The effect of pericardium on the diastolic properties of the heart--experimental studies on volume load and on acute ischemia in open chest dogs.

We studied the effect of the pericardium on the end-diastolic pressure-segment length (P-L) relation in volume loading (Experiment I) and in acute ischemia (Experiment II). Experiment I: In 6 open chest dogs, segment length of left and right ventricles were measured using ultrasonic crystals during blood infusion. Drawing end-diastolic pressure (P, on ordinate) against segment length (L, on abscissa), the P-L curve with pericardium positioned upward compared to that without pericardium. The slopes (b) of the exponential curve (P = aebL) with pericardium were steeper than those without pericardium in both ventricles. The difference between the slopes with and without pericardium was significantly larger in the right ventricle (RV, 0.30 +/- 0.10, mean +/- SEM) than in the left ventricle (LV, 0.05 +/- 0.02, p less than 0.05). These results show that the pericardium inhibits the distensibility of the free wall more in RV than in LV, and enhances a mechanical coupling of both ventricles during volume over-load. Experiment II: In 8 open chest dogs, segment lengths of ischemic and non-ischemic regions in LV were measured after left circumflex coronary occlusion. When the segment lengths and LV pressure became stable, a pericardiectomy was performed. After the pericardiectomy, whereas heart rate and LV systolic pressure did not change, end-diastolic segment length in the ischemic region further lengthened (12.0 +/- 0.2 to 12.5 +/- 0.2 mm, p less than 0.01) and that in the non-ischemic region did not change despite the concomitant fall in LV end-diastolic pressure (EDP, 11.9 +/- 0.6 to 9.8 +/- 0.6 mmHg, p less than 0.01). These results suggest that the pericardium alters the LV end-diastolic pressure-volume relation and is one of the factors contributing to an increase in LVEDP during acute ischemia.