Journal of Applied Physiology Journal of Applied Physiology
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J Appl Physiol 82: 592-598, 1997;
8750-7587/97 $5.00
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Journal of Applied Physiology
Vol. 82, No. 2, pp. 592-598, February 1997
PULMONARY CIRCULATION AND LUNG FLUID BALANCE

Thromboxane A2 mediates increased pulmonary microvascular permeability after intestinal reperfusion

Richard H. Turnage1, John L. Lanoue1, Kevin M. Kadesky1, Yan Meng1, and Stuart I. Myers2

1 Department of Surgery, University of Texas Southwestern Medical School, Dallas 76235-9031; 1 Dallas Veterans Administration Medical Center, Dallas, Texas 75216; and 2 Department of Surgery, Temple University School of Medicine, Philadelphia, Pennsylvania 19140

Received 9 July 1996; accepted in final form 30 September 1996.

Turnage, Richard H., John L. LaNoue, Kevin M. Kadesky, Yan Meng, and Stuart I. Myers. Thromboxane A2 mediates increased pulmonary microvascular permeability after intestinal reperfusion. J. Appl. Physiol. 82(2): 592-598, 1997.---This study examines the hypothesis that intestinal reperfusion (IR)-induced pulmonary thromboxane A2 (TxA2) release increases local microvascular permeability and induces pulmonary vasoconstriction. Sprague-Dawley rats underwent 120 min of intestinal ischemia and 60 min of IR. Sham-operated animals (Sham) served as controls. After IR or Sham, the pulmonary vessels were cannulated, and the lungs were perfused in vitro with Krebs buffer. Microvascular permeability was quantitated by determining the filtration coefficient (Kf), and pulmonary arterial (Ppa), venous (Ppv), and capillary (Ppc) pressures were measured to calculate vascular resistance (Rt). After baseline measurements, imidazole (TxA2 synthase inhibitor) or SQ-29,548 (TxA2-receptor antagonist) was added to the perfusate; then Kf, Ppa, Ppv, and Ppc were again measured. The Kf of lungs from IR animals was four times greater than that of Sham (P = 0.001), and Rt was 63% greater in the injured group (P = 0.01). Pc of IR lungs was twice that of controls (5.4 ± 1.0 vs. 2.83 ± 0.3 mmHg, IR vs. Sham, respectively; P < 0.05). Imidazole or SQ-29,548 returned Kf to baseline measurements (P < 0.05) and reduced Rt by 23 and 17%, respectively (P < 0.05). IR-induced increases in Pc were only slightly reduced by 500 µg/ml imidazole (14%; P = 0.05) but unaffected by lower doses of imidazole (5 or 50 µg/ml) or SQ-29,548. These data suggest that IR-induced pulmonary edema is caused by both increased microvascular permeability and increased hydrostatic pressure and that these changes are due, at least in part, to the ongoing release of TxA2.

capillary filtration coefficient; hydrostatic pressure; pulmonary vascular resistance; pulmonary edema


0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society




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