Effects of l-NA and Sodium Nitroprusside on Ischemia/Reperfusion-Induced Leukocyte Adhesion and Macromolecular Leakage in Hamster Cheek Pouch Venules

Author： Simões C. Svensjö E. Bouskela E.

Publisher： Academic Press

ISSN： 0026-2862

Source： Microvascular Research, Vol.62, Iss.2, 2001-09, pp. : 128-135

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Abstract

Our objective was to study how the topical application of a nitric oxide synthase inhibitor (l-NA, Nω-nitro-l-arginine) and a nitric oxide donor, sodium nitroprusside (SNP), could modulate leukocyte adhesion (sticking) and microvascular permeability as altered by ischemia/reperfusion (I/R) and topically applied histamine after I/R. Golden hamsters were prepared for intravital microscopy. Ischemia was induced by an inflatable silicon rubber cuff mounted around the neck of the cheek pouch prepared for intravital microscopy. Saline, l-NA, sodium nitroprusside, and histamine were applied in the superfusion solution. FITC–dextran was injected iv 30 min before initiation of ischemia as a marker of microvascular permeability. l-NA 10^-5 M inhibited both the increase in number of sticking leukocytes and the increase in vascular permeability after I/R compared with the untreated control group of hamsters. SNP neutralized this effect of l-NA on leukocytes and vascular permeability and caused arteriolar dilation at the concentration used, 10^-6 M. Both SNP and l-NA + SNP enhanced the I/R-induced macromolecular leakage. The topical application of SNP and SNP + l-NA did not modify the response to histamine after I/R compared with the untreated control group. In hamsters not subjected to I/R, histamine-induced macromolecular leakage was inhibited by l-NA and l-NA + SNP but was unchanged by SNP. It is concluded that inhibition of nitric oxide formation by l-NA reduced both leukocyte adhesion in postcapillary venules and the increase in macromolecular leakage and that a NO donor such as SNP could enhance the macromolecular leakage response to I/R.