scholarly journals Left coronary artery occlusion in an adult after aortopulmonary window closure

Author(s):  
Anton Vladimirovich Minaev ◽  
Eugene Pavlovich Golubev ◽  
Timur Yurievich Danilov
Resuscitation ◽  
2009 ◽  
Vol 80 (3) ◽  
pp. 295-296 ◽  
Author(s):  
Bernd A. Leidel ◽  
Michael Kunzelmann ◽  
Harro Bitterling ◽  
Florian Reichle ◽  
Stefan Wirth ◽  
...  

1963 ◽  
Vol 41 (1) ◽  
pp. 511-517 ◽  
Author(s):  
D. R. Varma ◽  
K. I. Melville

In dogs under pentobarbitone anesthesia, acute occlusion of the anterior descending branch of the left coronary artery at normal body temperature induced ventricular fibrillation in 30% of the animals, while hypothermia by surface cooling led to fibrillation in 40% of the animals. On the other hand, temporary coronary occlusion with hypothermia at 23 °C oesophageal temperature invariably induced ventricular fibrillation (15 experiments) within an average of 5.4 minutes of occlusion. Prior injections of quinidine and quinacrine protected 40 and 70%, respectively, of the dogs against this type of ventricular fibrillation (10 experiments each). Oxytocin (1–2 i.u./kg) offered no protection (six experiments) nor did it reverse established fibrillation under these conditions. It is concluded that temporary coronary artery occlusion at 23 °C oesophageal temperature in dogs is an effective and consistent method of producing ventricular fibrillation. It is also postulated that reduction of the coronary blood supply to the heart might be a precipitating factor in hypothermic ventricular fibrillation in surgery.


Circulation ◽  
1968 ◽  
Vol 37 (4s2) ◽  
Author(s):  
FRED A. CRAWFORD ◽  
BEN M. WILLWERTH ◽  
ROBERT E. CLINE ◽  
ANDREW G. WALLACE ◽  
WILL C. SEALY

1963 ◽  
Vol 41 (2) ◽  
pp. 511-517 ◽  
Author(s):  
D. R. Varma ◽  
K. I. Melville

In dogs under pentobarbitone anesthesia, acute occlusion of the anterior descending branch of the left coronary artery at normal body temperature induced ventricular fibrillation in 30% of the animals, while hypothermia by surface cooling led to fibrillation in 40% of the animals. On the other hand, temporary coronary occlusion with hypothermia at 23 °C oesophageal temperature invariably induced ventricular fibrillation (15 experiments) within an average of 5.4 minutes of occlusion. Prior injections of quinidine and quinacrine protected 40 and 70%, respectively, of the dogs against this type of ventricular fibrillation (10 experiments each). Oxytocin (1–2 i.u./kg) offered no protection (six experiments) nor did it reverse established fibrillation under these conditions. It is concluded that temporary coronary artery occlusion at 23 °C oesophageal temperature in dogs is an effective and consistent method of producing ventricular fibrillation. It is also postulated that reduction of the coronary blood supply to the heart might be a precipitating factor in hypothermic ventricular fibrillation in surgery.


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