in heart rate, aortic pressure, LV systolic pressure, first derivative for LV pressure (LV dP/dt), CI, and CI during a volume load. LV pressure-volume relation was shifted to the right, muscle stiffness was unchanged, and LV relaxation was prolonged. There was a decrease in mean circulatory filling pressure (MCFP) to 6.3 +/- 0.2 from 7.6 +/- 0.2 mmHg in control rats. This was associated with an 11% decrease in unstressed vascular volume and 12% decrease in total blood volume but no change in venous compliance. In hyperthyroid rats there was an increase in heart rate, LV systolic pressure, LV dP/dt, CI, and CI during a volume load. LV chamber stiffness was increased, but muscle stiffness and LV relaxation were unchanged. There was an increase in MCFP to 9.5 +/- 0.3 mmHg and a decrease in venous compliance to 2.65 +/- 0.12 compared with 3.20 +/- 0.09 ml.mmHg-1.kg-1 in control rats. Unstressed vascular volume and total blood volume were unchanged. In conclusion, hyperthyroid rats have augmented LV systolic function and altered diastolic function which, combined with changes in the venous circulation, result in increased venous return and thus cardiac output. In hypothyroid rats both LV systolic and diastolic function are altered. When combined with changes of the venous circulation the changes result in a decrease in cardiac output.

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