Greyson C, Xu Y, Cohen J, Schwartz G G
San Francisco Department of Veterans Affairs Medical Center, CA, USA.
Cardiovasc Res. 1997 May;34(2):281-8. doi: 10.1016/s0008-6363(97)00038-2.
Acute pulmonary hypertension may cause right ventricular (RV) contractile failure. While it has been assumed that restoration of normal loading conditions after acute pulmonary hypertension is sufficient for complete recovery of RV function, this has not been rigorously examined. The purpose of this study was to test the hypothesis that acute RV pressure overload produces RV contractile dysfunction that persists following restoration of control loading conditions.
We subjected 18 autonomically-blocked, chloralose-anesthetized, open-chest pigs to 1 h of pulmonary artery constriction to increase RV systolic pressure from 35 +/- 1 to 55 +/- 1 mmHg, followed by 2 h of measurements after pulmonary artery constriction release. We determined regional RV free wall function from pressure-segment length loops and preload recruitable stroke work relations, and global RV function from stroke work vs. end-diastolic pressure relations.
As expected, RV free wall systolic shortening diminished during pulmonary artery constriction, but the endo/epi blood flow ratio, lactate uptake, and coronary venous pH were not significantly changed. Following release of pulmonary artery constriction, RV systolic and diastolic pressure returned to control values. Nonetheless, contractile dysfunction persisted, with depressed RV free wall systolic shortening (70 +/- 22% of control), RV regional external work (59 +/- 11% of control at control end-diastolic length), and global RV stroke work (56 +/- 14% of control at control end-diastolic pressure). Depressed regional work was due to a parallel, rightward shift of the preload recruitable stroke work relation. Five pigs identically instrumented but not subjected to pulmonary artery constriction showed no significant over 3 h.
Acute pulmonary hypertension causes RV contractile dysfunction that persists at least 2 h after restoration of control loading conditions. Contractile dysfunction is not attributable to RV ischemia during pressure overload.
急性肺动脉高压可能导致右心室（RV）收缩功能衰竭。虽然一直认为急性肺动脉高压后恢复正常负荷条件足以使RV功能完全恢复，但这一点尚未得到严格检验。本研究的目的是检验以下假设：急性RV压力过载会导致RV收缩功能障碍，在恢复对照负荷条件后这种功能障碍仍会持续。
我们对18只自主神经阻断、用氯醛糖麻醉、开胸的猪进行1小时的肺动脉收缩，使RV收缩压从35±1 mmHg升高至55±1 mmHg，然后在解除肺动脉收缩后进行2小时的测量。我们通过压力-节段长度环和可募集前负荷的搏功关系来确定RV游离壁局部功能，并通过搏功与舒张末期压力关系来确定RV整体功能。
正如预期的那样，肺动脉收缩期间RV游离壁收缩期缩短减少，但内膜/外膜血流比值、乳酸摄取和冠状静脉pH值无显著变化。解除肺动脉收缩后，RV收缩压和舒张压恢复到对照值。尽管如此，收缩功能障碍仍然存在，RV游离壁收缩期缩短降低（为对照值的70±22%），RV局部外部功（在对照舒张末期长度时为对照值的59±11%），以及RV整体搏功（在对照舒张末期压力时为对照值的56±14%）。局部功降低是由于可募集前负荷的搏功关系平行向右移位。五只同样植入仪器但未进行肺动脉收缩的猪在3小时内无显著变化。
急性肺动脉高压导致RV收缩功能障碍，在恢复对照负荷条件后至少持续2小时。收缩功能障碍并非归因于压力过载期间的RV缺血。
