[Protective effect of protein kinase C on heart function: an experiment with isolated rabbit hearts].
OBJECTIVE
To investigate the protective effect of protein kinase C on heart function.


METHODS
The hearts of 40 rabbits were isolated, underwent Langendorff perfusion, and randomly divided into 4 equal groups: Group I (control group, the heart underwent long ischemia or preservation for I hour, was re-warmed and re-infused, and then re-perfused with K-H fluid), Group II (ischemic preconditioning group, perfusion was stopped for 5 minutes before the long ischemia, then the aorta was re-infused), Group III (specific activator of PKC, phorbol myristate acetate was infused inversely via the aorta before the perfusion of K-H fluid), and Group IV (polymyxin B, a specific antagonist of PKC, was infused after the infusion of PKC). Before the preservation and by the end of reperfusion left ventricle end systolic pressure (LVESP), and left ventricle end diastolic pressure (LVDSP) were measured. At the end of experiment specimens of myocardium were collected from each heart to measure the water content, the levels of lactic dehydrogenase and MB isoenzyme of creatine kinase (CK-MB), superoxide dismutase (SOD), and malonyldialdehyde (MDA). TUNEL method was used to measure the number of apoptotic cardiomyocyte.


RESULTS
All heart resumed beating. The LVESP of Group II and III were both significantly higher than those of Groups I and IV (all P < 0.05) and the LVESP of Group III was significantly higher than that of Group II too (P < 0.05). The LVEDP of Group II and III were both significantly lower than those of Groups I and IV (all P < 0.05) and the LVEDP of Group III was significantly lower than that of Group II too (P < 0.05). The levels of CK-MB, LDH, and SOD of Group II and III were all significantly higher than those of Groups I and IV (all P < 0.05) and the levels of CK-MB and LDH of Group III was significantly higher than that of Group II too (P < 0.05). The level of MDA of Group II and III were both significantly lower than those of Groups I and IV (all P < 0.05) and the level of MDA of Group III was significantly lower than that of Group II too (P < 0.05). The water contents of Group II and III were both significantly lower than those of Groups I and IV (all P < 0.05). The numbers of TUNEL positive cell and apoptotic cells of Group II and III were all significantly lower than those of Groups I and IV (all P < 0.05).


CONCLUSIONS
PKC can be activated by transient ischemia and PMA. PKC protects the heart function effectively.
Zhang
Xin
X
Department of Thoracic Surgery, Second Hospital Affiliated to Zhejiang University College of Medicine, Hangzhou 310031, China.
Chen
Ru-kun
RK
Niu
Jian-li
JL
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D005260:Female; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D019157:Ischemic Preconditioning, Myocardial; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D015428:Myocardial Reperfusion Injury; D009206:Myocardium / Q000201:enzymology* / Q000378:metabolism; D011112:Polymyxin B / Q000494:pharmacology; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011817:Rabbits; D011897:Random Allocation; D013482:Superoxide Dismutase / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase; D011493:Protein Kinase C; D011112:Polymyxin B; D013755:Tetradecanoylphorbol Acetate