Microcirculation and hemorrhagic shock.
Blood loss is followed by compensatory cardiovascular readjustments that favor the maintenance of blood flow to central vital organs rather than to peripheral tissues. The microcirculatory changes that occur in skeletal muscle in shock states are of major importance, since skeletal muscle is not only the largest cell mass of the body but also one of the major target organs for neurohumorally mediated compensatory vascular readjustments. Intravital microscopic studies show that the microvascular blood flow in skeletal muscle is intermittent in the early posthemorrhagic period. This probably reflects an interplay between alpha-adrenergic vasoconstrictor and beta-adrenergic vasodilator activities, which serves to enhance a compensatory mobilization of interstitial fluid into the vascular compartment. A period of complete microcirculatory arrest is then seen, followed by reperfusion engaging only 30% to 50% of the capillaries that were seen perfused in resting skeletal muscle. The microvascular blood flow in shock is further characterized by a pronounced heterogeneity in distribution. Many capillaries remain constantly unperfused, while in others a slow, intermittent blood flow is seen. Obstruction of many capillaries by white blood cells and their slow passage through other capillaries seem to be the main reasons for the maldistribution of capillary blood flow in shock. Red blood cell aggregates obstructing capillary blood flow are not seen. The heterogeneous tissue perfusion is accompanied by local variations in cellular hypoxic injury, as is evidenced by multifocal measurements of tissue oxygen tension and by cellular transmembrane potential registrations.(ABSTRACT TRUNCATED AT 250 WORDS)
D004630:Emergencies; D004907:Erythrocyte Deformability; D004912:Erythrocytes / Q000502:physiology; D005440:Fluid Therapy; D006801:Humans; D007962:Leukocytes / Q000502:physiology; D008833:Microcirculation; D009132:Muscles / Q000098:blood supply; D010100:Oxygen / Q000502:physiology; D012771:Shock, Hemorrhagic / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy
D010100:Oxygen