Auckland Bioengineering Institute, The University of Auckland, New Zealand.
Respir Physiol Neurobiol. 2011 Mar 15;175(3):365-74. doi: 10.1016/j.resp.2010.12.018. Epub 2010 Dec 31.
Embolus occlusion of pulmonary arteries can result in elevated pulmonary blood pressures, often resulting in pulmonary hypertension (PH). Experimental observations have shown that small emboli (diameter <170 μm) can have a disproportionate effect on pulmonary vascular resistance (PVR) compared with larger emboli for the same tissue occlusion. We present an anatomically based theoretical model of perfusion in the acinar blood vessels designed to investigate changes in PVR following occlusion of arteries <500 μm in diameter. The model predicts that emboli lodged near proximal capillary beds have a greater effect on PVR--regardless of their size--than emboli occluding 200 μm diameter arterioles, with PH occurring for 10% less tissue occlusion. Capillary blood pressures are predicted to exceed 24 mmHg (levels initiating capillary wall damage) in regions of the capillary bed at approximately the onset of PH. This study focuses on the effect of mechanical obstruction alone; however, we present simple models of vasoconstriction illustrating an increased impact on PVR.
肺动脉栓塞可导致肺动脉血压升高,常导致肺动脉高压(PH)。实验观察表明,与相同组织阻塞的较大栓塞相比,小栓塞(直径<170μm)对肺血管阻力(PVR)的影响不成比例。我们提出了一种基于解剖学的肺泡血管灌注理论模型,旨在研究直径<500μm的动脉阻塞后 PVR 的变化。该模型预测,位于近端毛细血管床附近的栓塞,无论其大小如何,对 PVR 的影响都比阻塞 200μm 直径的小动脉更大,组织阻塞减少 10%即可发生 PH。在 PH 发生的大约同时,毛细血管床的毛细血管血压预计将超过 24mmHg(引发毛细血管壁损伤的水平)。本研究仅关注机械阻塞的影响;然而,我们提出了简单的血管收缩模型,说明了对 PVR 的影响增加。