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• W2080334804 abstract "It has been postulated nitric oxide (NO) can react with superoxide anion (·O⁻₂) to generate hydroxyl (·OH) radical. If this is correct inhibition of NO synthesis could attenuate ·OH radical mediated ischemia/reperfusion injury. Therefore we studied the effects of N^G-nitro-l-arginine (l-NNA), a competitive inhibitor of the NO synthase enzyme on ischemia/reperfusion injury in isolated perfused rat hearts. Three groups of rats (<i>n</i>= 12–15) were studied. Group I: Untreated ischemia/reperfusion control (37.5 min of global ischemia follows by 20 min reperfusion); Group II: ischemia/reperfusion with 25μm N^G-nitro-l-arginine; and Group III: ischemia/reperfusion in the presence of l-NNA and 2mm l-arginine, the substrate for NO synthase. Coronary flow (in ml/min) and ventricular developed pressure +dP/dt and -dP/dt were measured 5 min prior to ischemia and at the end of reperfusion. Baseline preischemic developed pressure was significantly lower in l-NNA perfused hearts than controls (76.8±5.9 <i>v</i> 97.6±2.9 mmHg, <i>P</i><0.05). However, the developed pressure following reperfusion was significantly greater in l-NNA perfused hearts (57.4±7.4 <i>v</i> 20.8±6.4 mmHg in control). This protective effect was reversed by the addition of l-arginine. Preischemic coronary flow was decreased significantly in the l-NNa group (6.4±0.5ml/min) compared to controls (11.6±0.7ml/min). The duration of sinus rhythm was significantly improved from 3.8±1.2 min in controls to 15.1±0.8 min in l-NNA perfused hearts. A corresponding significantly lower incidence of arrhythmias was observed (10.2±1.5 in ischemia/reperfusion group <i>v</i> 1.7±0.8 min with l-NNA). Again, hearts perfused with l-NNA plus l-arginine had more arrhythmias and a shorter duration of sinus rhythm. The results show that despite the reduction of myocardial contractility and coronary flow prior to ischemia l-NNA significantly preserved myocardial contractility and reduced arrhythmias following reperfusion. Electron spin resonance or cytochrome <i>c</i> reduction assay demonstrated that l-NNA did not scavenge ·OH nor ·O⁻₂ radical directly. These results suggest that ischemia/reperfusion injury observed in this model may in part be due to ·OH radical formed as a result of NO interaction with ·O⁻₂ and that inhibition of this pathway by l-NNA leads to recovery of myocardial function." @default.
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• W2080334804 date "1995-01-01" @default.
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• W2080334804 title "Sustain inhibition of nitric oxide by NG-nitro-l-arginine improves myocardial function following ischemia/reperfusion in isolated perfused rat heart" @default.
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• W2080334804 doi "https://doi.org/10.1016/s0022-2828(08)80038-7" @default.
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