[Protection of HOE642 against cardiomyocyte injury caused by anoxia and reoxygenation].
OBJECTIVE
To investigate the protective effect of calcium antagonists (A/R) injury of cardiomyocytes.


METHODS
Primary-cultured cardiomyocytes were divided A/R, A/R+nicardipine(Nic), A/R+HOE642, A/R+H7, A/R+PD98059 and control parameters were measured in all groups, intracellular calcium concentration ([Ca2+]i), content, lactate dehydrogenase (LDH) and creative phosphokinase(CK) activity in the activity. The calpain (u-calpain and m-calpain) protein expression levels were measured In comparison with A/R group, A/R + nicardipine (Nic) and A/R + Nic groups showed [Ca2+]i, m-calpain protein expression, LDH and CK content in the medium, a higher activity of PKC and MAPK (P < 0.01). On the contrary, A/R+H7 and A/R+PD98059 LDH and CK content in the medium, and lower ATP content and cell viability as compared 0. 05).


CONCLUSIONS
The A/R mediated Ca2+ overload resulting from cardiomyocyte injury blocking Ca2+ entry and H+/Na+ exchange, and very likely PKC and MAPK are involved protection against the A/R injury of cardiomyocytes.
Zhang
Xin
X
Department of Cardiology, General Hospital of Chengdu Army, Chengdu 610083, China.
Liu
Han-Min
HM
Yang
Yong-Jian
YJ
Zhou
Tong-Fu
TF
D000818:Animals; D000831:Animals, Newborn; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D002154:Calpain / Q000378:metabolism; D015687:Cell Hypoxia / Q000502:physiology; D002478:Cells, Cultured; D006146:Guanidines / Q000494:pharmacology*; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000166:cytology*; D051381:Rats; D017208:Rats, Wistar; D013450:Sulfones / Q000494:pharmacology*
D000889:Anti-Arrhythmia Agents; D006146:Guanidines; D013450:Sulfones; C093373:cariporide; D002154:Calpain