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Biomedical subjects

P Visweswaran

Publications and source records attributed to P Visweswaran.

6 recordsLinked to original sources
PubMed1999

Rhabdomyolysis.

Dissolution of the skeletal muscle, resulting in extravasation of the intracellular toxic metabolites into the circulatory system, and the accompanying manifestations, constitutes the clinical syndrome of rhabdomyolysis. The most frequent complication of this syndrome is acute renal failure, and its most life threatening side effects are hyperkalemia and metabolic acidosis. Intracellular release of free iron from hemeprotein and the oxidant stress is the principle mechanism by which the proximal tubular cytotoxicity is produced. The potential pathogenic mechanisms and the strategies to prevent rhabdomyolysis induced acute renal failure are discussed in this article.

Acute Kidney Injury↗
PubMed1997

Mannitol-induced acute renal failure.

The osmotic diuretic mannitol may be used in diverse clinical settings, such as providing "renal protection" in patients at risk for acute renal failure, decreasing intracranial pressure in patients with intracranial trauma, and preventing the dialysis-disequilibrium syndrome. Mannitol is commonly used after cardiac catheterization, cardiovascular surgery, and exposure to intravenous contrast dyes. This study presents a case in which a long-term renal transplant recipient receiving cyclosporine therapy concomitantly developed acute renal failure after the administration of high-dose mannitol in an attempt to induce an osmotic diuresis. The diagnosis of "osmotic nephrosis" was confirmed by renal biopsy, and the condition was reversed by cessation of the agent. Studies in experimental animals indicate that cyclosporin A can potentiate the tubular toxicity of mannitol, but such an association has not been verified in humans. Numerous studies confirm the nephrotoxic potential of high-dose mannitol, especially in patients with renal insufficiency. The clinical utility of the osmolar gap in preventing mannitol nephrotoxicity is emphasized.

Acute Kidney Injury↗
PubMedDate not supplied

Stimulation of growth and migration of vascular endothelial cells by vascular endothelial growth factor transduced smooth muscle cells in co-culture.

Vascular endothelial growth factor (VEGF) is a secreted mitogen with high specificity toward endothelial cells. Expression of VEGF by smooth muscle cells in vivo may be an important stimulus for the regrowth of the endothelium after damage caused by interventions such as angioplasty. The levels of VEGF secreted by cultured smooth muscle cells minimally stimulated growth of endothelial cells in co-culture. Full length cDNA for the 165 amino acid residue, bovine VEGF (VEGF165), was isolated from calf liver total RNA by reverse transcriptase polymerase chain reaction (RT-PCR) techniques, and used to generate plasmid constructs for transfection. Bovine aortic smooth muscle cells (BSMC), stably transfected with VEGF165 plasmid DNA, secreted mitogen into conditioned culture medium at levels that are physiologically relevant (2-4 ng/ml). Transformed BSMC stimulated growth of bovine aortic endothelial cells (BAEC) in co-culture, to a significantly greater extent than mock transfected BSMC. Migration of BAEC was also enhanced by the presence of VEGF transduced BSMC. These data suggest that smooth muscle cells, genetically engineered to produce VEGF, may provide biologic linings in cardiovascular prostheses that could promote the growth of endogenous endothelial cells.

Animals↗