Effects of L‐Arginine on Impaired Acetylcholine‐Induced and Ischemic Vasodilation of the Forearm in Patients With Heart Failure
作者:
Yoshitaka Hirooka,
Tsutomu Imaizumi,
Tatsuya Tagawa,
Masanari Shiramoto,
Toyonari Endo,
Shin-ichi Ando,
Akira Takeshita,
期刊:
Circulation
(OVID Available online 1994)
卷期:
Volume 90,
issue 2
页码: 658-668
ISSN:0009-7322
年代: 1994
出版商: OVID
关键词: acetylcholine;heart failure, congestive;endothelium;relaxing factors;nitric oxide
数据来源: OVID
摘要:
BackgroundEndothelium-dependent vasodilation in response to acetylcholine (ACh) and ischemic vasodilation during reactive hyperemia are attenuated in the forearm of patients with heart failure (HF). It has been shown that L-arginine augments endothelium-dependent vasodilation in healthy subjects. Thus, the aim of the present study was to determine if L-arginine improves endothelium-dependent and ischemic vasodilation in the forearm in HF.Methods and ResultsForearm blood flow was measured by a strain-gauge plethysmograph in 20 patients with HF and in 24 age-matched control subjects (C). Resting forearm vascular resistance (FVR) was significantly higher in HF than in C (37±4 versus 22±2 U,P<.01). Intra-arterial infusions of ACh or sodium nitroprusside (SNP) at graded doses progressively decreased FVR in HF as well as in C. The magnitude of ACh-induced vasodilation was attenuated in HF (P<.01), whereas SNP-induced vasodilation was similar between the two groups. The minimal FVR during reactive hyperemia after 10 minutes of arterial occlusion was significantly higher in HF (n= 12) than in C (n= 12) (3.2±0.4 versus 2.1±0.1 U,P<.05). L-Arginine significantly augmented maximal vasodilation evoked with ACh and decreased minimal FVR during reactive hyperemia in HF (P<.01) but not in C. L-Arginine did not affect SNP-induced vasodilation in HF or C.ConclusionsOur results suggest that defective endothelial function may contribute to impaired ischemic vasodilator capacity in HF.
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