Suppression of Ventricular Arrhythmias After Coronary Artery Ligation by Pinacidil, a Vasodilator Drug

1985 ◽  
Vol 7 (5) ◽  
pp. 875-883 ◽  
Author(s):  
M J Kerr ◽  
R Wilson ◽  
R G Shanks
Keyword(s):  
Coronary Artery ◽  
Ventricular Arrhythmias ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Vasodilator Drug

Suppression of ventricular arrhythmias resulting from acute coronary artery ligation in rat by imipramine

1990 ◽  
Vol 42 (5) ◽  
pp. 360-362
Author(s):  
Samiha A. M. El-Mahdy ◽  
A. A. Alhaider ◽  
Afaf A. Mahgoub ◽  
Abdulwahab M. Bashandy
Keyword(s):  
Coronary Artery ◽  
Ventricular Arrhythmias ◽  
Coronary Artery Ligation ◽  
Artery Ligation

scholarly journals Inhibition of N-type calcium channels in cardiac sympathetic neurons attenuates ventricular arrhythmogenesis in heart failure

2020 ◽  
Author(s):  
Dongze Zhang ◽  
Huiyin Tu ◽  
Chaojun Wang ◽  
Liang Cao ◽  
Wenfeng Hu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Coronary Artery ◽  
Ventricular Arrhythmias ◽  
Sympathetic Neurons ◽  
Coronary Artery Ligation ◽  
Channel Blockers ◽  
Artery Ligation ◽  
Cell Excitability ◽  
Ventricular Arrhythmogenesis

Abstract Aims Cardiac sympathetic overactivation is an important trigger of ventricular arrhythmias in patients with chronic heart failure (CHF). Our previous study demonstrated that N-type calcium (Cav2.2) currents in cardiac sympathetic post-ganglionic (CSP) neurons were increased in CHF. This study investigated the contribution of Cav2.2 channels in cardiac sympathetic overactivation and ventricular arrhythmogenesis in CHF. Methods and results Rat CHF was induced by surgical ligation of the left coronary artery. Lentiviral Cav2.2-α shRNA or scrambled shRNA was transfected in vivo into stellate ganglia (SG) in CHF rats. Final experiments were performed at 14 weeks after coronary artery ligation. Real-time polymerase chain reaction and western blot data showed that in vivo transfection of Cav2.2-α shRNA reduced the expression of Cav2.2-α mRNA and protein in the SG in CHF rats. Cav2.2-α shRNA also reduced Cav2.2 currents and cell excitability of CSP neurons and attenuated cardiac sympathetic nerve activities (CSNA) in CHF rats. The power spectral analysis of heart rate variability (HRV) further revealed that transfection of Cav2.2-α shRNA in the SG normalized CHF-caused cardiac sympathetic overactivation in conscious rats. Twenty-four-hour continuous telemetry electrocardiogram recording revealed that this Cav2.2-α shRNA not only decreased incidence and duration of ventricular tachycardia/ventricular fibrillation but also improved CHF-induced heterogeneity of ventricular electrical activity in conscious CHF rats. Cav2.2-α shRNA also decreased susceptibility to ventricular arrhythmias in anaesthetized CHF rats. However, Cav2.2-α shRNA failed to improve CHF-induced cardiac contractile dysfunction. Scrambled shRNA did not affect Cav2.2 currents and cell excitability of CSP neurons, CSNA, HRV, and ventricular arrhythmogenesis in CHF rats. Conclusions Overactivation of Cav2.2 channels in CSP neurons contributes to cardiac sympathetic hyperactivation and ventricular arrhythmogenesis in CHF. This suggests that discovering purely selective and potent small-molecule Cav2.2 channel blockers could be a potential therapeutic strategy to decrease fatal ventricular arrhythmias in CHF.

Ventricular arrhythmias following coronary artery occlusion in the streptozotocin diabetic rat

1988 ◽  
Vol 66 (3) ◽  
pp. 312-317 ◽  
Author(s):  
G. N. Beatch ◽  
J. H. McNeill
Keyword(s):  
Coronary Artery ◽  
Ventricular Arrhythmias ◽  
Streptozotocin Diabetes ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Diabetic Rat ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Conscious Rat ◽  
Streptozotocin Diabetic Rat

The following investigation was designed to assess whether or not streptozotocin diabetes has an influence on the number and severity of ventricular arrhythmias following coronary artery occlusion in the conscious rat. In addition, electrocardiogram and haemodynamic data were compared between streptozotocin diabetic groups and control. Diabetes was induced in male Sprague–Dawley rats with streptozotocin (55 mg/kg iv) and left anterior descending coronary artery ligation was performed either 6 or 9 weeks later. Rats were allowed to recover from preparative surgery for 1 week prior to ligation. Streptozotocin diabetes (untreated or insulin controlled) appeared to have little influence on the variables tested. When exposed to equivalent degrees of ischaemia (the rat is a microangiopathy-resistant species), the streptozotocin diabetic rat heart was not appreciably more prone to arrhythmias of any type compared with control.

scholarly journals Differential Effects of Propofol and Sevoflurane on Ischemia-induced Ventricular Arrhythmias and Phosphorylated Connexin 43 Protein in Rats

2009 ◽  
Vol 110 (1) ◽  
pp. 50-57 ◽  
Author(s):  
Naoyuki Hirata ◽  
Noriaki Kanaya ◽  
Noriko Kamada ◽  
Saori Kimura ◽  
Akiyoshi Namiki
Keyword(s):  
Coronary Artery ◽  
Survival Rate ◽  
Myocardial Ischemia ◽  
Ventricular Arrhythmias ◽  
Connexin 43 ◽  
Acute Myocardial Ischemia ◽  
High Dose ◽  
Coronary Artery Ligation ◽  
Sodium Pentobarbital ◽  
Artery Ligation

Background The effects of anesthetics on ischemia-induced ventricular arrhythmias remain poorly studied. This study investigated the effects of propofol and sevoflurane on the survival rate and morbidity as a result of ventricular arrhythmias, and defined a possible mechanism for the arrhythmogenic properties of anesthetics during acute myocardial ischemia. Methods Under anesthesia with intraperitoneal sodium pentobarbital, Sprague-Dawley rats underwent 30 min of left anterior descending coronary artery ligation. The rats were divided into a low-dose propofol (Prop-LD) group (39 mg X kg(-1) X hr(-1), n = 18), a high-dose propofol group (78 mg x kg(-1) x hr(-1), n = 18), a sevoflurane group (2.5%, n = 18) and a control group (n = 18). The survival rate and morbidity as a result of ventricular arrhythmias were determined, and the amount of phosphorylated connexin 43 protein was measured 30 min after coronary artery ligation. Results The survival rate was 83% (15 of 18), 94% (17 of 18), 89% (16 of 18), and 67% (12 of 18, P = 0.038 vs. Prop-LD) in the control, Prop-LD, high-dose propofol, and sevoflurane groups, respectively. Sustained ventricular tachycardia was observed in 83% (15 of 18), 39% (7 of 18, P = 0.011 vs. control), 50% (9 of 18, P = 0.039 vs. control) and 94% (17 of 18, P < 0.01 vs. Prop-LD) in the control, Prop-LD, high-dose propofol, and sevoflurane groups, respectively. Immunoblotting showed a marked reduction in the amount of phosphorylated connexin 43 in the control and sevoflurane groups, as compared with the Prop-LD and high-dose propofol groups (P < 0.05). Conclusion The authors' results suggest that propofol preserves connexin 43 phosphorylation during acute myocardial ischemia, as compared with sevoflurane, and this might protect the heart from serious ventricular arrhythmias during acute coronary occlusion.

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