Critical timing of -arginine treatment in post-ischemic myocardial apoptosis?role of NOS isoforms

Liang, Feng; Gao, Erhe; Tao, Ling; Liu, Huirong; Qu, Yan; Christopher, Theodore A.; Lopez, Bernard L.; L, Xin

doi:10.1016/j.cardiores.2004.01.025

Cited by 34 publications

(17 citation statements)

References 26 publications

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“…We hypothesized that this is likely NO accumulation during the myocardial infarction due to the excessive supplement of NO released from the NO moiety plus a large amount of NO induced from endogenous iNOS, where a high concentration of NO is believed to be detrimental to cardiac tissue (8,44,48). Interestingly, Liang et al (22) demonstrated that L-arginine (a substrate for NO production) administered at different time points during ischemia-reperfusion exerted different effects on postischemic myocardial injury. Thus, in the present study, we limited the treatment period of NOaspirin before the induction of MI/R and evaluated its cardioprotective effect by evaluating infarct size and left ventricular (LV) function recovery at an extended reperfusion time (48 h) compared with those of vehicle-and aspirin-treated groups against lethal reperfusion injury, as well as the possible biochemical and molecular mechanisms involved in endogenous NO production blocked by NOS inhibitor to define the NO role from exogenous NO donor in ischemia-reperfused rats.…”

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confidence: 99%

Cardioprotective effects of nitric oxide-aspirin in myocardial ischemia-reperfused rats

Fu¹,

Wang²,

Chen³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Cardioprotective effects of nitric oxide-aspirin in myocardial ischemia-reperfused rats. Am J Physiol Heart Circ Physiol 293: H1545-H1552, 2007. First published May 25, 2007; doi:10.1152/ajpheart.00064.2007.-In this study, the cardioprotective effects of nitric oxide (NO)-aspirin, the nitroderivative of aspirin, were compared with those of aspirin in an anesthetized rat model of myocardial ischemia-reperfusion. Rats were given aspirin or NO-aspirin orally for 7 consecutive days preceding 25 min of myocardial ischemia followed by 48 h of reperfusion (MI/R). Treatment groups included vehicle (Tween 80), aspirin (30 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ), and NO-aspirin (56 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ). NO-aspirin, compared with aspirin, displayed remarkable cardioprotection in rats subjected to MI/R as determined by the mortality rate and infarct size. Mortality rates for vehicle (n ϭ 23), aspirin (n ϭ 22), and NO-aspirin groups (n ϭ 22) were 34.8, 27.3, and 18.2%, respectively. Infarct size of the vehicle group was 44.5 Ϯ 2.7% of the left ventricle (LV). In contrast, infarct size of the LV decreased in the aspirin-and NOaspirin-pretreated groups, 36.7 Ϯ 1.8 and 22.9 Ϯ 4.3%, respectively (both P Ͻ 0.05 compared with vehicle group; P Ͻ 0.05, NO-aspirin vs. aspirin ). Moreover, NO-aspirin also improved ischemiareperfusion-induced myocardial contractile dysfunction on postischemic LV developed pressure. In addition, NO-aspirin downregulated inducible NO synthase (iNOS; 0.37-fold, P Ͻ 0.01) and cyclooxygenase-2 (COX-2; 0.61-fold, P Ͻ 0.05) gene expression compared with the vehicle group after 48 h of reperfusion. Treatment with N G -nitro-L-arginine methyl ester (L-NAME; 20 mg/kg), a nonselective NOS inhibitor, aggravated myocardial damage in terms of mortality and infarct size but attenuated effects when coadministered with NO-aspirin. L-NAME administration did not alter the increase in iNOS and COX-2 expression but did reverse the NO-aspirin-induced inhibition of expression of the two genes. The beneficial effects of NO-aspirin appeared to be derived largely from the NO moiety, which attenuated myocardial injury to limit infarct size and better recovery of LV function following ischemia and reperfusion. nitroaspirin; aspirin; cardioprotection; ischemia-reperfusion; infarct size ISCHEMIC MYOCARDIAL TISSUE will inevitably induce necrosis if blood flow is not restored immediately. Early reperfusion after coronary obstruction is well established to recover injured myocardium; nevertheless, reperfusion itself is believed to bring about additional cellular injury (25,30). During the last two decades, numerous studies have been done that focus on the roles of nitric oxide (NO) in the pathogenesis progress and pharmacological intervention of myocardial ischemia and reperfusion. Of them, exogenous NO donors may provide therapeutic benefit and are also a recent conceptual advance in the management of reperfusion damage (1,17,19,39). However, conventional NO donors (e.g., organic nitrates) frequently result in unwanted hemodynamic effects due to the ...

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confidence: 99%

Cardioprotective effects of nitric oxide-aspirin in myocardial ischemia-reperfused rats

Fu¹,

Wang²,

Chen³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…Third: we measured the enzymatic activity for assessment of oxidative stress and cellular damage due to myocardial infarction in the immediately reperfusion period when typically it is at its greatest 35 and published its result which the most changes was during first 15 min of reperfusion 36 so we measured these parameters every 15 min like other studies method 35 because the I/R injury was worsened by the time and our object was to investigate the preventive role of antioxidant or mPTP inhibitor and combined effect of both during total time of experiment . We were going to check the severity of I/R injury after 60 min of reperfusion when the No production derived from eNOS was affected by pretreatment with different doses of antioxidant 37,38 only or in combination with a mPTP inhibitor (CsA). Because other studies have shown that inhibition of mitochondria permeability transition pore with this drug can prevents the eNOS expression.…”

Section: Discussionmentioning

confidence: 99%

Gallic Acid and Cyclosporine Mixture and their Effects on Cardiac Dysfunction Induced by Ischemia/Reperfusion and eNOS/iNOS Expression

Badavi

Sadeghi

Dianat

et al. 2017

International Journal of Cardiovascular Sciences

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“…already reported that superoxide (O2 .-) is produced in ischemic tissue at the time of reperfusion, and reacts with NO to form peroxynitrite [43]. Peroxynitrite is a potent oxidant that directly oxidizes sulfhydryl groups at a 1000-fold greater rate than hydrogen peroxide.…”

Section: Discussionmentioning

confidence: 99%

Biphasic Action of Inducible Nitric Oxide Synthase in a Hindlimb Ischemia Model

Kimura

Goto

Yagi

et al. 2006

J. Clin. Biochem. Nutr.

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Summary We investigated the influence of inducible nitric oxide synthase (iNOS) on acute ischemic injury and chronic angiogenesis. In a hindlimb ischemia model, NO produced by endothelial NO synthase (eNOS) reduces ischemic injury and promotes angiogenesis. However, the effect of the large amounts of NO generated by induced iNOS is unclear. Experimental groups of mice were as follows: (1) wild-type group (Wild), (2) iNOS-knockout group (iNOS-KO), and (3) aminoguanidine-treated wild-type group (Wild + AG), which received aminoguanidine from day 0 to day 3 after ischemia. Acute ischemic injury was evaluated by measuring the plasma CK value and ischemic score. Chronic angiogenesis was evaluated by microangiography and with a non-contact type Doppler blood flowmeter on day 3. Compared with the Wild group (251 ± 34.7 IU/l), the CK value was significantly elevated in the iNOS-KO (497 ± 126.7 IU/l) and Wild + AG (587.2 ± 128.7 IU/l) groups. The ischemic score was significantly increased in the iNOS-KO (92%) and Wild ± AG (66.6%) groups compared with the Wild group (23%). Blood flow was significantly increased in the iNOS-KO group (58.7 ± 15.3%) compared with the Wild (38.1 ± 15.9%) and Wild ± AG (43.5 ± 9.8%) groups in the chronic stage. Microangiography revealed a significantly increased number of blood vessels in the iNOS-KO (0.29 ± 0.02) group compared with the Wild (0.12 ± 0.01) and Wild + AG (0.15 ± 0.02) groups. Our findings indicate that NO generated by iNOS has a biphasic action, reducing acute ischemic injury and inhibiting angiogenesis in the chronic stage.

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Critical timing of -arginine treatment in post-ischemic myocardial apoptosis?role of NOS isoforms

Cited by 34 publications

References 26 publications

Cardioprotective effects of nitric oxide-aspirin in myocardial ischemia-reperfused rats

Cardioprotective effects of nitric oxide-aspirin in myocardial ischemia-reperfused rats

Gallic Acid and Cyclosporine Mixture and their Effects on Cardiac Dysfunction Induced by Ischemia/Reperfusion and eNOS/iNOS Expression

Biphasic Action of Inducible Nitric Oxide Synthase in a Hindlimb Ischemia Model

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