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Abnormalities of Vascular Reactivity in the Sepsis Syndrome FREE TO VIEW

William J. Sibbald; George Fox; Claudio Martin
Author and Funding Information

The Richard Ivey Critical Care Trauma Centre, Victoria Hospital Corporation, and the Program of Critical Care, Faculty of Medicine, the University of Western Ontario, London, Ontario, Canada.


1991, by the American College of Chest Physicians.


Chest. 1991;100(3_Supplement):155S-159S. doi:10.1378/chest.100.3_Supplement.155S
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Abstract

A discussion of changes in vascular responsiveness during sepsis is rendered difficult by virtue of the many different animals models that have been used to mimic sepsis and the fact that this disease represents a spectrum of injury to the host. Thus, differences in vascular reactivity during sepsis are likely different in the early and late stages of this host response to a focus of infection.

In early sepsis, vasodilation Within the coronary and splanchnic circulations likely subserves an increase in the respective organ Q, thereby supporting increased O2 needs within these organs. In this circumstance, these vascular responses would be considered appropriate.

However, early sepsis also initiates a process that depresses the ability of the gut to utilize its O2E reserve to support increased O2 needs. Therefore, this organ does not easily give up its Q to support increases in O2 needs within other organs imposed during sepsis. Again, vascular responsiveness at the local level in the gut would be considered appropriate in this regard, given that local metabolic needs establish priority in the governance of Q over the effect of sympathetic activity, which would otherwise distribute Q to other organs.

In contrast to the apparent appropriateness of vascular responsiveness in the early phases of sepsis, the later stages of this syndrome seem accompanied by a well-characterized depression in vascular responsiveness. Both in vivo and in vitro studies have demonstrated a depression in vascular responsiveness at most levels of the arterial circulation in animal models that mimic the later stages of sepsis. The precise cause of this abnormality remains undefined, although altered adrenoreceptor or smooth muscle function, the influence of vasoconstrictor prostanoids, and the presence of other circulating mediators may be involved. The clinical correlate of this failure of normal vascular responsiveness seems to be the inability to demonstrate increased systemic resistance in nonsurvivors of septic shock when systemic Q has fallen. At the organ level, failure of normal vascular responsiveness to metabolic and neurohumeral signals likely establishes conditions in which Qo2 to some organs is depressed below need, so that organ ischemic injury results, a process that would accentuate or indeed cause MOF.


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