Distribution of capillary blood flow in rat kidney during postischemic renal failure

Abstract

Changes in distribution of intrarenal blood flow were studied in anesthetized rats during the acute phase of postischemic renal failure (1 h renal artery occlusion, 1 h reflow). Distribution of capillary plasma flow was determined by injecting fluorescein-isothiocyanate-globulin and lissamine-rhodamine-B200-globulin 1, 3, or 10 min prior to rapid freezing of the kidney. In histological sections it was possible to differentiate among the vessels perfused during the time of labeling because of their respective fluorescence. In these experiments all glomeruli became labeled within 1 min, although in contrast to the controls, the glomerular capillary network itself was not filled completely in the postocclusion organs. Incomplete labeling was far more pronounced, however, in the postglomerular network of the occlusion experiments. Due to this effect in the cortex and in the medulla, 11 and 58% of tissue, respectively, were found lying at a distance of more than 60 microns from the next vessel labeled after 1 min of dye circulation. In the control experiments there was no tissue within this distance. Prolonging the time of labeling up to 10 min caused little change in this pattern of distribution. In the occlusion experiments, the globulins were observed in nearly all Bowman spaces, but in less than half of the tubular lumina. The results strengthen the view that the ischemic insult leads primarily to disturbance of the postglomerular perfusion, which then results in trophic damage of the tubular system mainly within the renal medulla.

Comparison of protective effects of trimetazidine against experimental warm ischemia of different durations: early and long-term effects in a pig kidney model

“…The reduction in regional blood flow to the outer medulla occurring during IRI is more pronounced than that to the cortical capillaries in the postischemic kidney (36). In the present study, we have demonstrated a strong correlation between C Cr evolution and WI times as previously suggested (26).…”

Shiga Toxin 1 Causes Direct Renal Injury in Rats

“…Because no increase in the both serum and urine (14), but in these cases lipopolysaccharide, a well-known TNF inducer, may also have contributed to TNF production. Although the induction of both apoptosis and cytokine biosynthesis by Stx has been shown for renal cells (9,15), it was also reported that both phenomena in the cells can be induced on May 10, 2018 by guest http://iai.asm.org/ by ischemia (3,22) and that tubular cells in the medulla, where these phenomena were observed with the present study, are particularly susceptible to ischemic injury (38). Because our light-microscopic examination showed a few changes in some samples of both sham-operated and Stx1-perfused groups until 24 h, suggesting that these changes potentially resulted from ischemia during the operation, we cannot exclude the possibility that ischemia is involved in the mechanism of the induction of apoptosis and TNF-␣.…”

Cell death induced by acute renal injury: a perspective on the contributions of apoptosis and necrosis

“…The outer medullary region is marginally oxygenated under normal conditions and has high energy demands. The blood flow to outer medullary or corticomedullary junction region remains ϳ10% of normal during reperfusion (234,235). The microvasculature in this region becomes congested due to interstitial edema, red blood cell trapping, leukocyte adherence, and extravasation (22).…”