OBJECTIVE: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. METHODS: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. RESULTS: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. CONCLUSIONS: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.

译文

目的:急性肺动脉高压可能导致右心室(RV)收缩衰竭。尽管已经假定急性肺动脉高压后恢复正常负荷状态足以使RV功能完全恢复,但尚未对此进行严格检查。本研究的目的是检验以下假设:急性RV压力超负荷会导致RV收缩功能障碍,并在控制负荷条件恢复后持续存在。
方法:我们对18头经氯醛糖麻醉的自闭式开胸猪进行了1小时的肺动脉收缩,以将RV收缩压从35 /-1增加到55 /-1 mmHg,然后在肺动脉进行2小时的测量收缩释放。我们从压力段长度环和预负荷可招募的卒中功关系中确定了区域RV无壁功能,并从卒中功与舒张末期压力关系中确定了整体RV功能。
结果:正如预期的那样,在肺动脉收缩期间右室游离壁收缩期缩短减少,但是内/外血流量比,乳酸摄取和冠状静脉pH没有明显变化。释放肺动脉收缩后,RV收缩压和舒张压恢复至控制值。然而,收缩功能障碍持续存在,右室游离壁收缩期缩短(控制区的70 /-22%),右室局部外部工作(在控制舒张末期的控制区为59 /-11%)和整体右室卒中工作持续存在(56)在对照舒张末期压力下为对照的14%)。较低的区域工作量是由于预载可招募中风工作关系的平行,向右移动。五只相同仪器但未经历肺动脉收缩的猪在3 h内无明显变化。
结论:急性肺动脉高压导致右室收缩功能障碍,在控制负荷恢复后至少持续2 h。压力超负荷期间收缩功能障碍不归因于RV缺血。

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