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Pressures in the primary arterioles of the cremaster muscle are reported to be approximately 50% of systemic, indicating that arterial resistance proximal to microvessels is high and may limit maximal blood flow. With no change in arterial resistance, increases in perfusion normally associated with muscle work either could not occur or would require increments in systemic pressure far greater than those actually observed in vivo. Therefore, we hypothesized that the small arteries feeding the muscle may participate in the hyperemic response. To test this hypothesis, male golden hamsters (n = 31, 118 g) were anesthetized (pentobarbital, 70 mg/kg i.p.), and the right cremaster was opened to expose its feed arteries, which originated from the iliac artery. Preparations were superfused and maintained at 35 +/- 1 degree C. Feed arteries had substantial tone, as shown by the fact that topical acetylcholine, applied at supramaximal concentration, dilated these vessels from 115 +/- 8 microns at rest to 158 +/- 9 microns (mean +/- SE; n = 38 vessels; p less than 0.01), corresponding to an estimated 4.4-fold increase in conductance. Stimulation of the sectioned motor nerve (8 Hz, 30 seconds) induced striated muscle contraction and increased feed vessel diameter from 93 +/- 5 microns to 116 +/- 5 microns (n = 14; p less than 0.01), consistent with a 2.6-fold increase in conductance. A 5-minute occlusion of the iliac artery resulted in feed artery dilation of similar magnitude. Supramaximal doses of acetylcholine applied topically to the distal portions of the cremaster resulted in striated muscle contraction and a dilation that propagated upstream to increase feed artery diameter by 25%.(ABSTRACT TRUNCATED AT 250 WORDS)

Communication between feed arteries and microvessels in hamster striated muscle: segmental vascular responses are functionally coordinated.