Enhanced metabolic vasodilation secondary to diuretic therapy in decompensated congestive heart failure secondary to coronary artery disease.
Enhanced metabolic vasodilation secondary to diuretic therapy in decompensated congestive heart failure secondary to coronary artery disease.
复制标题
冠状动脉疾病继发的失代偿性充血性心力衰竭中利尿治疗继发的代谢性血管舒张增强。
DOI：
10.1016/0002-9149(87)90995-7
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Zelis,R
中科院分区：
文献类型：
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作者：
Sinoway,L;Minotti,J;Musch,T;Goldner,D;Davis,D;Leaman,D;Zelis,R
由于钠和水潴留被认为是限制充血性心力衰竭（CHF）最大代谢血管舒张的主要因素，我们对9例失代偿性CHF住院患者进行了严格利尿对最大血管舒张能力的影响的系统研究。反应性充血的峰值血流量，通过应变体积描记仪测量，被用作最大血管扩张能力的指标。利尿24h后体重减轻2.2 kg，最大流量由19.9 ml/min·100 ml增加至26.1 ml/min·100 ml （p < 0.05）。尽管在24至48小时内体重进一步减轻1.4 kg，但最大血流量没有增加（26.1至25.8 ml/min·100 ml）。由于血压没有明显变化，前臂最小阻力和最大电导也有类似的改善。血管收缩激素的变化不太可能解释这种影响，因为8名受试者中只有2名血浆去甲肾上腺素显著下降，只有1名受试者血浆肾素活性下降。作为一个组，去甲肾上腺素水平没有显著变化，仍远高于正常水平（1,525至1,148 pg/ml），血浆肾素活性（12.3至18.9 ng/ml/hour）。由于尽管持续利尿，血管舒张能力的改善在24小时内达到平台期，并且由于峰值反应性充血血流量仍比正常低32%，因此建议除了钠和水潴留之外的另一种机制是导致CHF周围血管舒张功能受损的重要原因。
Since sodium and water retention have been implicated as major factors limiting maximal metabolic vasodilation in congestive heart failure (CHF), the effect of rigorous diuresis on maximal vasodilatory capacity was studied systematically in 9 subjects hospitalized with decompensated CHF. Peak reactive hyperemic blood flow, measured by straingauge plethysmography, was used as an index of maximal vasodilatory capacity. After 24 hours of diuresis and a 2.2-kg weight loss, maximal flow increased from 19.9 to 26.1 ml/min · 100 ml (p < 0.05). Despite a further 1.4-kg weight loss between 24 and 48 hours, maximal blood flow increased no more (26.1 to 25.8 ml/min · 100 ml). Since blood pressure did not change significantly, minimal forearm resistance and maximal conductance showed similar improvements. It is unlikely that vasoconstrictor hormone changes could account for this effect since a marked decrease in plasma norepinephrine occurred in only 2 of 8 subjects and plasma renin activity decreased in only 1 subject. As a group there was no significant change in norepinephrine level, which remained substantially above normal (1,525 to 1,148 pg/ml), or in plasma renin activity (12.3 to 18.9 ng/ml/hour). Because the improvement in vasodilator capacity reached a plateau by 24 hours despite continued diuresis, and because peak reactive hyperemic blood flow was still 32% below normal, it is suggested that a second mechanism besides sodium and water retention is responsible for a significant portion of the impaired peripheral vasodilation in CHF.