Heart reperfusion free radicals produced

In an attempt to quantify free radicals produced in ischemic and reperfused myocardium, Zweier et al. [73,74] have used low-temperature ESR and concluded that oxy radicals (peroxyl and superoxide radicals) are produced in myocardial rat hearts. In these studies, heart tissues were subjected to pulverization prior to ESR studies. At about the same time that we became interested in the application of direct ESR in myocardial research, we also became immediately aware of the grinding artifact in myocardial tissues. 

We then asked the question, can we detect free radicals produced during ischemia and reperfusion in myocardial tissues using a more gentle tissue processing technique, namely by chopping of the heart tissues ... 

Although the major thrust of this chapter is centered on the free radical hypothesis of myocardial injury, it is essential to realize that calcium overload in myocardial cells during ischemia and reperfusion could be the primary cause of myocardial injury [40,41]. It is also likely that mechanisms of free radical production and calcium overload are related and not mutually exclusive [40]. Alterations in intracellular calcium homeostasis are often accompanied by depletion of cellular antioxidants [42]. The mitochondrial Ca2+ homeostasis has been shown to affect oxy radicals produced through the electron-transport chain [43], Reperfusion and reoxygenation of hearts are characterized by marked increase in cytosolic and mitochondrial levels of Ca2+ [44]. Ruthenium red, which inhibits mitochondrial Ca2+ uptake, also protects the heart against reperfusion-induced damage [45,46],... 

---