Literature DB >> 9612356

Flow-generating capability of the isolated skeletal muscle pump.

D D Sheriff1, R Van Bibber.   

Abstract

We sought to test directly whether the mechanical forces produced during rhythmic muscle contraction and relaxation act on the muscle vasculature in a manner sufficient to initiate and sustain blood flow. To accomplish this goal, we evaluated the mechanical performance of the isolated skeletal muscle pump. The hindlimb skeletal muscle pump was isolated by reversibly connecting the inferior vena cava and terminal aorta with extracorporeal tubing in 15- to 20-kg anesthetized pigs (n = 5). During electrically evoked contractions (1/s), hindlimb muscles were made to perfuse themselves by diverting the venous blood propelled out of the muscles into the shunt tubing, which had been prefilled with fresh arterial blood. This caused arterial blood to be pushed into the distal aorta and then through the muscles (shunt open, proximal aorta and vena cava clamped). In essence, the muscles perfused themselves for brief periods by driving blood around a "short-circuit" that isolates muscle from the remainder of the circulation, analogous to isolated heart-lung preparations. Because the large, short shunt offers a negligible resistance to flow, the arterial-venous pressure difference across the limbs was continuously zero, and thus the energy to drive flow through muscle could come only from the muscle pump. The increase in blood flow during normal heart-perfused contractions (with only the shunt tubing clamped) was compared with shunt-perfused contractions in which the large veins were preloaded with extra blood volume. Muscle blood flow increased by 87 +/- 11 and 110 +/- 21 (SE) ml/min in the first few seconds after the onset of shunt-perfused and heart-perfused contractions, respectively (P > 0.4). We conclude that the mechanical forces produced by muscle contraction and relaxation act on the muscle vasculature in a manner sufficient to generate a significant flow of blood.

Entities:  

Mesh:

Year:  1998        PMID: 9612356     DOI: 10.1152/ajpheart.1998.274.5.H1502

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


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