Relationship between arterial pressure and blood flow in the generation of slow-wave flowmotion in rat skeletal muscle.

The objective of this study was to determine the role of hypotension and hypoperfusion in the induction of regular slow-wave flowmotion (SWFM) in skeletal muscle in vivo. SWFM and microcirculatory muscle blood flow (MBF) were assessed by laser Doppler flowmetry in anesthetized rats exposed to: (1) graded hemorrhage (n = 15); (2) partial occlusion of the feeding artery (n = 6); (3) partial occlusion of the vein (n = 6), and (4) the vasodilator hydralazine (n = 10). Mean arterial pressure (MAP) was significantly reduced to 65 +/- 2.1% after hemorrhage and hydralazine before (64 +/- 2.4%) and after (42 +/- 1.8%) additional blood loss, but remained unchanged after venous occlusion. The pressure of the feeding artery fell to 38 +/- 1.2% after partial occlusion. MBF dropped significantly to 74 +/- 4.2% after hemorrhage, 54 +/- 5.6% after arterial and 53 +/- 3.0% after venous occlusion. Hydralazine caused MBF to rise to 192 +/- 21.8% before additional blood withdrawal and returned to normal values after it. SWFM was observed in all animals after hemorrhage and arterial occlusion, but in none after venous occlusion. In the hydralazine group, SWFM occurred only after blood loss. The hemoglobin concentration was reduced to 82 +/- 2.1% after hemorrhage. It remained normal after hydralazine administration, but decreased to 79 +/- 1.2% after the subsequent blood withdrawal. We conclude that arterial hypotension, but not hypoperfusion, induces SWFM, and hyperperfusion prevents it. Our results support the hypothesis that SWFM is generated by a reduction of vascular wall tension.