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 a nd hypoperfusion in the induction of regular slow-wave flowmotion (SWF M) in skeletal muscle in vivo. SWFM and microcirculatory muscle blood flow (MBF) were assessed by laser Doppler flowmetry in anesthetized ra ts exposed to: (1) graded hemorrhage (n = 15); (2) partial occlusion o f the feeding artery (n = 6); (3) partial occlusion of the vein (n = 6 ), and (4) the vasodilator hydralazine (n = 10). Mean arterial pressur e (MAP) was significantly reduced to 65 +/- 2.1% after hemorrhage and hydralazine before (64 +/- 2.4%) and after (42 +/- 1.8%) additional bl ood 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% af ter arterial and 53 +/- 3.0% after venous occlusion. Hydralazine cause d MBF to rise to 192 +/- 21.8% before additional blood withdrawal and returned to normal values after it. SWFM was observed in all animals a fter hemorrhage and arterial occlusion, but in none after venous occlu sion. In the hydralazine group, SWFM occurred only after blood loss. T he hemoglobin concentration was reduced to 82 +/- 2.1% after hemorrhag e. 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 hyperp erfusion prevents it. Our results support the hypothesis that SWFM is generated by a reduction of vascular wall tension.