Comparison of Arterial Occlusion and Ischaemic Exercise for the Study of Vasodilatation in the Human Calf

Abstract

1. Calf blood flow was measured by venous occlusion plethysmography to compare two stimuli for eliciting maximal calf vascular conductance: (i) 10 min of arterial occlusion and (ii) isolated exhaustive calf exercise with ischaemic occlusion. The subjects were semi-supine with the calf in position for immediate blood flow measurements after release of the occluding cuff. Three groups of subjects were studied: young [35 years (SD 9, n = 9)], old [57 years (SD 5, n = 10)] and patients with congestive heart failure [63 years (SD 7, n = 7)]. 2. Occlusion and ischaemic exercise were equally effective in producing maximal calf vascular conductance in each of the subject groups. Maximal calf vascular conductance (ml min−1 100 ml−1 mmHg−1) was equivalent in the young [ischaemic exercise 0.54 (SEM 0.03), occlusion 0.54 (SEM 0.05)] and old [ischaemic exercise 0.47 (SEM 0.05), occlusion 0.48 (SEM 0.04)] subjects. However, patients with congestive heart failure exhibited significantly reduced maximal calf vascular conductance [ischaemic exercise 0.20 (SEM 0.02), occlusion 0.20 (SEM 0.01)]. 3. Analysis of the curves, generated by plotting serial calf vascular conductance values obtained immediately and every 15 s after occlusion cuff release for 165 s, revealed differences in the pattern of vasodilatation after occlusion and ischaemic exercise. Maximal calf vascular conductance was more sustained after ischaemic exercise, and the shape of the calf vascular conductance curve was similar in all subject groups. After occlusion in the patients with congestive heart failure, maximal calf vascular conductance occurred at 6 s (SEM 3) after cuff release and declined rapidly, whereas, in the healthy subjects, calf vascular conductance increased after the first measurement, with maximal calf vascular conductance at 20 s (SEM 4) in the old and 27 s (SEM 6) in the young groups. The time delay for maximal calf vascular conductance in the healthy subjects is consistent with a velocity-mediated proximal arterial dilatation, and the rapid decline in the patients with congestive heart failure may reflect sympathetic vasoconstriction and endothelial dysfunction. 4. In conclusion, both occlusion and ischaemic exercise are equally useful for the determination of vasodilatory capacity of the human calf. The prolonged vasodilatation after ischaemic exercise allows more time for the measurement of maximal calf vascular conductance. However, analysis of the entire calf vascular conductance recovery curve after occlusion provides more information on the relative contributions of factors which sustain vasodilatation after a maximal stimulus.