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Am J Physiol Heart Circ Physiol 267: H1928-H1935, 1994;
0363-6135/94 $5.00
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AJP - Heart and Circulatory Physiology, Vol 267, Issue 5 1928-H1935, Copyright © 1994 by American Physiological Society

ARTICLES

Capillary hemodynamics in hemorrhagic shock and reperfusion: in vivo and model analysis

M. C. Mazzoni, K. C. Warnke, K. E. Arfors and T. C. Skalak
Department of Applied Mechanics and Engineering Sciences-Bioengineering, University of California, San Diego, La Jolla 92093.

A computer network model and in vivo measurements of microcirculatory blood flow in skeletal muscle were used to study the mechanisms responsible for low flow in hemorrhagic shock and reperfusion, with focus on the potential importance of capillary diameters and leukocyte rheology. Model flows were determined by the network pressure gradient, systemic hematocrit and leukocrit, leukocyte cytoplasmic viscosity, and vessel dimensions. After 1 h of shock (40% acute bleed) in anesthetized rabbits, pressure was reduced by 45%, hemodilution occurred, and capillary diameters decreased by 21%. The 45-50% flow reduction found experimentally in gastrocnemius muscle by laser Doppler flowmetry (LDF) and a microsphere technique matched model flow predictions with one-half of the proximal capillaries narrowed. Ringer-lactate (RL) reperfusion only partially restored control LDF flow, whereas a small-volume bolus of hypertonic saline-dextran followed by RL gave complete LDF flow recovery. The model predicted these flows for moderate hemodilution states, with the added insight that low-flow conditions are exacerbated by leukocytes only if they become activated, which is often a complication in ischemia/reperfusion.


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