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We briefly review what appear to be the most important elements responsible for renal cell injury during and after oxygen deprivation. Recent studies in numerous laboratories have vastly improved our understanding of the changes in cell function that occur during ischemia and yet, the underlying mechanisms by which tubule damage and cell death occur remain elusive. We attempt to separate the effects that occur during ischemia or anoxia from those occurring during reperfusion (reoxygenation). These are not always separable, especially because it appears that ischemia initiates a series of complex events that may only become manifested during reperfusion. Ischemia-induced renal dysfunctions are clearly multifactorial events that will require major efforts to unravel.
K G Dickman, and
W R Jacobs, and
L J Mandel
January 1987,
Advances in experimental medicine and biology,
K G Dickman, and
W R Jacobs, and
L J Mandel
January 1998,
Mineral and electrolyte metabolism,
K G Dickman, and
W R Jacobs, and
L J Mandel
September 1970,
Polski tygodnik lekarski (Warsaw, Poland : 1960),
K G Dickman, and
W R Jacobs, and
L J Mandel
December 1983,
Kidney international. Supplement,
K G Dickman, and
W R Jacobs, and
L J Mandel
October 1987,
Kidney international. Supplement,
K G Dickman, and
W R Jacobs, and
L J Mandel
October 1990,
The American journal of clinical nutrition,
K G Dickman, and
W R Jacobs, and
L J Mandel
May 1968,
The Journal of laboratory and clinical medicine,
K G Dickman, and
W R Jacobs, and
L J Mandel
April 1991,
The American journal of clinical nutrition,
K G Dickman, and
W R Jacobs, and
L J Mandel
January 1983,
Nihon rinsho. Japanese journal of clinical medicine,
K G Dickman, and
W R Jacobs, and
L J Mandel
July 1983,
Nihon Jinzo Gakkai shi,
