Belenkie I, Horne S G, Dani R, Smith E R, Tyberg J V
Department of Medicine, Faculty of Medicine, University of Calgary, Alberta, Canada.
Circulation. 1995 Aug 1;92(3):546-54. doi: 10.1161/01.cir.92.3.546.
Acute right ventricular (RV) hypertension may result in hemodynamic collapse. The associated reduction in left ventricular (LV) end-diastolic volume is thought to result from reduced RV output (secondary to RV ischemia) and adverse direct ventricular interaction. Aortic constriction improves cardiac function in these circumstances; this has been attributed to a reversal of the RV ischemia caused by an increased coronary perfusion pressure. We hypothesized that altered ventricular interaction, potentially via altered septal mechanics, may also contribute to the beneficial effects of aortic constriction.
We instrumented nine dogs with ultrasonic dimension crystals to measure RV segment length, septum-to-RV free wall and septum-to-LV free wall diameters, and LV anterioposterior diameter. Catheter-tipped manometers were used to measure LV and RV pressures. Pericardial pressure was measured with flat, liquid-containing balloon transducers. Inflatable cuff constrictors were placed on the pulmonary artery (PA) and aorta, and a flow probe was placed on the PA. The right coronary artery (RCA) was perfused independently by a roller pump calibrated for flow. During moderate PA constriction, while RCA pressure was maintained at control level, RCA flow did not change significantly (15.8 +/- 6.2 to 16.9 +/- 11.5 mL/min) and was similar during severe PA constriction (18.6 +/- 9.8 mL/min). During severe PA constriction, RV stroke volume decreased from a control value of 10.3 +/- 4.9 to 2.3 +/- 1.4 mL/beat (P < .05). When aortic constriction was added while RCA pressure was maintained at control level, there was an increase in RV stroke volume to 4.5 +/- 2.0 mL/beat (P < .05) with no associated change in RCA flow (17.8 +/- 9.5 mL/min). However, pressure-dimension loops clearly demonstrated changes in diastolic and systolic ventricular interaction; with aortic constriction, there was a large increase in the transeptal pressure gradient associated with a rightward septal shift. During either isolated severe PA constriction or simultaneous severe PA and aortic constriction, RCA flow was increased until RCA pressure was approximately equal to that in the aorta. This produced an increase in RCA flow of 50% (P < .05); however, this increase in coronary flow was ineffective in improving any measure of RV function.
In this model of acute RV hypertension, aortic constriction improves cardiac function, at least in part, by altering ventricular interaction independent of changes in RCA flow. Changes in RCA flow do not appear to have a significant impact on cardiac function in this model in which coronary artery pressure was maintained at normal or increased levels.
急性右心室（RV）高血压可能导致血流动力学崩溃。左心室（LV）舒张末期容积的相关减少被认为是由于右心室输出量减少（继发于右心室缺血）和不利的直接心室相互作用所致。在这些情况下，主动脉缩窄可改善心脏功能；这归因于冠状动脉灌注压升高导致的右心室缺血的逆转。我们推测，心室相互作用的改变，可能是通过间隔力学的改变，也可能有助于主动脉缩窄的有益作用。
我们给9只狗植入超声尺寸晶体，以测量右心室节段长度、间隔至右心室游离壁和间隔至左心室游离壁直径以及左心室前后径。使用导管尖端压力计测量左心室和右心室压力。心包压力用扁平的含液气囊换能器测量。在肺动脉（PA）和主动脉上放置可充气袖带收缩器，并在肺动脉上放置流量探头。右冠状动脉（RCA）由校准流量的滚轴泵独立灌注。在中度肺动脉缩窄期间，当右冠状动脉压力维持在对照水平时，右冠状动脉血流量没有显著变化（15.8±6.2至16.9±11.5 mL/min），在重度肺动脉缩窄期间也相似（18.6±9.8 mL/min）。在重度肺动脉缩窄期间，右心室搏出量从对照值10.3±4.9降至2.3±1.4 mL/搏（P<.05）。当在右冠状动脉压力维持在对照水平的同时增加主动脉缩窄时，右心室搏出量增加至4.5±2.0 mL/搏（P<.并伴有右冠状动脉血流量无相关变化（17.8±9.5 mL/min）。然而，压力-尺寸环清楚地显示了舒张期和收缩期心室相互作用的变化；随着主动脉缩窄，跨间隔压力梯度大幅增加，伴有间隔向右移位。在单独的重度肺动脉缩窄或同时的重度肺动脉和主动脉缩窄期间，右冠状动脉血流量增加，直到右冠状动脉压力大致等于主动脉压力。这使右冠状动脉血流量增加了50%（P<.05）；然而，冠状动脉血流量的这种增加在改善任何右心室功能指标方面均无效。
在这个急性右心室高血压模型中，主动脉缩窄至少部分通过改变心室相互作用而改善心脏功能，而与右冠状动脉血流量的变化无关。在这个冠状动脉压力维持在正常或升高水平的模型中，右冠状动脉血流量的变化似乎对心脏功能没有显著影响。
