Role of the microcirculation to skeletal muscle during shock.
Our laboratory has performed a number of experiments to outline the role of the skeletal muscle microcirculation during hemorrhage and sepsis. We have suggested that the transition from the compensated to decompensated state in hemorrhagic shock could be attributed to the loss of vascular smooth muscle tone in small precapillary arterioles. This loss of tone is not due to a decrease in vascular smooth muscle reactivity to norepinephrine. However, tissue acidosis which is a uniform finding in the shock state contributes to this loss of vascular smooth muscle tone in large arterioles but not in small arterioles. The skeletal muscle responses to hyperdynamic sepsis were a mild constriction of large arterioles with a marked dilation of small vessels. It is this latter dilation which contributes to decreased systemic vascular resistance in sepsis. The microvessels reacted similarly in the hypodynamic septic state and do not appear to be responsible for the transition from the hyper- to the hypodynamic state in sepsis. The marked constrictor influence of large vessels seen in hemorrhage were not present in sepsis, indicating a possible vasodilator influence or loss of vasoconstrictor reactivity during sepsis but not hemorrhage. Similar findings were noted in both hyper- and hypodynamic endotoxemia suggesting that the energy metabolism effect of high dose endotoxin does not play a major role in skeletal muscle microvascular responses. Overall skeletal muscle vascular tone is due to a balance of vasoconstrictor influences that predominate in large arterioles which appear to be mediated by adrenergic nerve activity and vasodilator influences in small arterioles which are due to an escape from adrenergic nerve activity along with activation of local control factors by mediators of the inflammatory process, such as complement. The initial vasodilator response appears to be mediated by release of EDRF from the endothelial cell. Prostaglandins but not histamine or serotonin appear to be important in the initiation of vasodilation in small arterioles and in the modulation of existing vasoconstricting influences.
Garrison
R N
RN
Department of Surgery, University of Louisville, School of Medicine, Kentucky 40202.
Cryer
H M
HM
D000138:Acidosis / Q000209:etiology; D000818:Animals; D001685:Biological Factors / Q000502:physiology; D003167:Complement Activation; D004927:Escherichia coli Infections / Q000150:complications; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D009132:Muscles / Q000098:blood supply*; D009569:Nitric Oxide; D051381:Rats; D018805:Sepsis / Q000150:complications; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D012772:Shock, Septic / Q000503:physiopathology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014666:Vasomotor System / Q000503:physiopathology
D001685:Biological Factors; D014662:Vasoconstrictor Agents; D009569:Nitric Oxide