Abstract
Nitric oxide and carbon monoxide exert vasodilatory effects that minimize ischaemia-reperfusion injury. An isolated porcine kidney model was used to assess the effects of administering the nitric oxide donor sodium nitroprusside (SNP) and carbon monoxide-releasing molecule (CORM) 3 during a period of warm preservation followed by reperfusion. Kidneys were perfused under warm preservation conditions after 10 min of warm ischaemia and 16 h of cold storage in four groups: SNP, control, CORM-3 and inactive CORM-3 (inactive control). Renal function and viability were assessed. SNP and CORM-3 increased renal blood flow (RBF) during warm preservation (P = 0.014). After reperfusion, RBF was significantly improved in the CORM-3 group compared with the control group (P = 0.019). The reduction in creatinine clearance was significantly less in the CORM-3 group than in the inactive CORM-3 group (P = 0.021), and serum creatinine levels were significantly lower (P = 0.029). There was a negative correlation between RBF during warm preservation and functional parameters during reperfusion (creatinine concentration: r(s) = - 0.722, P < 0.001; sodium excretion: r(s) = - 0.912, P < 0.001). The beneficial vasodilatory effects of CORM-3 during warm preservation improved renal function during reperfusion; SNP exerted similar, although less pronounced, effects.
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