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Am J Physiol Regul Integr Comp Physiol 280: R959-R967, 2001;
0363-6119/01 $5.00
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Vol. 280, Issue 4, R959-R967, April 2001

Nitric oxide increases fluid extravasation from the splenic circulation of the rat

Peter S. Andrew, Yiming Deng, Richard Sultanian, and Susan Kaufman

Departments of Physiology and Medicine, University of Alberta, Edmonton, Alberta T6G 2S2, Canada

We hypothesized that nitric oxide (NO) contributes to intrasplenic fluid extravasation by inducing greater relaxation in splenic resistance arteries than veins such that intrasplenic microvascular pressure (PC) rises. Fluid efflux was estimated by measuring the difference between splenic blood inflow and outflow. Intrasplenic infusion of the NO donor S-nitroso-N-acetylpenicillamine (SNAP) (0.3 µg · 10 µl-1 · min-1) caused a significant increase in intrasplenic fluid efflux (baseline: 0.8 ± 0.4 ml/min, n = 10 vs. peak rise during SNAP infusion: 1.3 ± 0.4 ml/min, n = 10; P < 0.05). Intrasplenic PC was measured in the isolated, blood-perfused rat spleen. Intrasplenic infusion of SNAP (0.1 µg · 10 µl-1 · min-1) caused a significant increase in PC (saline: 10.9 ± 0.2 mmHg, n = 3 vs. SNAP: 12.2 ± 0.2 mmHg, n = 3; P < 0.05). Vasoreactivity of preconstricted splenic resistance vessels to sodium nitroprusside (SNP) (1 × 10-12-1 × 10-4 M) and SNAP (1 × 10-10-3 × 10-4 M) was investigated with the use of a wire myograph system. Significantly greater relaxation of arterioles than of venules occurred with both SNP (%maximal vasorelaxation: artery 96 ± 2.3, n = 9 vs. vein 26 ± 1.9, n = 10) and SNAP (%maximal vasorelaxation: artery 50 ± 3.5, n = 11 vs. vein 32 ± 1.7, n = 8). These results are consistent with our proposal that differential vasoreactivity of splenic resistance arteries and veins to NO elevates intrasplenic PC and increases fluid extravasation into the systemic lymphatic system.

spleen; microvascular pressure; blood flow


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