| Autor: |
Ramani, Kishin, Lust, W. David, Whittingham, Tim S., Lesnefsky, Edward J. |
| Zdroj: |
Journal of the American College of Cardiology; February 1995, Vol. 25 Issue: 2, Number 2 Supplement 1 p372A-372A, 1p |
| Abstrakt: |
Myocardial injury following ischemia and reperfusion is increased in the aging heart, including in the aging 24 mo Fischer 344 rat (mean survival 29 mo) compared to the Fischer 344 adult (6 mo). Adenosine (ADO) has been increasingly appreciated as a cardioprotective agent in myocardial ischemia. We hypothesized that a potential mechanism of the increased injury in the aging heart is decreased production of ADO in response to ischemia. Isolated buffer perfused (glucose 5 mM — insulin 5 μ/1) hearts from aging and adult Fischer 344 rats were subjected to stop-flow ischemia for either 2, 5, 10, 15 or 25 min after a 15 min equilibration phase. ADO and hypoxanthine (HX) were measured by HPLC. Tissue total adenylates, ATP, glycogen and lactate were measured.IschemiaPre-ischemia2 min5 min10 min15 min25 min(n=5)(n=5)(n=5)(n=5)(n=5)(n=5)ADO 6 mo0.2±0.10.7±0.10.7±0.12.2±0.237±0.64.5±0.324 mo0.2±0.105±0.10.3±0.1*1.1±0.3*2.1±0.3*3.5±0.4HX 6 mo2.0±0.21.6±0.22.3±0.32.2±0.125±0.22.8±0.224mo1.9±0.21.4±0.11.4±0.2*2.1±0.22.2±0.83.5±0.3(Mean±SE, nmol/mg protein)*p<0.05 vs 6 mo |
| Databáze: |
Supplemental Index |
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