Wilson J R, Hoyt R W, Ferraro N, Janicki J S, Weber K T
J Am Coll Cardiol. 1984 Sep;4(3):529-34. doi: 10.1016/s0735-1097(84)80097-2.
The direct smooth muscle vasodilator hydralazine has been used to treat exertional fatigue in patients with chronic heart failure. However, prior studies suggest that arteriolar vasodilators such as hydralazine may actually impair nutritive flow to working skeletal muscle by interfering with the distribution of blood flow within muscle. To investigate this possibility, tension development and metabolism were measured in nine vascularly isolated gracilis muscle preparations perfused at 90 mm Hg and stimulated to contract progressively at rates of 1, 3 and 6/s with each stage lasting 3 minutes. Studies were then repeated after 30 minutes of intraarterial hydralazine (0.02 to 0.12 mg/min). At rest, hydralazine decreased mean vascular resistance (+/- SEM) from 15.1 +/- 1.4 to 8.6 +/- 0.9 X 10(2) units (p less than 0.001) and increased blood flow from 6.4 +/- 0.7 to 11.4 +/- 1.2 ml/min (p less than 0.001), but did not change oxygen consumption (VO2) control, 18 +/- 1 versus hydralazine, 17 +/- 2 microliter/min). Hydralazine also decreased vascular resistance and increased flow at a contraction rate of 1/s, but not at 3 and 6/s. Hydralazine had no effect on maximal VO2 (control, 254 +/- 18 versus hydralazine, 236 +/- 19 microliter/min), maximal developed tension (control, 353 +/- 90 versus hydralazine, 334 +/- 74 kg X min) or the response in venous lactate (control, 20.6 +/- 2.3 versus hydralazine, 18.1 +/- 2.0 mg/dl). Hydralazine also did not change muscle metabolism and function at contraction rates of 1 and 3/s. These data suggest that hydralazine does not adversely affect nutritive flow to working skeletal muscle.
