Fadel Elie, Michel René P, Eddahibi Saadia, Bernatchez Renée, Mazmanian Guy-Michel, Baudet Bruno, Dartevelle Philippe, Herve Philippe
Laboratoire de Chirurgie Expérimentale, Hôpital Marie Lannelongue, Université Paris Sud, France.
J Thorac Cardiovasc Surg. 2004 Apr;127(4):1009-17. doi: 10.1016/j.jtcvs.2003.07.048.
Pulmonary vascular resistance decreases dramatically after pulmonary thromboendarterectomy and further improves in time. This may reflect the slow regression of postobstructive pulmonary vasculopathy. We hypothesized that postobstructive pulmonary vasculopathy may regress after reperfusion in a piglet model of chronic (5 weeks) left pulmonary artery obstruction.
The ligated left pulmonary artery was reimplanted into the pulmonary arterial trunk. Pulmonary artery blood flow and pressure were measured 2 days and 5 weeks after reperfusion. Pulmonary artery smooth muscle thickness, endothelium-dependent relaxation, and left lung endothelial nitric oxide synthase activity and expression were assessed 5 weeks after ligation (n = 10) and 5 weeks after reperfusion (n = 10), and compared with a sham group (n = 10). Patency of the anastomoses and systemic blood supply to the lung were assessed by pulmonary angiography and nonselective thoracic aortography, respectively.
Angiography showed that pulmonary artery anastomoses were patent in all animals. Five weeks after reperfusion, left pulmonary blood flows were similar to those in the sham animals, and systemic blood supply to the left lung decreased. Left pulmonary vascular resistance decreased by 50% at 5 weeks after reperfusion compared with 2 days after reperfusion (P =.0009). Medial muscle thickness of the left pulmonary artery greater than 600 microm increased 5 weeks after ligation and regressed to sham values 5 weeks after reperfusion (P =.001). Endothelium-dependent relaxation was only partially restored 5 weeks after reperfusion, whereas left lung endothelial nitric oxide synthase expressions and activities returned to sham values.
This study shows that postobstructive pulmonary vasculopathy induced by ligation of the pulmonary artery for 5 weeks regresses after reperfusion, accounting for the progressive improvement in hemodynamics after thromboendarterectomy.
肺动脉血栓内膜剥脱术后肺血管阻力显著降低,并随时间进一步改善。这可能反映了阻塞性肺血管病的缓慢消退。我们假设在慢性(5周)左肺动脉阻塞的仔猪模型中,再灌注后阻塞性肺血管病可能会消退。
将结扎的左肺动脉重新植入肺动脉干。在再灌注后2天和5周测量肺动脉血流和压力。在结扎后5周(n = 10)和再灌注后5周(n = 10)评估肺动脉平滑肌厚度、内皮依赖性舒张以及左肺内皮型一氧化氮合酶活性和表达,并与假手术组(n = 10)进行比较。分别通过肺血管造影和非选择性胸主动脉造影评估吻合口的通畅情况和肺的体循环血液供应。
血管造影显示所有动物的肺动脉吻合口均通畅。再灌注5周后,左肺血流与假手术动物相似,左肺的体循环血液供应减少。与再灌注后2天相比,再灌注后5周左肺血管阻力降低了50%(P =.0009)。结扎后5周,左肺动脉中膜肌层厚度大于600微米增加,再灌注后5周恢复至假手术组水平(P =.001)。再灌注5周后内皮依赖性舒张仅部分恢复,而左肺内皮型一氧化氮合酶的表达和活性恢复至假手术组水平。
本研究表明,肺动脉结扎5周诱导的阻塞性肺血管病在再灌注后消退,这解释了血栓内膜剥脱术后血流动力学的逐渐改善。