Nitrates and Angina: an insight into arterialand venular involvement in blood flow regulation.

This study tested the hypothesis that venular resistance increases during ischaemia and that a prevalent nitrates-induced venodilationis the cruc a mechanism underlying their ability to relieve ischaemia. Using the model of postreactive hyperaemia we used mercuryin-rubber surain gauges to measure forearm blood flow (FBF) and forearm circumference (FC) before and after 5 mg sublingual isosorbide dinitrate in twelve healthy volunteers. The FC change during reactive hyperaemia was evaluated according to a hydraulic model which assumes that arteriolar resistance (AR) controls the blood inflow and that venular resistance (VR) controls the blood outflow of the vascular capillary reservoir. In this setting FC represents the reservoir volume and any change in this parameter represents the instantaneous difference between input and output flows. In the absence of nitrates and five minutes of arterial closure, the hyperaemic FC curve shows a rapid increase followed by a slow recovery demonstrating a rapid inflow followed by a delayed outflow of the reservoir. This behaviour may be explained by assuming an initial very low arterial resistance and high venular resistance, followed by a slow requilibrium of the two. Repeating the experiment after nitrates intake, the hyperaemic FC curve shows a reduced dimension and a faster recovery to the baseline. Compared with the previous condition, this finding may be explained by assuming a reduced initial venular resistance, which facilitates the blood outflow and hence muscle perfusion. Our findings are coherent with an ischaemia-induced arteriolar dilatation which facilitates filling, and a simultaneous venular constriction which opposes emptying (arteriovenous ischaemic mismatch): the action of the nitrates seems to restore the mismatch by acting on the venous side.