Kingsbury Martyn P, Huang Wenxin, Donnelly J Leo, Jackson Emma, Needham Emma, Turner Mark A, Sheridan Desmond J
Academic Cardiology Unit, Imperial College School of Medicine, St. Mary's Campus, 10th floor QEQM Wing, South Wharf Road, LondonW2 1NY, UK.
Basic Res Cardiol. 2003 Sep;98(5):295-303. doi: 10.1007/s00395-003-0419-6. Epub 2003 May 16.
In order to determine whether morphological changes could account for a previously reported reduction in pulmonary capillary filtration in heart failure, we studied pulmonary morphology in lungs from a guinea-pig chronic heart failure model. Heart failure was induced by banding the ascending aorta with sham operated animals serving as controls; all animals were studied at 158 +/- 6 days post-operation. Following banding, a reduction in aortic flow, increased peripheral vascular resistance and raised left ventricular end diastolic, left atrial and right ventricular pressures together with increased right ventricle to body weight ratio (all p < 0.05) are indicative of established pulmonary hypertension and heart failure. This was associated with an increase in pulmonary septal volume fraction (38.1 +/- 3.1% vs 24.6 +/- 2.3 %, p < 0.01) and reticulin fibre density. There was also evidence of siderophage infiltration and examination of pulmonary ultra structure revealed a significantly thicker alveolar-capillary barrier in heart failure (1278 +/-76 vs 638 +/- 32 nm, p < 0.001), thickening of both the alveolar (89%, p < 0.01) and capillary (69%, p < 0.05) basal laminae with pericyte and collagen in filtration of the alveolar-capillary barrier. We hypothesise that these pulmonary adaptations provide protection from oedema formation, but whilst initially protective, are also likely to confer major long-term disadvantages in chronic heart failure.
为了确定形态学变化是否能够解释先前报道的心力衰竭时肺毛细血管滤过减少的现象，我们研究了豚鼠慢性心力衰竭模型肺脏的形态学变化。通过结扎升主动脉诱导心力衰竭，假手术动物作为对照；所有动物均在术后158±6天进行研究。结扎后，主动脉血流减少、外周血管阻力增加、左心室舒张末期、左心房和右心室压力升高，同时右心室与体重之比增加（所有p<0.05），提示已发生肺动脉高压和心力衰竭。这与肺间隔体积分数增加（38.1±3.1%对24.6±2.3%，p<0.01）和网状纤维密度增加有关。也有含铁血黄素巨噬细胞浸润的证据，肺超微结构检查显示心力衰竭时肺泡-毛细血管屏障明显增厚（1278±76对638±32nm，p<0.001），肺泡（89%，p<0.01）和毛细血管（69%，p<0.05）基底膜增厚，伴有周细胞和胶原纤维浸润到肺泡-毛细血管屏障中。我们推测这些肺部适应性变化可防止水肿形成，但虽然最初具有保护作用，但在慢性心力衰竭中也可能带来重大的长期不利影响。
