Abstract
We recently observed that 30 min of bilateral renal arterial, venous, or pedicle occlusion with 2-h reperfusion differentially induced acute kidney injury (AKI), which was suggested to be probably resulted from their directly exerting dissimilar impacts on kidney during the ischemic period. The present study was further designed to evaluate and prove this suggestion. Anesthetized male Sprague-Dawley rats were divided in two distinct supragroups with 30-min bilateral renal ischemia alone (BI) or followed by 30-min reperfusion (BIR), which each had four different groups (n = 8) of subjecting to renal artery, vein, or pedicle clamping and also sham operation. In the BI groups, artery clamping caused lower renal tissue injury than pedicle clamping but vein occlusion caused the highest levels of kidney histological damages along with the widespread hemorrhagic congestion. In the BIR groups, renal vascular congestion, intratubular cast, and edema decreased, but tubular epithelial injury did not significantly change in comparison to their equivalents BI groups. However, the orders of total renal tissue damages in the BIR groups were still as clamping renal veins > > pedicles > arteries and in association with their proportionally developed renal hemodynamic, excretory, and urine-concentrating dysfunctions. The transmission of high arterial pressure into renal microvessels and rupturing of their walls during venous-clamping augment, but the retrograde blood flow from veins into kidney during artery clamping attenuates induction of renal tissue injury with respect to pedicle clamping not only at the ischemic period but also at the early reperfusion period and along with the proportional development of renal dysfunctions.
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