Bhargava V, Shabetai R, Ross J, Shirato K, Pavelec R S, Mason P A
Am Heart J. 1983 Jun;105(6):995-1001. doi: 10.1016/0002-8703(83)90402-7.
The pericardium is largely responsible for displacement of the left ventricular diastolic pressure-volume curve observed after acute volume loading in dogs. Likewise the pericardium has been considered likely to play a role in displacement of the curve in patients with acute cardiac failure and in shifts following manipulation of afterload. This study was designed to examine the influence of the pericardium on the diastolic pressure-volume relation of the left ventricle when volume load is more sustained, a setting relevant to observations made in patients with heart failure. We measured left ventricular pressure and volume in six conscious dogs with sustained volume overload (mean left ventricular end-diastolic pressure 21 mm Hg, left ventricular end-diastolic volume 149% of the upper limit of normal for our laboratory) produced by aortocaval shunt created 7 to 29 days earlier. Simultaneous left ventriculograms and pressures were obtained before and during nitroprusside infusion with the pericardium intact and in four dogs the studies were repeated 7 to 15 days after pericardiectomy. In all six dogs with intact pericardium, nitroprusside displaced the entire pressure-volume curve downward whereas after pericardiectomy, the pressure-volume data points obtained before and during nitroprusside infusion fell on a single curve. These results were similar to those previously reported for acute volume overload. Nitroprusside did not alter the time course of left ventricular pressure fall during the isovolumic period of diastole either before pericardiectomy (28.8 +/- 10.2 sec,-1, 28.4 +/- 11.9 sec-1) or after (28.8 +/- 6.7 sec-1, 26.1 +/- 7.2 sec-1). These data indicate that in dogs subjected to volume overload sustained for periods of up to 29 days, the pericardium affects the left ventricular diastolic pressure-volume curve and contributes to the elevation of left ventricular filling pressure through upward displacement of this curve.
心包在很大程度上导致了犬急性容量负荷后观察到的左心室舒张压力-容积曲线的移位。同样,心包被认为可能在急性心力衰竭患者的曲线移位以及后负荷操纵后的移位中起作用。本研究旨在探讨在容量负荷更持久的情况下心包对左心室舒张压力-容积关系的影响,这种情况与心力衰竭患者的观察结果相关。我们测量了6只清醒犬的左心室压力和容积,这些犬因7至29天前建立的主动脉腔静脉分流而出现持续容量超负荷(平均左心室舒张末期压力21 mmHg,左心室舒张末期容积为我们实验室正常上限的149%)。在硝普钠输注前及输注期间,在完整心包状态下同时获取左心室造影和压力数据,并且在4只犬心包切除术后7至15天重复这些研究。在所有6只心包完整的犬中,硝普钠使整个压力-容积曲线向下移位,而心包切除术后,硝普钠输注前及输注期间获得的压力-容积数据点落在同一条曲线上。这些结果与先前报道的急性容量超负荷的结果相似。硝普钠在心包切除术前(28.8±10.2秒⁻¹,28.4±11.9秒⁻¹)或术后(28.8±6.7秒⁻¹,26.1±7.2秒⁻¹)均未改变舒张期等容期左心室压力下降的时间过程。这些数据表明,在经历长达29天持续容量超负荷的犬中,心包影响左心室舒张压力-容积曲线,并通过该曲线的向上移位导致左心室充盈压升高。