Ischemic Cells

The main differences between necrosis and apoptosis are in the triggers (accidental v. physiological), the process (energy-independent vs. dependent), and the outcomes (with vs. without inflammation). However, apoptosis and/or necrosis can be induced by the same causes in some cases (K16). Alteration of mitochondrial permeability is involved in both apoptosis and necrosis (K16). Both apoptosis and necrosis are found in conditions such as stroke and myocardial infraction (F5), and necrosis can occur secondary to apoptosis (T4). To preserve the usefulness of the two terms for denoting different modes of cell death while still recognizing possible overlap of the two processes (H7), some more descriptive terms have been proposed primary necrosis (oncosis, ischemic cell death) (Ml) and secondary necrosis (apoptotic necrosis, necrosis secondary to apoptosis) (K15). 

Kristian T., and Siesjo B.K. 1998 Calcium in ischemic cell death. Stroke 29, 705-718. 

Bretylium lengthens the ventricular (but not the atrial) action potential duration and effective refractory period. This effect is most pronounced in ischemic cells, which have shortened action potential durations. Thus, bretylium may reverse the shortening of action potential duration caused by ischemia. 

Lipton, P. (1999). Ischemic cell death in brain neurons. Physiol. Rev. 79, 1431—1568. 

In healthy cardiac cells, the recovery time from inactivation of sodium channels (back to the resting state) is quite rapid, so that the maximum number of channels is available for activation. In contrast, in sick cells, the recovery time is quite slow. In these sick cells, the action potential develops from the opening of fewer sodium channels, so the action potential is a slow sluggish upstroke as opposed to the fast upstroke in a healthy cell. A slow sluggish upstroke results in poor and perhaps no propagation of the action potential. Chronically depolarized or ischemic cells may (1) fail to conduct an action potential and therefore fail to contract or to transmit the action potential to neighboring cells or (2) become an ectopic pacemaker (due to a... 

Zhang R. L., ChoppM., Chen H., Garcia J.H., and Zhang Z. G. (1993) Postischemic (1 hour) hypothermia significantly reduces ischemic cell damage in rats subjected to 2 hours of middle cerebral artery occlusion. Stroke 24,1235-1240. 

Meldrum, B. S., Brierley, J. B. (1973, January). Prolonged epileptic seizures in primates Ischemic cell change and its relation to ictal physiological events. Archives of Neurology, 28, 10-17. 

Inhibitor 1 Inhibitor 2 Inhibitor 3 Effects on ischemic cell death... 

Brierley, J.B., Meldrum, B.S., Brown, A.W. (1973). The threshold and neuropathology of cerehral anoxic-ischemic cell change. Arch. Neurol. 29 367-74. 

M. Chopp, R. L. Zhang, H. Chen, Y. Li, N. Jiang, and J. R. Rusche, Postischemic Administration of an Anti-Mac-1 Antibody Reduces Ischemic Cell Damage after Transient Middle Cerebral Artery Occlusion in Rats, Stroke, 25 (1994) 869-876. 

Reimer KA, Lowe JE, Rasmussen MM, Jennings RB. The wavefront phenomenon of ischemic cell death I. 

K. A. Reimer, J. E. Lowe, M. M. Rassmussen and R. B. Jennings, The wavefront phenomenon of ischemic cell death. I. Myocardial infarct size vs. duration of coronary occlusion in dogs, Circulation 56,786-794, (1977). 

With a single channel conductance of more than 100 pS,1,20,22 only ten hemichannels need to be open to produce a millimolar cellular sodium influx,83 and such a millimolar increase in the intracellular sodium concentration has been measured during ischemia in whole hearts.84-86 The osmotic imbalance resulting from increased AMP, inorganic phosphate and sodium concentrations results in swelling and finally membrane rupture of the ischemic cells. 

Kempsi, O., Zimmer, M., Neu, A., Vonrosen, F., Jansen, M., and Baethmann, A., Control of glial cell volume in anoxia. In vitro studies on ischemic cell swelling,... 

Brown, A. W. and Brierly, J. B., Anoxic-ischemic cell change in rat brain light microscopic and fine-structural observations, J. Neurol. Sci., 16, 59, 1972. 

Bretylium increases action potential duration in ischemic cells. 

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