[Immunohistochemical study of Cx43 dephosphorylation in human left ventricular myocardium suffered by acute ischemia].

Objective: This study was performed to detect the phosphorylation state of Cx43 in human left ventricular myocardium among sudden deaths caused by acute myocardial ischemia (AMI) especially sudden coronary death (SCD) and control groups. And then evaluate the significance of these findings in diagnosing the early pathological changes of acute myocardial ischemia.

Methods: Immunohistochemistry (IHC) SP techniques were adopted to detect the phosphorylation state of Cx43 in the left ventricular myocardium samples of 45 deceased, which classified as group I--SCD, group II & III (other two groups of AMI) and Group IV & V (two control groups, sudden death caused by lethal acute cranio-cerebral injury or pathologic intracranial hemorrhage). In addition, we selected anti-Pan-Cadherin (construction protein of adherent junctions on the intercalated disc) and PHA-E+L/Bio, to detect the integration of myocardial mechanical coupling and membranes (applying affinityhistochemistry, AHC) respectively.

Results: (1) Phosphorylated Cx43 positive staining was almost invisible in Group I, II and III or scattered in sarcoplasm in few samples; but it was assembling at the IDs clearly in group IV and V. (2) Strongly positive staining of Pan-Cadherin could be observed at the IDs and (3) integrated myocardial membranes were found in all samples.

Conclusion: These findings suggested that compared with the control groups, the integration of myocardial mechanical coupling and membranes did not alter in AMI. But Cx43, the key protein of electrical coupling on myocardial gap junctions, occurred dephosphorylation remarkably in AMI. Thus applying IHC techniques to detect the Cx43 dephosphorylation in human left ventricular myocardium maybe useful to recognize the onset of arrhythmia in AMI, especially in SCD whose myocardium without apparent morphological changes.