Renal microcirculation and function were studied in the unilateral clamp-induced
ischemia/reperfusion model in anesthetized rats. After 60-min reperfusion fluorochromelabeled
globulin was injected i.v. allowing histological determination of capillary plasma flow patterns (CPFP). In the 60-min
ischemia protocol the untreated group revealed poor capillary labeling in the outer medulla (OM), whereas cortical perfusion patterns were only slightly altered. Pre- and postischemic treatment with
diltiazem led to significant improvement of CPFP in the OM: 4.9% of tissue areas were lying more than 60 microns from the next perfused capillary vs 70.2% after untreated
ischemia. Postischemic treatment with
diltiazem proved much less effective.
Inulin clearance (CIn) amounted to less than 2% of baseline values irrespective of the treatment regimen. However, in the 30-min
ischemia protocol, displaying normal CPFP, preservation of CIn was evident and most effective after pre- and postischemic
diltiazem treatment (53% vs 8% after untreated
ischemia). Measurements of tubular function, however, did not reveal any significant improvement after
diltiazem treatment. This observation and the fact that the drugs has a vasodilating effect lend support to the view that the preservation of glomerular filtration rate (GFR) is most likely mediated by vascular mechanisms. In conclusion, in this experimental model
diltiazem significantly reduced postischemic disturbances of renal microcirculation occurring after prolonged periods of
ischemia and was clearly efficient in maintaining GFR after shorter ischemic episodes; however, tubular function was not preserved. Our results, as well as those of other authors, strongly suggest that
diltiazem causes the aforementioned effects mainly by actions at the vascular site.