Na+ overload-induced mitochondrial damage in the ischemic heart.
Ischemia induces a decrease in myocardial contractility that may lead more or less to contractile dysfunction in the heart. When the duration of ischemia is relatively short, myocardial contractility is immediately reversed to control levels upon reperfusion. In contrast, reperfusion induces myocardial cell death when the heart is exposed to a prolonged period of ischemia. This phenomenon is the so-called "reperfusion injury". Numerous investigators have reported the mechanisms underlying myocardial reperfusion injury such as generation of free radicals, disturbance in the intracellular ion homeostasis, and lack of energy for contraction. Despite a variety of investigations concerning the mechanisms for ischemia and ischemia-reperfusion injury, ionic disturbances have been proposed to play an important role in the genesis of the ischemia-reperfusion injury. In this present study, we focused on the contribution of Na+ overload and mitochondrial dysfunction during ischemia to the genesis of this ischemia-reperfusion injury.
Takeo
Satoshi
S
Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji 192-0392, Japan. takeos@ps.toyaku.ac.jp
Tanonaka
Kouichi
K
D000818:Animals; D004734:Energy Metabolism; D066298:In Vitro Techniques; D008929:Mitochondria, Heart / Q000378:metabolism / Q000473:pathology*; D017202:Myocardial Ischemia / Q000378:metabolism / Q000473:pathology*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology; D011188:Potassium / Q000502:physiology; D051381:Rats; D012964:Sodium / Q000378:metabolism / Q000633:toxicity*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D019831:Sodium-Calcium Exchanger / Q000037:antagonists & inhibitors
D026941:Sodium Channel Blockers; D019831:Sodium-Calcium Exchanger; D012964:Sodium; D011188:Potassium