Ultrastructural damage associated with reoxygenation of the anoxic myocardium

Hearse, David J.; Humphrey, S.M.; Nayler, Winifred G.; Slade, A.M.; Border, D. J.

doi:10.1016/0022-2828(75)90121-2

Cited by 183 publications

(47 citation statements)

References 11 publications

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“…The concept of myocardial necrosis due to reperfusion, as distinguished from necrosis due to ischemia, was introduced by Hearse et al in 1975. 1 They reported that there was evidence of damage to the ultrastructure of the myocardium in hearts subjected to ischemia followed by reperfusion that was not present in hearts exposed to ischemia alone. After early reperfusion of animal models of myocardial infarction or stroke, up to 60% of the total damage to the heart 2 and 73% of the damage to the brain 3 was caused by processes initiated during reperfusion.…”

Section: Role Of Iron In Reperfusion Injurymentioning

confidence: 99%

Iron-mediated cardiovascular injury

Horwitz

Rosenthal

1999

Vasc Med

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Abstract:Iron is an essential element for normal cellular function and general health. However, iron may play a pathologic role in certain cardiac conditions including reperfusion injury, hemochromatosis, ␤-thalassemia and coronary atherosclerosis. It also may play a role in injury due to anthracycline cardiotoxicity. Removal of iron via phlebotomy for hemochromatosis and chelation therapy for ␤-thalassemia are proven treatments. Cell culture, and isolated organ and animal studies suggest that depleting iron stores may prevent reperfusion injury, restenosis and even atherogenesis. This article will review mechanisms by which iron overload states and normal iron stores contribute to cardiovascular pathophysiology and the accumulating evidence that iron chelation may prevent restenosis and atherogenesis.

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Section: Role Of Iron In Reperfusion Injurymentioning

confidence: 99%

Iron-mediated cardiovascular injury

Horwitz

Rosenthal

1999

Vasc Med

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“…This rigor was partly reversible in 60% of the cells. Rigor in isolated heart cells has been described by several groups and has been attributed to a drop in cytosolic ATP below 50 #m (Hearse, Humphrey, Nayler, Slade & Border, 1975;Stern et al 1985). The rigor is thought to further consume ATP which leads via a positive feedback to an acceleration of the process.…”

Section: Anoxia Causes Rigor Only If Cells Are Not Openedmentioning

confidence: 99%

Anoxia induces time‐independent K+ current through KATP channels in isolated heart cells of the guinea‐pig.

Benndorf

Bollmann

Friedrich

et al. 1992

The Journal of Physiology

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SUMMARY1. Isolated ventricular heart cells of the guinea-pig were exposed to anoxia (Po2 < 01 Torr) which induced a time-independent K+ current. This current was studied with the patch clamp technique in the whole-cell and cell-attached configuration.2. The latency until anoxia-induced changes of whole-cell current developed was distributed exponentially (mean 10-5 min; n = 41). The current was abolished within 2-4 s of reoxygenation.

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“…Reperfusion injuries are often attributed to elevated oxygen tension, i.e., the `oxygen paradox' [5] and elevated intracellular Ca 2+, i.e., the `calcium paradox' [4]. The intracellular Ca 2+ concentration is controlled by ATP-dependent Ca 2+ pumps in the SL and SR.…”

Section: Discussionmentioning

confidence: 99%

“…In the ischemic myocardium, disruptions in the supply of oxygen and in fatty acid metabolism result in accelerated glycolysis and the accumulation of lactate [1][2][3]. Ischemia-reperfusion injuries are believed to be due to abrupt and large increase in flows of Ca2+ and oxygen into cells, known as the `calcium paradox' [4] and `oxygen paradox' [5]. Adenosine 5'-triphosphate (ATP) provides energy not only for muscular contraction but also for cellular ionic homeostasis as well.…”

Section: Increasementioning

confidence: 99%