CONDUCTED VASODILATION ELEVATES FLOW IN ARTERIOLE NETWORKS OF HAMSTER STRIATED-MUSCLE

Our purpose was to investigate blood flow responses to local and conducted vasodilation in arteriole networks supplying the cremaster muscle of anesthetized (pentobarbital sodium) male hamsters. We tested the hypothesis that with local release of a vasodilator onto an arteriole segment, conduction is necessary to increase arteriolar perfusion. The tips (OD, 1-2 mu m) of micropipettes containing acetylcholine (ACh; 1.0 M) or sodium nitroprusside (NP; 0.2 M) were positioned similar to 1 mm distal to the origin of a 3A arteriole (resting diameter, 16 +/- 2 mu m) originating at a ''Y'' bifurcation. Responses were monitored (n = 9) at the site of release (local) and at three upstream locations: at the vessel origin, in the parent (2A) arteriole (diameter, 24 +/- 3 mu m), and in the paired (3A) daughter branch (diameter, 17 +/- 3 mu m). At each upstream site, diameter and red blood cell velocity (V-rbc) were quantified at rest and during the peak of diameter responses; these variables were used to calculate blood flow and wall shear rate (WSR). Microiontophoresis (1 mA, 500 ms) of ACh increased local diameter by 13 +/- 4 mu m (P < 0.05); vasodilation was conducted to each of the upstream sites (typical magnitude, 4-6 mu m; P < 0.05). Blood flow into branches increased 25-80% above corresponding values at rest without changing V-rbc; thus WSR consistently decreased with dilation (P < 0.05). Microiontophoresis of NP induced similar dilation locally yet had no effect on diameter, blood flow, or WSR in network branches. Thus dilation of a distal arteriole segment alone had no effect on muscle blood flow. Our findings indicate that, with local release of a vasodilator, the conduction of vasodilation into parent and daughter branches promotes hyperemia throughout the supplying network.