[Effects of sympathetic nerve stimulation on connexin43 and ventricular arrhythmias during acute myocardial ischemia: experiment with rats].
OBJECTIVE
To investigate the effects of sympathetic nerve stimulation (SNS) on connexin43 (Cx43) and ventricular arrhythmias during acute myocardial ischemia (MI).


METHODS
Ninety five Wistar rats were randomly divided into four groups: MI group (n=25), undergoing: ligation of the anterior descending coronary; MII-SNS group (n=25); undergoing electric stimulation of sympathetic nerve since the beginning of ligation of the anterior descending coronary and lasting till 30 min after the ligation, sympathetic nerve stimulation preconditioning + myocardial ischemia (pSNS-MI) group (n=25), undergoing electric stimulation of sympathetic nerve since the beginning of ligation of the anterior descending coronary that ended just after the ligation; and sham operation (SO) group (n=20), without coronary ligation. Ventricular arrhythmias were monitored by electrocardiography. Western blotting and RT-PCR were used to detect the protein and mRNA expression of Cx43 respectively. Immunofluorescence analysis was used to observe the changes of Cx43 protein distribution.


RESULTS
One and 3 rate died due to ventricular fibrillation in the MI group and MI-SS group respectively. The incidence of ventricular tachycardia (VT)/VF within 30-minute after ligation in the MI-SNS group was 80.0%, significant higher than that of the MI group (52.0%, P < 0.05). The incidence of VT/VF within 30-minute after ligation of the pSNS-MI group was 20.0%, significantly lower than that of the MI-SNS group (P < 0.05). 30 minutes after the ligation, the percentage of phosphorylated Cx43 of the pSNS-MI and MI-SNS groups were 71.2% +/- 7.0% and 73.4% +/- 6.7% respectively, both significantly higher than that of the MI group (46.7% +/- 6.3%) (both P < 0.05). The total contents of Cx43 of the MI and pSNS-MI groups were 1.29 +/- 0.14 and 1.25 +/- 0.13 respectively, both similar to that of the SO group [(1.30 +/- 0.10), both P > 0.05], while the total Cr43 content of the MI-SNS group was 0.73 +/- 0. 12, significantly lower than that of the SO group [(1.30 +/- 0.10), P < 0.05]. The Cx43 mRNA levels of the 3 experimental groups were all significantly lower than that of the SO group (all P < 0.05). Immunofluorescence analysis confirmed that ischemia and sympathetic nerve stimulation induced the changes of connexin43 distribution and sympathetic nerve stimulation preconditioning inhibited the changes of connexin43 distribution induced by ischemia.


CONCLUSIONS
SNS promotes ventricular arrhythmias by promoting Cx43 degradation, and sympathetic nerve stimulation preconditioning inhibits ventricular arrhythmias by preventing Cx43 dephosphorylation.
Hu
Xiao-rong
XR
Department of Cardiology, Renmin Hospital, Wuhan University, Wuhan 430060, China.
Jiang
Hong
H
Wen
Hua-zhi
HZ
Lu
Zhi-bing
ZB
Zhao
Dong-dong
DD
Huang
Cong-xin
CX
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D015153:Blotting, Western; D018031:Connexin 43 / Q000235:genetics / Q000378:metabolism*; D004558:Electric Stimulation / Q000379:methods; D005455:Fluorescent Antibody Technique; D008297:Male; D017202:Myocardial Ischemia / Q000503:physiopathology*; D010766:Phosphorylation; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D018031:Connexin 43; D012333:RNA, Messenger