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Blunted response of L-type calcium current to simulated ischemia and reperfusion in ventricular myocytes from diabetic rabbits / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 2155-2160, 2010.
Article Dans Chinois | WPRIM | ID: wpr-402325
ABSTRACT

AIM:

To evaluate the effects of simulated acute ischemia and reperfusion on L-type calcium current (ICa,L) in ventricular myocytes from diabetic and non-diabetic rabbits.

METHODS:

Using whole-cell patch clamp techniques, ICa,L was measured in left ventricular myocytes isolated from 6-week alloxan-induced diabetic rabbits and age-matched control ones at baseline, 5 min of simulated ischemia, and 5 min of reperfusion.

RESULTS:

There were no significant differences on baseline maximum ICa,L densities between diabetic and control ventricular myocytes. In control cells (n=11), maximal ICa,L densities of baseline, ischemia and reperfusion were (-8.36±1.63)pA/pF, (-5.90±1.75)pA/pF and (-4.22±1.02)pA/pF, respectively. The ICa,L of ischemia was less than that of baseline (P<0.01), while the ICa,L of reperfusion was less than those of baseline (P<0.01) and ischemia (P<0.05). In diabetic cells (n=9),the ICa,L of baseline, ischemia and reperfusion were (-7.55±1.62)pA/pF, (-6.05±1.58)pA/pF and (-5.12±1.13)pA/pF, respectively. Only ICa,L of reperfusion was less than that of baseline (P<0.01), while ICa,L of ischemia was not significantly different from that of baseline (P>0.05) or reperfusion (P>0.05).

CONCLUSION:

ICa,L in diabetic ventricular myocytes represents blunted response to acute ischemic injury, being decreased more slowly than that in control cells. Post-ischemic reperfusion is still a potent inhibitor against ICa,L in both diabetic and non-diabetic cells. This study may be indicative of the mechanism about ischemia-reperfusion injury to diabetic myocardium and the therapy for diabetic patients with ischemic heart disease.

Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) langue: Chinois Texte intégral: Chinese Journal of Pathophysiology Année: 2010 Type: Article

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Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) langue: Chinois Texte intégral: Chinese Journal of Pathophysiology Année: 2010 Type: Article