Mahy I R, Shore A C, Smith L D, Tooke J E
Department of Vascular Medicine, University of Exeter, UK.
Cardiovasc Res. 1995 Dec;30(6):939-44.
Previous studies of peripheral microvascular function in human heart failure have concentrated on changes in flow, and there is little information concerning the impact of heart failure on the principal determinants of transcapillary fluid exchange. This study investigated whether alterations in capillary pressure and microvascular fluid permeability can be detected in subjects with idiopathic dilated cardiomyopathy.
Finger nailfold capillary pressure and calf capillary filtration coefficient (CFC) were measured in parallel studies of two overlapping groups of 12 non-oedematous subjects with idiopathic dilated cardiomyopathy and mild to moderate heart failure and in age- and sex-matched healthy controls. Capillary pressure was measured by direct cannulation using an electronic resistance feedback servonulling technique, and CFC by mercury-in-silastic strain gauge plethysmography using a modification of the technique which avoids assumptions concerning isovolumetric venous pressure.
Following correction for differences in skin temperature, capillary pressure was lower in the subjects with heart failure (P = 0.02). Both CFC and isovolumetric venous pressure were greater in the subjects with heart failure than in controls (3.4 +/- 0.9 vs. 2.6 +/- 0.7 ml.min-1.mmHg-1.100 ml-1, P = 0.03; 27.1 +/- 8.4 vs. 17.2 +/- 7.2 mmHg, P = 0.01).
These data suggest that factors other than changes in arterial inflow and venous outflow pressures are likely to play an important role in the disruption of microvascular homeostasis which occurs in heart failure. Changes in capillary hydraulic conductance may contribute to the pathogenesis of oedema.
以往关于人类心力衰竭外周微血管功能的研究主要集中在血流变化上,而关于心力衰竭对跨毛细血管液体交换主要决定因素的影响的信息较少。本研究调查了特发性扩张型心肌病患者是否能检测到毛细血管压力和微血管液体通透性的改变。
在两组重叠的研究中,对12名患有特发性扩张型心肌病和轻至中度心力衰竭的非水肿患者以及年龄和性别匹配的健康对照者进行了平行研究,测量了指甲襞毛细血管压力和小腿毛细血管滤过系数(CFC)。毛细血管压力通过使用电子电阻反馈伺服零技术的直接插管测量,CFC通过使用改良技术的硅橡胶汞应变片体积描记法测量,该技术避免了对等容静脉压力的假设。
校正皮肤温度差异后,心力衰竭患者的毛细血管压力较低(P = 0.02)。心力衰竭患者的CFC和等容静脉压力均高于对照组(3.4±0.9 vs. 2.6±0.7 ml·min-1·mmHg-1·100 ml-1,P = 0.03;27.1±8.4 vs. 17.2±7.2 mmHg,P = 0.01)。
这些数据表明,除动脉流入和静脉流出压力变化外的其他因素可能在心力衰竭时发生的微血管内环境稳态破坏中起重要作用。毛细血管水力传导率的变化可能有助于水肿的发病机制。