Effects of L-arginine on impaired acetylcholine-induced and ischemic vasodilation of the forearm in patients with heart failure

Yoshitaka Hirooka, Tsutomu Imaizumi, Tatsuya Tagawa, Masanari Shiramoto, Toyonari Endo, Shin Ichi Ando, Akira Takeshita

    研究成果: ジャーナルへの寄稿学術誌査読

    147 被引用数 (Scopus)

    抄録

    Background: Endothelium-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 Results: Forearm 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. Conclusions: Our results suggest that defective endothelial function may contribute to impaired ischemic vasodilator capacity in HF.

    本文言語英語
    ページ(範囲)658-668
    ページ数11
    ジャーナルCirculation
    90
    2
    DOI
    出版ステータス出版済み - 8月 1994

    !!!All Science Journal Classification (ASJC) codes

    • 循環器および心血管医学
    • 生理学(医学)

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