In vivo heat shock preconditioning mitigates calcium overload during ischaemia/reperfusion in the isolated, perfused rat heart.

Autor: Szenczi, Orsolya, Kemecsei, Péter, Mikló;s, Zsuzsanna, Ligeti, László, Snoeckx, Luc, Riel, Natal, Buijs, Jorn, Vusse, Ger, Ivanics, Tamás
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Zdroj: Pflügers Archiv: European Journal of Physiology; Mar2005, Vol. 449 Issue 6, p518-525, 8p
Abstrakt: Heat shock (HS) pretreatment of the heart is effective in mitigating the deleterious effects of ischaemia/reperfusion. The main objective of this study was to determine whether the beneficial effect of HS is associated with the preservation of intracellular Ca2+ handling in the ischaemic/reperfused, isolated rat heart. Twenty-four hours after raising body core temperature to 42 °C for 15 min, rat hearts were perfused according to Langendorff and subjected to 30 min ischaemia followed by 20 min reperfusion. Cyclic changes of cytoplasmic calcium ion [Ca2+i] levels were measured by surface fluorometry using Indo-1 AM. Reperfused HS hearts showed improved recovery of contractile function compared with control hearts: end-diastolic pressure: 45±11 vs. 64±22 mm Hg; developed pressure: 72±12 vs. 41±20 mm Hg; maximum rate of pressure increase (+dP/dtmax): 1,513±305 vs. 938±500 mm Hg/s; maximum rate of pressure decrease (-dP/dtmax): -1,354±304 vs. -806±403 mm Hg/s. HS hearts displayed a significantly lower end-diastolic cytosolic [Ca2+] ([Ca2+]i) after reinstallation of flow. The dynamic parameters of the Ca2+i transients, i.e. the maximum rate of increase/decrease (±dCa2+i/dtmax) and amplitude, did not differ between reperfused control and HS hearts. The novel finding of this study is that improved performance of the HS-preconditioned heart after an ischaemic insult is associated with a reduced end-diastolic Ca2+i load, and most likely, preserved Ca2+ sensitivity of the myocardial contractile machinery. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index