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Circulation, Vol 90, 658-668, Copyright © 1994 by American Heart Association
Y Hirooka, T Imaizumi, T Tagawa, M Shiramoto, T Endo, S Ando and A Takeshita
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.
ARTICLES
Effects of L-arginine on impaired acetylcholine-induced and ischemic vasodilation of the forearm in patients with heart failure
Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
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