Nitric oxide and thromboxane A2 modulate pulmonary pressure after ischemia and intestinal reperfusion

Transplantation Proceedings
M SłupskiA T Sinjab

Abstract

Nitric oxide (NO) and thromboxane A(2) (TxA(2)) are paracrine substances that likely contribute to IR-induced lung injury. This study examined the hypothesis that pulmonary vasoconstriction during ischemia is induced by NO synthesis and ischemia/reperfusion (IR)-induced TxA(2). Wistar rats underwent 30 or 60 minute of intestinal ischemia with 60 minute of IR in situ. Sham-operated animals (Sham) served as the controls. After ischemia and IR or Sham, the pulmonary vessels were cannulated to perfuse the lungs with Krebs buffer in vitro. Pulmonary arterial (Ppa) and venous (Ppv) pressures were measured to calculate vascular resistance (Rt). After baseline measurements, the nonselective inhibitor (N(omega)-nitro-L-arginine methyl ester), the selective nNOS inhibitor 1-(2-trifluoromethylphenyl) imidazole (TRIM), TxA(2) synthase inhibitor imidazole or TxA(2)-receptor antagonist SQ-29,548 was added to the perfusate prior to measurements of Ppa, Ppv, and Ppc. The Rt was 73% greater in the injured group (P = .01). Pc of in the IR lungs was about twice that of controls (7.2 +/- 0.71 vs 2.43 +/- 0.36 mm Hg, respectively; P < .01). The nNOS inhibitor TRIM, imidazole, or SQ-29,548 reduced Rt by 45%, 33%, and 26%, respectively. IR-induced in...Continue Reading

References

Nov 16, 2002·American Journal of Physiology. Heart and Circulatory Physiology·Norbert WeissmannFriedrich Grimminger

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Citations

Sep 18, 2012·Experimental and Therapeutic Medicine·Katarzyna Szadujkis-SzadurskaGrzegorz Matusiak
Feb 15, 2013·Experimental and Therapeutic Medicine·Katarzyna Szadujkis-SzadurskaGrzegorz Matusiak

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