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Effects of calcitonin gene-related peptide receptor antagonist on ventricular arrhythmia after acute myocardial infarction in rats |
WANG Lili ZHANG Ruilin GUO Zheng▲ |
Department of Anesthesiology, the Second Hospital of Shanxi Medical University, Shanxi Province, Taiyuan 030001, China |
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Abstract [Abstract] Objective To observe the effect of calcitonin gene-related peptide (CGRP) receptor antagonist CGRP8-37 on ventricular arrhythmia after acute myocardial infarction in rats. Methods Twenty-four healthy adult male Sprague-Dawley rats weighing 250-300 g were selected and randomly assigned into three groups (n = 8): control group (sham group), coronary artery occlusion group (CAO group) and CGRP8-37 intervention for coronary artery occlusion in advance group (CGRP8-37-CAO group). The times of ventricular arrhythmia from 10 min before CAO to 60 min after CAO were calculated and analyzed statistically according to the types of ventricular arrhythmia including one ventricular premature beat, two consecutive ventricular premature beats, three consecutive ventricular premature beats, more than three consecutive ventricular premature beats. Results CAO could induce the occurrence of ventricular arrhythmias, the occurrence time was concentrated on 0-12 min of early ischemia and peaked around 6 min after CAO. Pretreatment of CGRP8-37 before CAO could significantly increase the frequency of arrhythmias, and the time course was significantly extended from 0-12 min in CAO group to 0-20 min in CGRP8-37-CAO group. Peaked time of ventricular premature beats appeared in 12 min after CAO. The occurrence of ventricular arrhythmias in sham group, CAO group and CGRP8-37-CAO group had no significant differences 10 min before CAO (P > 0.05). Compared with sham group, the occurrence of ventricular arrhythmias was increased in CAO group and CGRP8-37-CAO group, the differences were highly statistically significant (P < 0.01). Compared with CAO group, the occurrence of ventricular arrhythmia in CGRP8-37-CAO group was increased, the difference was highly statistically significant (P < 0.01). The time of differences appeared in ventricular arrhythmia was concentrated on 20, 30, 40 min after CAO. Conclusion CGRP8-37 can significantly increase the occurrence of ventricular arrhythmia after acute myocardial infarction in rats.
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[参考文献]
[1] Pires LA,Wagshal AB,Lancey R,et al. Arrhythmias and conduction disturbances after coronary artery bypass graft surgery:epidemiology,management,and prognosis [J]. Am Heart J,1995,129(4):799-808.
[2] Bril A. Cellular mechanisms of cardiac arrhythmias in the ischemic and reperfused heart [J]. Birkh■user Basel,1996, 76:135-153.
[3] Huikuri HV,Castellanos A,Myerburg RJ. Sudden death due to cardiac arrhythmias [J]. N Engl J Med,2001,345(20):1473-1482.
[4] Opitz CF,Mitchell GF,Pfeffer MA,et al. Arrhythmias and death after coronary artery occlusion in the rat:continuous telemetric ECG monitoring in conscious,untethered rats [J]. Circulation,1995,92(2):253-261.
[5] Manning AS,Hearse DJ. Reperfusion-induced arrhythmias:mechanisms and prevention [J]. J Mol Cell Cardiol,1984, 16(6):497-518.
[6] Zhang RL,Guo Z,Wang LL,et al. Degeneration of capsaicin sensitive sensory nerves enhances myocardial injury in acute myocardial infarction in rats [J]. Int J Cardiol,2012,160(1):41-47.
[7] Li YJ,Xiao ZS,Peng CF,et al. Calcitonin gene-related peptide-induced preconditioning protects against ischemia-reperfusion injury in isolated rat hearts [J]. Eur J Pharmacol,1996,311(2-3):163-167.
[8] Amara SG,Jonas V,Rosenfeld M. Alternative RNA processing in calciton in gene expression generates mRNAs encoding different polypeptide products [J]. Nature,1982,298(5871):240-244.
[9] Keith IM,Tjen-A-Looic S,Kraiczi H,et al. Three week neonatal hypoxia reduces blood CGRP and cause persistent pulmonary hypertension in rats [J]. Am J Physiol Heart Cire Physiol,2000,279(4):1571-1578.
[10] 继东,甘立军,张春卉.降钙素基因相关肽与冠心病[J].山东医药,2001,41(7):59-60.
[11] 李圻,陈张根,贾兵,等.降钙素基因相关肽对体外循环心功能的影响[J].复旦学报,2001,28(4):326-329.
[12] 刘琳,邢宇彤,魏军营.降钙素基因相关肽对心力衰竭大鼠心肌组织中肿瘤坏死因子-α表达的影响[J].临床医学,2014,34(4):98-100.
[13] Chadha PS,Jepps TA,Carr G,et al. Contribution of kv7.4/kv7.5 heteromers to intrinsic and calcitonin gene-related peptide-induced cerebral reactivity [J]. Arterioscler Thromb Vasc Biol,2014,34(4):887-893.
[14] Roustit M,Khouri C,Blaise S,et al. Pharmacology of Raynaud's phenomenon [J]. Therapie,2014,69(2):115-128.
[15] 陈璐,赵鑫,郭政.降钙素基因相关肽对高糖下新生大鼠心肌细胞缺氧复氧损伤的影响[J].中华麻醉学杂志,2014,34(10):1185-1188.
[16] 岳维,朱国斌,杜秋香,等.降钙素基因相关肽对高脂复合缺氧/复氧诱导乳鼠心肌细胞凋亡的影响[J].中国组织工程研究,2014,18(11):1761-1764.
[17] Shi B,Long X,Zhao R,et al. Transplantation of mesenchymal stem cells carrying the human receptor activity-modifying protein 1 geneimproves cardiac function and inhibits neointimal proliferation in the carotid angioplasty and myocardial infarction rabbit model [J]. Exp Biol Med,2014,239(3):356.
[18] Bell D,Schluter KD,Zhou XJ,et al. Hypertrophic effects of calcitonim gene-related peptide(CGRP)and amylin on a adult mammalian ventricular cardiomyocytes [J]. J Mol Cell Cardiol,1995,27(11):2433-2443.
[19] 陈前,崔长琮,杨琳,等.降钙素基因相关肽对缺血-再灌注心肌细胞电生理的影响[J].中华心律失常学杂志,2001,5(1):49.
[20] Zhang JF,Liu J,Liu XZ,et al. The effect of calcitonin gene-related peptide on ischemic reperfusion-induced arrhythmias in rats [J]. Int J Cardiol,1994,46(1):33-36. |
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