Improved mitochondrial Ca2+ handling and functional recovery after ischemia reperfusion injury in hearts from old vs. young guinea pigs

We hypothesized that aging‐induced oxidative damage to mitochondria would result in mitochondrial [Ca2+] (m[Ca2+]) overload, depressed contractile function, and decreased NADH after ischemia reperfusion (IR) injury in old vs. young guinea pig hearts. Unpaced hearts (n=7 each) from young (< 2 mo)...

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Bibliographic Details
Published in:The FASEB journal 2007, Vol.21 (6), p.A1223-A1223
Main Authors: Johnson, Christopher, Camara, Amadou KS, Aldakkak, Mohammed, Varadarajan, Srinivasan G, Heisner, James S, Stowe, David F, Rhodes, Samhita S
Format: Article
Language:English
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Summary:We hypothesized that aging‐induced oxidative damage to mitochondria would result in mitochondrial [Ca2+] (m[Ca2+]) overload, depressed contractile function, and decreased NADH after ischemia reperfusion (IR) injury in old vs. young guinea pig hearts. Unpaced hearts (n=7 each) from young (< 2 mo) and old (> 24 mo) animals were perfused with Krebs‐Ringer’s solution (2.1 mM [Ca2+]) at 37°C. Left ventricular pressure (LVP, mmHg) was recorded with a saline filled latex balloon and transducer. Simultaneously, m[Ca2+] (nM) was measured ratiometrically by indo‐1 fluorescence with a fiber optic probe on the LV free wall. Hearts were subjected to 30 min global ischemia and 60 min reperfusion (RP). All data ± SEM, p
ISSN:0892-6638
1530-6860
DOI:10.1096/fasebj.21.6.A1223