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Myocardial leukocyte transit time and retention during acute endotoxemia

University of British Columbia

During sepsis, endotoxins are released into the circulation which cause the activation of both cellular and humoral mediators of inflammation. Following activation of the cytohumoral cascade of sepsis the transit time of leukocytes through the microvasculature of the heart is increased. Increased transit time contributes to the retention of increased numbers of activated leukocytes in the heart. Leukocytes are retained primarily within the capillaries of the heart. The neutrophil fraction of leukocytes is slowed and retained to a much greater extent than the lymphocyte fractions. The retention of activated neutrophils is mediated more by the effects of humoral inflammatory mediators on the heart than on the neutrophils themselves. The retention of increased numbers of activated neutrophils within the capillaries of the heart is associated with the development of myocardial edema and myocyte structural changes. These myocardial changes are associated with decreased myocardial contractile function. Reduced myocardial contractility contributes to the pathogenesis of the septic shock state which increases the mortality due to sepsis. Exclusion of activated neutrophils from the capillary circulation of the heart during sepsis protects the myocardium from pathologic changes associated with sepsis and decreases the loss of myocardial contractile function.

Thesis/Dissertation

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2009-05-28

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http://hdl.handle.net/2429/8410

Experimental Medicine

University of British Columbia

UBCV

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