Invited Symposium: Cerebral Artery Pharmacology and Physiology



1. Cell calcium metabolism and ischemia

2. Mitochondria and ischemic cell death



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Calcium and Mitochondria in Ischemic Cell Death

Kristian, T (Center for the Study of Neurological Disease, The Queen's Medical Center, Honolulu, USA)
Siesjo, BK (Center for the Study of Neurological Disease, The Queen's Medical Center, Honolulu, USA)

Contact Person: Tibor Kristian (tibor@www.cns.queens.org)


Ischemia is accompanied by mitochondrial dysfunction leading to fall in ATP concentration and phosphorylation potential, and loss of cellular ion homeostasis. Particularly, the raise in intracellular calcium concentration due to bioenergetical failure is believed to be harmful for cells. Following brief ischemic insults, mitochondrial function is usually normalized in the early reperfusion period and the ion concentration gradients are re-instituted. However reperfusion, especially following long-lasting ischemic periods, may be accompanied by secondary mitochondrial failure, which can trigger a lethal cascade of events known as apoptosis, or cause necrotic cell death. Recently there is accumulating evidence revieling the possible scenario of pathophysiological and biochemical mechanisms which orchestrate the events playing a significant role in ischemic cell death.

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Presentation Number SAkristian0829

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Kristian, T; Siesjo, BK; (1998). Calcium and Mitochondria in Ischemic Cell Death. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/laher/kristian0829/index.html
© 1998 Author(s) Hold Copyright