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重度慢性左心衰竭时肺微血管通透性降低

Reduced pulmonary microvascular permeability in severe chronic left heart failure.

作者信息

Davies S W, Bailey J, Keegan J, Balcon R, Rudd R M, Lipkin D P

机构信息

Cardiac Department, Royal Free Hospital, London, England.

出版信息

Am Heart J. 1992 Jul;124(1):137-42. doi: 10.1016/0002-8703(92)90931-k.

Abstract

Pulmonary edema is a serious complication of heart failure, but often patients with chronic heart failure resist pulmonary edema despite elevated pulmonary venous pressures. This protection might be a result of decreased pulmonary microvascular permeability. Double-isotope scintigraphy with 113mindium-labeled transferrin and 99mtechnetium-labeled erythrocytes allows noninvasive estimation of pulmonary microvascular permeability; an index of transferrin accumulation is calculated that reflects microvascular permeability. Fourteen patients with severe chronic left ventricular dysfunction were compared with a control group of 15 patients with mild coronary artery disease. In the control group the transferrin accumulation index was 0.35 (range -0.3 to 1.0) x 10(-3)/min, and in patients with heart failure the index was 0.0 (range -1.0 to 0.7) x 10(-3)/min, which was significantly lower (p less than 0.01). The reduction in the transferrin accumulation index correlated weakly with the duration of heart failure (R = -0.5, p less than 0.02). These data indicate reduced protein efflux consistent with a decrease in pulmonary microvascular permeability in patients with severe chronic heart failure. Similar changes have been observed in severe mitral stenosis and may reflect a generalized adaptation to chronic pulmonary venous hypertension.

摘要

肺水肿是心力衰竭的一种严重并发症,但慢性心力衰竭患者尽管肺静脉压升高,却常常能抵御肺水肿。这种保护作用可能是肺微血管通透性降低的结果。用113铟标记的转铁蛋白和99锝标记的红细胞进行双同位素闪烁扫描可对肺微血管通透性进行无创评估;计算出一个反映微血管通透性的转铁蛋白积聚指数。将14例严重慢性左心室功能不全患者与15例轻度冠状动脉疾病患者组成的对照组进行比较。对照组的转铁蛋白积聚指数为0.35(范围为-0.3至1.0)×10⁻³/分钟,心力衰竭患者的该指数为0.0(范围为-1.0至0.7)×10⁻³/分钟,显著更低(p<0.01)。转铁蛋白积聚指数的降低与心力衰竭持续时间呈弱相关(R = -0.5,p<0.02)。这些数据表明,严重慢性心力衰竭患者的蛋白外渗减少,这与肺微血管通透性降低一致。在严重二尖瓣狭窄中也观察到了类似变化,这可能反映了对慢性肺静脉高压的一种普遍适应性反应。

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