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Protection of Glycyl-L-Glutamine against myocardial ischemia-reperfusion injury in the isolated rat heart / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12)1989.
Artículo en Chino | WPRIM | ID: wpr-532249
ABSTRACT

AIM:

To study the protection of Glycyl-L-Glutamine(Gly-Gln) against myocardial ischemia/reperfusion(I/R) injury in the isolated rat heart.

METHODS:

A model of myocardial ischemia-reperfusion injury was established with a Langendorff apparatus.Thirty male SD rats were randomly divided into four groupscontrol group,Gly-Gln group,I/R group and I/R+Gly-Gln group.Both I/R and I/R+Gly-Gln group were pre-perfused for 30 min,followed by 20 min ischemia and 40 min reperfusion.During reperfusion I/R+Gly-Gln group was perfused with Gly-Gln perfusate.Control group was kept perfused for 90 min.Gly-Gln group Gly-Gln perfusate was also kept perfused for 90 min.The left ventricular end-diastolic pressure(LVEDP),left ventricular developed pressure(LVDP),?dp/dtmax,heart rate(HR),monophasic action potentials(MAP) was measured during perfusion.The coronary effluent fluid was collected at different certain times.The activities of lactic dehydrogenase(LDH) and creatine kinase(CK) were determined.

RESULTS:

The isolated rat heart function decreased severely after 20 min ischemia and 40 min reperfusion(I/R)the LVEDP increased and the LVDP,?dp/dtmax decreased.But the LVEDP decreased and the LVDP,?dp/dtmax increased in I/R+Gly-Gln group compared with I/R group.Moreover,the activities of LDH and CK in the coronary effluent fluid decreased remarkably in I/R+Gly-Gln group compared with I/R group.

CONCLUSION:

Gly-Gln can play a protective role against myocardial I/R injury in isolated rat hearts via maintaining the left ventricular function and decreasing the release of LDH and CK.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Pathophysiology Año: 1989 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Pathophysiology Año: 1989 Tipo del documento: Artículo