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Skeletal Microcirculatory Responses to Hyperdynamic Escherichia coli Sepsis in Unanesthetized Rats
Henry M. Cryer, MD;
R. Neal Garrison, MD;
Herman W. Kaebnick, MD;
Patrick D. Harris, PhD;
Lewis M. Flint, MD
Arch Surg. 1987;122(1):86-92.
Abstract
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To determine the microvascular site of vasodilation during hyperdynamic sepsis, we measured arteriolar and venular responses to live Escherichia coli bacteremia in the rat cremaster muscle by direct in vivo videomicroscopy. Our data indicate that cardiac output (by thermodilution) increased, systemic vascular resistance decreased, and a differential arteriolar response occurred, with constriction of large arterioles and dilation of small terminal arterioles. We conclude that dilation of small terminal arterioles in skeletal muscle could contribute to decreased systemic vascular resistance during hyperdynamic sepsis. This may be an appropriate response to increased oxygen demand or decreased tissue utilization of oxygen. Alternatively, small-arteriole dilation may be an inappropriate response and secondary to release of vasoactive inflammatory mediators. If the latter is true, there is a potential therapeutic role for selective manipulation of the tone of small terminal arterioles in hyperdynamic sepsis.
(Arch Surg 1987;122:86-92)
Author Affiliations
From the Departments of Surgery (Drs Cryer, Garrison, Kaebnick, and Flint) and Physiology and Biophysics (Dr Harris), University of Louisville (Ky) School of Medicine.
Footnotes
Accepted for publication Sept 10, 1986.
Read before the Sixth Annual Meeting of the Surgical Infection Society, Chicago, April 22, 1986.
Reprint requests to Department of Surgery, University of Louisville, 550 S Jackson, Louisville, KY 40292 (Dr Cryer).
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