Mélot C, Delcroix M, Closset J, Vanderhoeft P, Lejeune P, Leeman M, Naeije R
Department of Intensive Care, Erasme University Hospital, Brussels, Belgium.
Am J Physiol. 1995 Feb;268(2 Pt 2):H817-27. doi: 10.1152/ajpheart.1995.268.2.H817.
We investigated whether the Starling resistor model (Mitzner et al. J. Appl. Physiol. 51: 1065-1071, 1981) or a distensible vessel model (Haworth et al. J. Appl. Physiol. 70: 15-26, 1991) best describes pulmonary vascular pressure-flow (Q) relationships in embolic pulmonary hypertension. Mean pulmonary arterial pressure (Ppa)-Q plots at constant left atrial pressure (Pla) and Ppa-Pla plots at constant Q were investigated in seven dogs before and after 500-micron glass bead pulmonary embolism. Embolization to a mean angiographic obstruction of 78% increased the slope and extrapolated pressure intercept (P(i)) of Ppa-Q plots and increased the inflection point of Ppa-Pla plots, above which an increase in Pla is transmitted to Ppa in a ratio of approximately 1:1. The Starling resistor and the distensible vessel model provided a reasonably good fit to the Ppa-Q and Ppa-Pla coordinates before and after embolism. However, contrary to the prediction of the Starling resistor model, no correlation was found between the inflection point of Ppa-Pla plots and P(i). We therefore conclude that an increased closing pressure is unlikely to contribute to embolic pulmonary hypertension.
我们研究了斯塔林电阻器模型（米茨纳等人，《应用生理学杂志》51: 1065 - 1071, 1981）或可扩张血管模型（霍沃思等人，《应用生理学杂志》70: 15 - 26, 1991）是否最能描述栓塞性肺动脉高压时的肺血管压力-流量（Q）关系。在7只犬500微米玻璃珠肺栓塞前后，研究了在恒定左心房压力（Pla）下的平均肺动脉压（Ppa）-Q图以及在恒定Q下的Ppa - Pla图。栓塞至平均血管造影阻塞率达78%，增加了Ppa - Q图的斜率和外推压力截距（P(i)），并增加了Ppa - Pla图的拐点，在此拐点以上，Pla的增加以约1:1的比例传递至Ppa。斯塔林电阻器模型和可扩张血管模型对栓塞前后的Ppa - Q和Ppa - Pla坐标拟合得相当好。然而，与斯塔林电阻器模型的预测相反，在Ppa - Pla图的拐点与P(i)之间未发现相关性。因此，我们得出结论，闭合压力升高不太可能导致栓塞性肺动脉高压。
