Cardioprotective activity of endogenous and exogenous nitric oxide on ischaemia reperfusion injury in isolated guinea pig hearts

Masini, Emanuela; Salvemini, Daniela; Ndisang, J. Fomusi; Gai, P.; Berni, L.A.; Moncini, M.; Bianchi, S.; Mannaioni, P. F.

doi:10.1007/s000110050504

Cited by 38 publications

(31 citation statements)

References 50 publications

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“…Second, inflammation induces expression of angiogenic growth factors associated with reduced infarct size, 21 and endogenous production of NO protects the myocardium from ischemia reperfusion injury. 22 Therefore, the clinical situation in which CRP levels are already elevated immediately after the onset of AMI may protect the ischemic myocardium. Because AMI with elevated CRP levels immediately after the onset may have less myocardial damage and a more fragile culprit lesion, 7 it may be best managed by early implementation of a reliable reperfusion strategy, such as stent replacement or treatment with abciximab.…”

Section: Discussionmentioning

confidence: 99%

Relationship Between Myocardial Damage and C-Reactive Protein Levels Immediately After Onset of Acute Myocardial Infarction

et al. 2001

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Section: Discussionmentioning

confidence: 99%

Relationship Between Myocardial Damage and C-Reactive Protein Levels Immediately After Onset of Acute Myocardial Infarction

et al. 2001

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“…Several recent studies suggest that HMG-CoA reductase inhibitors increase eNOS activity (4,(22)(23)(24). And recent studies have provided evidence that endogenous production of NO provides significant myocardial protection from ischemia-reperfusion injury (25,26). HMG-CoA reductase inhibitors increase eNOS expression through an increase in eNOS mRNA stability (23).…”

Section: Discussionmentioning

confidence: 99%

Effects of an HMG-CoA Reductase Inhibitor in Combination with an ACE Inhibitor or Angiotensin II Type 1 Receptor Antagonist on Myocardial Metabolism in Ischemic Rabbit Hearts

2002

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We investigated the effects of a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, pravastatin, an angiotensin converting enzyme (ACE) inhibitor, temocaprilat, and an angiotensin II type 1 (AT1) receptor antagonist, CV-11974, on myocardial metabolism during ischemia in isolated rabbit hearts using phosphorus 31-nuclear magnetic resonance ( 31 P-NMR) imaging. Forty-five minutes of continuous normothermic global ischemia was carried out. Pravastatin, temocaprilat, CV-11974 or a nitric oxide synthase inhibitor, L-NAME was administered from 60 min prior to the global ischemia. Japanese white rabbits were divided into the following experimental groups, a control group (n 7), a group treated with pravastatin (P group; n 7), a group treated with pravastatin and temocaprilat (P T group; n 7), a group treated with pravastatin and CV-11974 (P CV group; n 7), and a group treated with pravastatin and L-NAME (P L-NAME group; n 7). During ischemia, P group, as well as either P T group or P CV group, showed a significant inhibition of the decreases in adenosine triphosphate (ATP) and intracellular pH (pHi) (p 0.01, respectively, at the end of ischemia compared to the control group as well as P L-NAME group), and a significant inhibition of the increase in inorganic phosphate (Pi) (p 0.01, respectively, compared with the control group as well as P L-NAME group). These results suggest that pravastatin significantly improved myocardial energy metabolism during myocardial ischemia. This beneficial effect was dependent on NO synthase.However, this beneficial effect was not enhanced by either temocaprilat or CV-11974.

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“…On these grounds, we hypothesized that pea seedling histaminase could effectively prevent the adverse effects of cardiac and intestinal ischemia-reperfusion. In fact, the heart is particularly susceptible to tissue damage by several key agents involved in the pathophysiological mechanisms of ischemia-reperfusion, such as ROS, histamine and NO [29,30]. During acute myocardial ischemia, the coronary sinus histamine concentration increases simultaneosly with the development of early arrhytmias [31].…”

Section: Plant Dao/histaminase Has a Protective Effect Against Ischemmentioning

confidence: 99%

Effects of Amine Oxidases in Allergic and Histamine-Mediated Conditions

Mondovı̀¹,

Fogel²,

Federico³

et al. 2012

IAD

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Cardioprotective activity of endogenous and exogenous nitric oxide on ischaemia reperfusion injury in isolated guinea pig hearts

Abstract: The endogenous production of NO provides significant myocardial protection from IR injury and histamine release. These effects were mimicked by various NO donors.

Cited by 38 publications

References 50 publications

Relationship Between Myocardial Damage and C-Reactive Protein Levels Immediately After Onset of Acute Myocardial Infarction

Relationship Between Myocardial Damage and C-Reactive Protein Levels Immediately After Onset of Acute Myocardial Infarction

Effects of an HMG-CoA Reductase Inhibitor in Combination with an ACE Inhibitor or Angiotensin II Type 1 Receptor Antagonist on Myocardial Metabolism in Ischemic Rabbit Hearts

Effects of Amine Oxidases in Allergic and Histamine-Mediated Conditions

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