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1

Effect of electrical cardioversion on stented coronary artery

100%

Sharifkazemi M. , Safai A. , Aslani A. , Dehghan S. , Rezakhani A. , Rezaian G.

Open Medicine

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2010

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tom 5

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nr 3

303-307

EN

Direct current cardioversion, which produces electrical energy, is highly effective for the termination of cardiac arrhythmia and sometimes is indicated in patients with coronary artery stents due to arrhythmias. Only a few reports have been published describing the potential adverse interactions between foreign bodies and electrical cardioversion. The aim of this animal study was to investigate the acute effect of repeated external defibrillation on coronary artery tissue and adjacent myocardium at the implantation site of coronary stents. Custom-made stainless steel stents were implanted in the coronary arteries of 7 dogs. Rapid ventricular pacing was performed to induce ventricular fibrillation. Defibrillation was achieved [5 J/kg; n=2 and 8 J/kg; n=3]. In 2 animals, coronary stent was implanted but defibrillation was not performed [control group]. The animal’s heart were excised and sent for microscopic examination. The light and electron micrographs of heart muscles showed no histological and ultrastructural changes in defibrillated and control dogs. It is concluded that nickel coating provides good resistance to heat in coronary stents and repeated defibrillation does not cause histopathological changes typical of thermal injury at the implantation site of coronary stent.

2

Myocardial remodeling in rats with metabolic syndrome: role of Rho-kinase mediated insulin resistance

100%

Li C.-B. , Li X.-X. , Chen Y.-G. , Gao H.-Q. , Bao C.-M. , Liu X.-Q. , Bu P.-L. , Zhang J. , Zhang Y. , Ji X.-P.

Acta Biochimica Polonica

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2012

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tom 59

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nr 2

249-254

EN

Insulin resistance (IR) plays a critical role in metabolic syndrome (MS). Previous studies have demonstrated that activated ROCK is increased in MS patients. However, the effect of Rho-kinase (ROCK) on IR has not been definitely determined. Thus, the aims of the present study were to determine whether ROCK activation induces IR or affects myocardial structure and function, as well as the possible mechanisms underlying this process. Wistar rats fed high fat, high glucose and high salt diet sewed as model of MS and we used transmission electron microscopy, echocardiogram technology, and terminal deoxynucleotidyl transferase-mediated DNA nick-end labeling staining to identify any myocardial damage. The protein levels of MYPT-1 (characteristic of ROCK activation), IRS-1 and AKT were analyzed by immunohistochemistry and Western blotting. In hearts from MS rats, we found increased protein levels of phospho-MYPT-1 and phospho-IRS-1 (Ser307) and decreased phospho-AKT compared to levels in normal rats. In conclusion, the results suggest that ROCK-mediated IR is involved in the development of myocardial impairments in MS rats and that this effect is mediated probably via the IRS-1/PI3-kinase/AKT pathway.

3

Light-dark dependence of electrocardiographic changes during asphyxia and reoxygenation in a rat model

100%

Bačová I. , Švorc P. , Kundrík M. , Fulton B.

Open Medicine

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2011

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tom 6

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nr 1

89-97

EN

The aim of this study was to evaluate the effect of ventilation on electrocardiographic time intervals as a function of the light-dark (LD) cycle in an in vivo rat model. RR, PQ, QT and QTc intervals were measured in female Wistar rats anaesthetized with both ketamine and xylazine (100 mg/15 mg/kg, i.m., open chest experiments) after adaptation to the LD cycle (12:12h) for 4 weeks. Electrocardiograms (ECG) were recorded before surgical interventions; after tracheotomy, and thoracotomy, and 5 minutes of stabilization with artificial ventilation; 30, 60, 90 and 120 seconds after the onset of apnoea; and after 5, 10, 15, and 20 minutes of artificial reoxygenation. Time intervals in intact animals showed significant LD differences, except in the QT interval. The initial significant (p<0,001) LD differences in PQ interval and loss of dependence on LD cycle in the QT interval were preserved during short-term apnoea-induced asphyxia (30–60 sec) In contrast, long-term asphyxia (90–120 sec) eliminated LD dependence in the PQ interval, but significant LD differences were shown in the QT interval. Apnoea completely abolished LD differences in the RR interval. Reoxygenation restored the PQ and QT intervals to the pre-asphyxic LD differences, but with the RR intervals, the LD differences were eliminated. We have concluded that myocardial vulnerability is dependent on the LD cycle and on changes of pulmonary ventilation.

4

Light-dark dependence of electrocardiographic changes during asphyxia and reoxygenation in a rat model

100%

Bačová I. , Švorc P. , Kundrík M. , Fulton B.

Open Medicine

|

2010

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tom 5

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nr 5

611-619

EN

The aim of this study was to evaluate the effect of ventilation on electrocardiographic time intervals as a function of the light-dark (LD) cycle in an in vivo rat model. RR, PQ, QT and QTc intervals were measured in female Wistar rats anaesthetized with both ketamine and xylazine (100 mg/15 mg/kg, i.m., open chest experiments) after adaptation to the LD cycle (12:12h) for 4 weeks. Electrocardiograms (ECG) were recorded before surgical interventions; after tracheotomy, and thoracotomy, and 5 minutes of stabilization with artificial ventilation; 30, 60, 90 and 120 seconds after the onset of apnoea; and after 5, 10, 15, and 20 minutes of artificial reoxygenation. Time intervals in intact animals showed significant LD differences, except in the QT interval. The initial significant (p<0,001) LD differences in PQ interval and loss of dependence on LD cycle in the QT interval were preserved during short-term apnoea-induced asphyxia (30–60 sec) In contrast, long-term asphyxia (90–120 sec) eliminated LD dependence in the PQ interval, but significant LD differences were shown in the QT interval. Apnoea completely abolished LD differences in the RR interval. Reoxygenation restored the PQ and QT intervals to the pre-asphyxic LD differences, but with the RR intervals, the LD differences were eliminated. We have concluded that myocardial vulnerability is dependent on the LD cycle and on changes of pulmonary ventilation.