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AJP - Heart and Circulatory Physiology, Vol 270, Issue 3 827-H836, Copyright © 1996 by American Physiological Society
ARTICLES |
H. Kerger, D. J. Saltzman, M. D. Menger, K. Messmer and M. Intaglietta
Department of Bioengineering, University of California, San Diego, La Jolla 92093-0412, USA.
The relationship between systemic and microvascular Po2 in subcutaneous connective tissue and hemodynamics was investigated during 4-h hemorrhagic shock (40 mmHg) in conscious Syrian hamsters (n = 66) fitted with a dorsal skinfold window. Systemic blood gases, metabolic parameters, arteriolar, venular, and tissue Po2, microvascular red blood cell velocity, and blood flow were evaluated in survivors (S) and nonsurvivors (NS). Surviving animals were resuscitated with shed blood. Microvascular and tissue Po2 were measured by phosphorescence decay of Pd-meso-tetra (4-carboxyphenyl) porphyrin (30 mg/kg body wt iv). Shock caused a significant dissociation between systemic arterial and microvascular arteriolar Po2 levels. Arterial Po2 increased from 59.7 +/- 12.0 to 110.8 +/- 19.7 mmHg (S) and from 64.0 +/- 13.7 to 128.5 +/- 10.1 mmHg (NS), whereas Po2 in large arterioles decreased from 56.9 +/- 5.5 (control) to 29.5 +/- 20.1 (S) and 6.0 +/- 5.7 mmHg (NS). Correspondingly, tissue Po2 fell from 24.1 +/- 6.8 (control) to 0.9 +/- 0.6 (S) and 0.4 +/- 0.3 mmHg (NS). Venous Po2 decreased from 28.8 +/- 3.7 to 20.4 +/- 4.1 (S) and from 28.0 +/- 2.9 to 16.3 +/- 0.5 mmHg (NS). Shock outcome and tissue oxygenation were predicted by arterial blood gases and metabolic and microcirculatory conditions but not by central venous Po2.
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