Left ventricular pressure-volume relations shift to the left after long-term loss of pericardial restraint.

The short-term effect of pericardiectomy is to shift the in vivo left ventricular (LV) pressure-volume curve to the right. We studied nine weight-matched pairs of male guinea pigs 28 to 39 days (mean 35) after complete pericardiectomy or sham thoracotomy to determine the long-term effects of pericardiectomy on LV pressure-volume relations. Hemodynamic and in vitro LV pressure-volume data were collected in matched pairs on the same day, 2 to 3 hr after catheter placement and recovery from anesthesia. Cardiac output was measured by the microsphere reference sample method. Postsurgical weight gain was similar in both groups: 823 +/- 6 (mean +/- SD) to 925 +/- 6 g in the pericardiectomy group and 829 +/- 7 to 927 +/- 7 g in the sham thoracotomy group. We found no difference in LV weight: 1.555 +/- 0.145 g in the pericardiectomy group vs 1.564 +/- 0.148 g in the sham thoracotomy group, nor any difference in heart rate, mean arterial, right atrial, or left ventricular end-diastolic pressures, cardiac outputs, or stroke volumes (p = NS). LV pressure-volume relations, however, were shifted to the left in the pericardiectomy group (p less than .005). At 10 mm Hg, LV volume in the pericardiectomy group (0.85 +/- 0.22 cc) was less than that in the sham thoracotomy group (1.02 +/- 0.15 cc; p less than .025). The LV stress-elastic modulus relationship was not different between groups (p greater than .30). One month after pericardiectomy, LV pressure-volume relations in vitro were shifted to the left without a change in LV weight, LV elastic modulus, or hemodynamics. We speculate that this shift compensates for the lack of pericardial restraint and returns LV volume and hemodynamics to normal in vivo.

Disturbances of calcium metabolism in the spontaneously hypertensive rat.

Ionized calcium is critical to the maintenance of normal cardiovascular function. Recently, vasoactive properties have also been attributed to parathyroid hormone (PTH). The present study characterizes the calcium-PTH axis in the spontaneously hypertensive rat (SHR) in order to determine the effects of chronic alterations in calcium intake on the development and maintenance of hypertension in this species. Thirty-six SHR and 36 Wistar-Kyoto (WKY) normotensive control rats were studied. The rats were fed one of three levels (percent of total diet) of calcium (normal 0.5%, low-normal 0.25%, high 4.0%) beginning at 10 weeks of age. Serum total and ionized calcium, serum PTHs, urinary electrolytes, and systolic blood pressures were assessed by repeated measurements between 10 and 48 weeks of age. Irrespective of calcium intake, the SHRs had lower serum ionized calcium concentrations (p less than 0.001) and higher PTH levels (p less than 0.001) than the WKYs. Serum total calcium were similar for the two strains. Urinary calcium excretion was greater in the SHR (p less than 0.001) relative to the WKY. The high (4.0%) calcium diet normalized the serum ionized calcium and attenuated the development of the SHRs' hypertension (p less than 0.001). The present study describes several previously unrecognized abnormalities of calcium metabolism in the SHR. These disturbances may be of pathogenetic importance in the development and maintenance of hypertension in the SHR.