J. Y. Cheung

Calcium and ischemic injury

ISCHEMIC diseases of the heart, kidney, and brain continue to be the primary causes of mortality and morbidity in the United States and other Western industrialized nations. The magnitude of the pr...

The Cellular Basis of Ischemic Acute Renal Failure

It has long been recognized that obstruction of the blood supply to the normothermic kidney for periods of greater than 1 hr will almost invariably result in tubular necrosis and the clinical picture of acute renal failure. As the duration of arterial obstruction increases from 30 to 60 min, the proportion of kidneys that suffer damage increases, as does the extensiveness of damage. In the past few years there has been heightened interest in the nature of the lesion(s) caused by ischemia which results in irreversible cell injury even if blood flow to the kidney is restored. Identifying the critical change or changes that doom the cell to certain death will not only add to our knowledge of cellular physiology but possibly provide the basis for therapeutic interventions aimed at preventing or delaying the onset of the irreversible change(s). It is this latter hope that has done much to stimulate research.

Determination of isolated myocyte viability: Staining methods and functional criteria

Single ventricular cells tolerant to physiological levels of calcium have been successfully isolated from adult rat heart. These cells exhibit morphological as well as functional characteristics of the intact myocardium. Under anaerobic incubations either in the absence of extracellular calcium or in the presence of 6% PEG, myocytes excluded Trypan blue despite severe derangements in biochemical functions. We suggest that Trypan blue entry may be a rather insensitive criterion of cell injury. We recommend the combination of rod-shape morphology, ATP levels and the ability to contract under external pacing as alternative simple tests of cell viability.