Effect of Anesthetization of A-V Node on Ventricular Fibrillation Following Acute Coronary Arterial Occlusion

Anesthetization of the A-V node with procaine to produce complete atrioventricular dissociation was found to reduce the incidence of ventricular fibrillation following left coronary artery ligation, which in all control animals resulted in ventricular fibrillation in less than 150 seconds. Of 14 dogs in which idioventricular rhythms were produced, three fibrillated at 30 seconds, 7 minutes and 18 minutes, respectively, while the remaining 11 hearts gradually slowed and stopped after periods up to 45 minutes without fibrillation or other arrhythmia. Of the two dogs which developed an atrioventricular nodal rhythm following procainization, one fibrillated at 9 minutes after coronary ligation, while the other gradually slowed to asystole in 11 minutes.

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Effect of chronic oral pretreatment with trandolapril on ventricular fibrillation threshold and hemodynamics in pigs with coronary artery ligation

European Journal of Pharmacology ◽

10.1016/0014-2999(90)93042-o ◽

1990 ◽

Vol 183 (2) ◽

pp. 205-206 ◽

Cited By ~ 1

Author(s):

C.A. Muller ◽

L.H. Opie ◽

A.M. Theron ◽

H.M. Basset

Keyword(s):

Coronary Artery ◽

Ventricular Fibrillation ◽

Coronary Artery Ligation ◽

Artery Ligation ◽

Ventricular Fibrillation Threshold

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Abstract 132: Cardiomyocyte Specific Conditional Overexpression Of Stromal Cell Derived Factor 1 Facilitates Cardiac Regeneration After Permanent Coronary Artery Ligation In Mice.

Circulation Research ◽

10.1161/res.115.suppl_1.132 ◽

2014 ◽

Vol 115 (suppl_1) ◽

Author(s):

Detlef Obal ◽

Kenneth Brittian ◽

Michael Book ◽

Aruni Bhatnagar ◽

Yiru Guo ◽

...

Keyword(s):

Coronary Artery ◽

Stromal Cell ◽

Cardiac Regeneration ◽

Left Ventricular ◽

Border Zone ◽

Coronary Artery Ligation ◽

Artery Ligation ◽

Casein Kinase 1 ◽

Coronary Ligation ◽

Stromal Cell Derived Factor

Background: Interruption of cardiac stromal cell derived factor 1 (SDF1)-CXCR4 axis by chronic AMD3100 administration increased myocardial injury after permanent coronary artery ligation demonstrating the important role of this chemokine in cardiac regeneration. Hypothesis: Cardiomyocyte specific conditional overexpression of SDF1 prevents heart failure after permanent coronary ligation and facilitates cardiac regeneration. Methods and Results: Tetracycline-controlled, αMyHC promoter directed overexpression of cardiac SDF1, resulted in a significant increase of SDF1 expression (SDF1: 8.1 ng/mg protein) compared to littermate WT mice (0.02 ng/mg protein) four weeks after doxycycline withdraw. SDF1 overexpression increased AKT and casein kinase 1 levels in the heart. Although there was no difference in cardiac function and scar size 1 week after infarction, SDF1 overexpression improved left ventricular (LV) ejection fraction (SDF1 [n=13]: 47±5% [mean±SEM] vs. WT [n=15]: 29±4%, p<0.05) decreased end-diastolic volume (78±10 vs. 158±30, p<0.05) and reduced infarct size measured by trichrome staining (13±3% vs. 23±3% of LV wall, p<0.05) 4 weeks after permanent ligation. Bromodeoxyuridine (BrdU) staining revealed increased regeneration indicated by a 5-fold increase in BrdU + cardiomyocyte (CM) nuclei in the borderzone of the infarct (22±3% vs. 5±1% CM nuclei, p<0.01). Increased proliferation in SDF1 mice was confirmed by a higher number of KI67 + cells compared to WT mice. Cardiomyocyte cross sectional area in the border zone was significantly reduced in SDF1 mice (365±13 μm 2 vs. 434±10 μm 2 , p<0.001) while capillary density was unchanged (2348±151/ mm 2 vs. 2498±153/ mm 2 ) compared to WT mice. Conclusion: This study demonstrates for the first time that cardiac specific overexpression of SDF1 increases myocardial regeneration and improves LV function 4 weeks after permanent coronary ligation.

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