Renal vascular response to vasodilators following warm ischemia and cold storage preservation in dog kidneys.

The purpose of this study was to determine whether warm ischemia (WIT) and cold storage preservation (CSP) impair endothelium-dependent vascular relaxation in the kidney. Twenty-four canine kidneys were harvested, preserved with CSP for 24 or 48 hours, and then perfused with canine blood at 37 C for the determination of glomerular filtration rate (GFR), perfusion flow rate, and renal vascular resistance (RVR). There were four experimental groups: Group I--no WIT followed by 24 hours CSP, Group II--30 minutes WIT followed by 24 hours CSP, Group III--no WIT followed by 48 hours CSP, Group IV--30 minutes WIT followed by 48 hours CSP. Endothelial function in each group was evaluated using acetylcholine (ACh, 1 mg. bolus) as an endothelial dependent vasodilator, and sodium nitroprusside (NP, 10 mg. bolus) as an endothelial independent vasodilator. Glomerular filtration rate was significantly less (P < .05) and RVR was significantly greater (P < .05) for kidneys from Groups II, III and IV compared to group I. The highest RVR was observed in kidneys from Groups II and IV. Nitroprusside administration caused an equivalent reduction in RVR among all four study groups. ACh administration caused a similar reduction in RVR in Groups I and III; however, the change in RVR was significantly less in Groups II and IV (P < .05). We hypothesize that the more severe ischemic insult in the latter groups led to vascular endothelial damage with a consequent loss of ability to secrete endothelium-derived relaxing factor in response to ACh administration.