Chronic renal insufficiency was modeled in rats by unilateral nephrectomy and electrocoagulation of both poles of the remaining kidney; acute renal failure was induced by 90-min clamping of the vascular pedicle of the only kidney. Injection of unfractionated culture of human fetal kidney cells or bone marrow mesenchymal stem cells into damaged kidney restored its function in rats with chronic renal insufficiency (observation period up to 2 months). After 2.5 months a relapse of chronic renal insufficiency was observed in 1 of 3 rats receiving human fetal kidney cells and in 1 of 2 animals receiving bone marrow mesenchymal stem cell culture. Injection of bone marrow mesenchymal stem cell culture to rats with acute renal failure improved recovery of renal function and prevented the death from uremia, while injection of total culture of human fetal kidney cells had virtually no effect on the course of acute renal failure.
The therapeutic effect of intravenous injection of human fetal bone marrow mesenchymal stem cells or summary culture of kidney cells were studied on models of chronic or acute renal failure in outbred albino rats. Both cell types promoted improvement and normalization of the renal function in rats with stable chronic renal insufficiency (2 weeks after kidney cell injection, 1 month after bone marrow mesenchymal stem cell injection). Renal function remained normal or subnormal during the delayed period (3-3.5 months after injection). In rats with latent stage of chronic renal insufficiency, exacerbation was induced by additional 40-min ischemia. All rats receiving intravenous injection of saline died. Improvement of the functional parameters started 2 weeks after injection of kidney cells or bone marrow mesenchymal stem cells, and normalization was observed after 1.1-5 months. During the delayed period (after 3-4 months), functional parameters retained at normal or subnormal levels. In experimental series III, all rats with acute renal failure intravenously injected with saline (control) died from uremia on days 2-4. After injection of kidney cells 50% rats survived and renal function in these animals returned to normal after 2 weeks. After injection of bone marrow mesenchymal stem cells 83% rats survived, functional parameters returned to normal after 3 weeks.
Blood supply to the pelvic organs of outbred male rats was diminished by graduated constriction of the distal part of the inferior vena cava. Deficiency of intramural blood supply in prostate and urinary bladder was revealed by bioimpedance harmonic analysis according to the magnitude of first cardiac peak in the bioimpedance spectrogram. In 1-1.5 months, the histological examination revealed the glandular-stromal form of progressive benign prostatic hyperplasia in all ischemic rats. The development of hyperplasia was not accompanied by the changes in testosterone, dihydrotestosterone, or estradiol in blood and prostatic tissue. Assessment of vesical functional status by recording the intravesical pressure during infusion cystometry revealed an increase in the amplitude of spontaneous fluctuations of detrusor tone and intravesical pressure during bladder filling, which can be considered as indicator of detrusor hyperactivity. The data conclude that chronic ischemia of pelvic organs is an individual pathogenic factor in the development of benign prostatic hyperplasia and associated urinary disorders.
The ability of cc-tocopherol in the form of an emulsion to augment the antioxidant reserve of kidneys during their ischemia or storage is explored. Over 10 min after an intravenous injection of the emulsion into rats or rabbits at 10 mg/kg body weight, the mean a-tocopherol concentration in the renal cortical layer rose from 6.7+0.2 to 7.4+0.2 gg/g (p<0.05); the injection also slowed the accumulation of malonic dialdehyde in cortical layer homogenates of intact and ischemic kidneys during ascorbate-induced lipid peroxidation. In kidneys stored at 4~ in a preservative solution to which the a-tocopherol emulsion had been added (10 mg/liter), lipid peroxidation was found to be inhibited after 24 and 48 h of storage.
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