Impermeant Solutes and Cellular Calcium Metabolism in Pathogenesis of Acute Renal Failure.
Abstract
Using a rat model of in vivo renal ischemia and one of gentamicin-induced nephrotoxicity as well as the freshly isolated preparation of rat proximal tubules, it was found that adenosine triphosphate levels of rat kidney cortex improves for 3-6 hours after anoxia but then subsequently declines with continued reperfusion; that calcium accumulates in mitochondria in vivo during reflow; that in vitro mitochondria return to normal buffering capacity soon after reflow begins but thereafter this capacity is lost. Finally, endoplasmic reticulum are better preserved as calcium transporting vessicles than are mitochondria and gentamicin in vivo induces early, and increases in an intracellular calcium compartment or pool even before functional and morphologic injury is seen. Keywords: Acute renal failure; norepinephrine; verapamil; nifedipine; mannitol.
Document Details
- Document Type
- Technical Report
- Publication Date
- Feb 01, 1985
- Accession Number
- ADA178516
Entities
People
- Robert W. Schrier
Organizations
- University of Colorado Boulder