Delayed cardioprotective effects of exercise in dogs are aminoguanidine sensitive: possible involvement of nitric oxide

Babai, László; SZIGETI, Zsolt; Parratt, J. R.; Végh, Ágnes

doi:10.1042/cs20010296

Cited by 23 publications

(11 citation statements)

References 36 publications

(51 reference statements)

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“…The findings presented herein appear to conflict with those of Babai et al (3), who reported that the iNOS inhibitor aminoguanidine (AG) blocked the preconditioning effects 24 h after a single, 21-min bout of exercise in dogs. They also found that the activity of iNOS increased threefold in the myocardium 24 h following exercise.…”

Section: Discussioncontrasting

confidence: 99%

Improved postischemic function following acute exercise is not mediated by nitric oxide synthase in the rat heart

Taylor

Olsen²,

Starnes³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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The mediators of acute exercise-induced preconditioning against ischemia-reperfusion injury are not understood. This study assesses the role of nitric oxide synthase (NOS), a reported mediator of other forms of preconditioning. Male Fischer 344 rats were divided into five groups (n = 6-7): sedentary (Sed); exercised 2 days on a treadmill at 20 m/min, 6 degrees grade, for 60 min (Run); sedentary, perfused with 100 microM N(omega)-nitro-l-arginine methyl ester hydrochloride (l-NAME) to inhibit NOS (Sed/L-N); exercised, perfused with l-NAME (Run/L-N); and exercised in a 4 degrees C environment, perfused with l-NAME (CRun/L-N). Twenty-four hours following exercise, isolated, perfused working hearts were subjected to 22.5 min of global ischemia plus 30 min of normoxic reperfusion. Left ventricle contents of several putative preconditioning mediators were determined. Postischemic recovery of cardiac output times systolic pressure was better in Run than Sed (78.4 vs. 50.2% of preischemia, P < 0.05). Inhibition of NOS did not abrogate the improved recovery in the exercise groups or alter recovery in Sed. All exercise groups also displayed improved myocardial efficiency (cardiac output times systolic pressure/oxygen consumption) postischemia and less lactate dehydrogenase release (P < 0.05). l-NAME appeared to lower lactate dehydrogenase release independent of exercise. The only change in antioxidant enzyme activity was a decrease in manganese superoxide dismutase in CRun/L-N (P < 0.05). Heat shock protein 72 expression increased only in Run and Run/L-N and endothelial NOS only in CRun/L-N (P < 0.05). Acute exercise-induced preconditioning of the Fischer 344 rat heart is not mediated by NOS and does not require increases in heat shock protein 72 or antioxidant enzymes.

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Section: Discussioncontrasting

confidence: 99%

Improved postischemic function following acute exercise is not mediated by nitric oxide synthase in the rat heart

Taylor

Olsen²,

Starnes³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…Kukreja's group ( Ockaili et al , 2002 ; Salloum et al , 2003 ) have shown that a delayed protection, as assessed by a reduction in infarct size, is evident at this time and that it is mediated by NO. The delayed antiarrhythmic effect of sildenafil could also involve NO, as with cardiac pacing ( Kis et al , 1999 ) and exercise ( Babai et al , 2002 ). The moderate prolongation of QT duration could also contribute, since drugs that prolong cardiac repolarisation, like sildenafil ( Geelen et al , 2000 ), can also be protective against ischaemia‐induced arrhythmias.…”

Section: Discussionmentioning

confidence: 99%

Sildenafil (Viagra) reduces arrhythmia severity during ischaemia 24 h after oral administration in dogs

Nagy

Hajnal

Parratt

et al. 2004

British J Pharmacology

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Sildenafil (Viagra) prolongs repolarisation in cardiac muscle, an effect that could lead to ventricular fibrillation (VF). Sildenafil (2 mg kg À1) was given by mouth to 12 mongrel dogs and, 24 h later, these dogs were anaesthetised, thoracotomised and subjected to a 25 min occlusion of the anterior descending coronary artery. Haemodynamic parameters were similar in this and the control group, but there were fewer and less serious ventricular arrhythmias during occlusion in the sildenafil group (VF 17 vs 60%; ventricular premature beats 140752 vs 4377127% and episodes of ventricular tachycardia 4.073.2 vs 19.377.7%, all Po0.05). However, reperfusion VF and indices of ischaemia severity (epicardial ST-segment mapping, inhomogeneity) were not modified by the drug. Sildenafil increased the QT interval, especially during ischaemia. Our conclusion is that ischaemia-induced ventricular arrhythmias are reduced by sildenafil, but this protection is less pronounced than that following cardiac pacing or exercise.

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“…First, in this series of experiments the collateral blood flow was not measured. We have previous evidence that in this arrhythmia model, the use of microspheres during the vulnerable, early (25 min) period of ischaemia can substantially modify arrhythmia severity (Babai et al, 2002). Therefore, we do not attempt to assess tissue blood flow in all of our studies, when the arrhythmias are assessed.…”

Section: Discussionmentioning

confidence: 99%

The activation of PI 3-kinase/Akt pathway is involved in the acute effects of simvastatin against ischaemia and reperfusion-induced arrhythmias in anaesthetised dogs

Kisvári

Kovács

Seprényi

et al. 2015

European Journal of Pharmacology

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The objective of this study was to examine whether the PI3-kinase/Akt pathway is involved in the activation of endothelial nitric oxide synthase (eNOS) and in the subsequent increase of nitric oxide (NO) production that has been proved to play a role in the antiarrhythmic effect of acute simvastatin treatment in anaesthetised dogs, subjected to a 25min occlusion and reperfusion of the left anterior descending coronary artery. Using the same model, 12 dogs out of the 26 controls (given the solvent of simvastatin) and 11 dogs out of the 23 animals treated with intracoronary administered simvastatin (0.1mg/kg), were now received wortmannin (1.5mg/kg, ic.), a selective inhibitor of PI3-kinase. In another 13 dogs the effects of DMSO (0.1%), the vehicle of wortmannin, were examined. Compared to the controls, simvastatin markedly reduced the severity of ischaemia (epicardial ST-segment, inhomogeneity) and ventricular arrhythmias that were reversed (except the occlusion-induced ventricular fibrillation [VF; 50%, 0%, 0%]) by the administration of wortmannin. Thus in these groups there were 310±45, 62±14, 307±59 ectopic beats, 7.1±1.4, 0.3± 0.2, 4.3±1.3 tachycardiac episodes that occurred 93%, 17% and 73% of the dogs during occlusion, whereas survival following reperfusion was 0%, 67% and 0%, respectively. Simvastatin also increased the phosphorylation of eNOS and the plasma nitrate/nitrite levels, but reduced myocardial superoxide production on reperfusion. These effects of simvastatin were also abolished in the presence of wortmannin. We conclude that the NO-dependent antiarrhythmic effect of simvastatin involves the rapid activation of eNOS through the stimulation of the PI3-kinase/Akt pathway.

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Delayed cardioprotective effects of exercise in dogs are aminoguanidine sensitive: possible involvement of nitric oxide

Cited by 23 publications

References 36 publications

Improved postischemic function following acute exercise is not mediated by nitric oxide synthase in the rat heart

Improved postischemic function following acute exercise is not mediated by nitric oxide synthase in the rat heart

Sildenafil (Viagra) reduces arrhythmia severity during ischaemia 24 h after oral administration in dogs

The activation of PI 3-kinase/Akt pathway is involved in the acute effects of simvastatin against ischaemia and reperfusion-induced arrhythmias in anaesthetised dogs

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