Antifibrillatory effects of α1-adrenoceptor blocking drugs in experimental coronary artery occlusion and reperfusion

1993 ◽  
Vol 71 (2) ◽  
pp. 103-111 ◽  
Author(s):  
B. G. Benfey
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Guinea Pig ◽  
Ventricular Arrhythmias ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Coronary Reperfusion ◽  
Isolated Hearts ◽  
Anesthetized Dogs

The myocardium of animals and man possesses α1-adrenoceptors in addition to β-adrenoceptors. Ischemia increases sympathetic tone, and ventricular arrhythmias can occur by β- and α1-adrenoceptor stimulation. I believe that α1-adrenoceptor blocking drugs have antifibrillatory effects and will review the data that support this condition. The effect of α1,-adrenoceptor blocking drugs on the incidence of ventricular fibrillation in acute coronary artery occlusion and (or) reperfusion has been determined in 24 studies in conscious and anesthetized dogs and rats, anesthetized cats and pigs, and rat and guinea-pig isolated hearts. The drugs reduced the incidence of fibrillation from 35 to 24% in coronary occlusion and from 61 to 29% in reperfusion.Key words: heart, coronary occlusion, coronary reperfusion, ventricular fibrillation, α1-adrenoceptor blocking drugs.

VENTRICULAR FIBRILLATION INDUCED BY CORONARY OCCLUSION DURING HYPOTHERMIA IN DOGS AND THE EFFECTS OF QUINIDINE, QUINACRINE, AND OXYTOCIN

1963 ◽  
Vol 41 (1) ◽  
pp. 511-517 ◽  
Author(s):  
D. R. Varma ◽  
K. I. Melville
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Left Coronary Artery ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Surface Cooling ◽  
Normal Body Temperature ◽  
Oesophageal Temperature ◽  
Consistent Method

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.

TxA2 inhibition and ischemia-induced loss of myocardial function and reactive hyperemia

1990 ◽  
Vol 258 (5) ◽  
pp. H1402-H1408 ◽  
Author(s):  
J. L. Mehta ◽  
W. W. Nichols ◽  
R. Schofield ◽  
W. H. Donnelly ◽  
V. K. Chandna
Keyword(s):  
Coronary Artery ◽  
Coronary Occlusion ◽  
Myocardial Function ◽  
Reactive Hyperemia ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Leukocyte Infiltration ◽  
Coronary Reperfusion ◽  
Reperfusion Arrhythmias ◽  
Premature Ventricular Contractions

To determine the contribution of thromboxane (Tx) A2 release in reperfusion injury, 17 dogs were subjected to total coronary occlusion for 1 h and reperfusion for 1 h. Eleven dogs were treated with saline, and six were treated with selective TxA2 synthetase inhibitor U63,557A (5 mg/kg iv) 30 min before coronary artery occlusion. In all saline-treated dogs, peak reactive hyperemia after 10-s total coronary artery occlusion was diminished (P less than 0.01) after reperfusion. Myocardial segmental shortening was also reduced (9.8 +/- 1.9 to -6.7 +/- 2.0%, P less than 0.01) in the reperfused region. Reperfusion was associated with 737 +/- 343 premature ventricular contractions (PVCs) per hour. Histology revealed extensive myocardial infiltration and capillary plugging by leukocytes in the reperfused region. Myeloperoxidase, an index of leukocyte infiltration, was also increased (P less than 0.02) in the reperfused region. In the U63,557A-treated animals, serum and plasma TxB2 levels were markedly (P less than 0.02) reduced. Decrease in myocardial shortening fraction was less in U63,557A- than in saline-treated animals (P less than 0.05). The frequency of reperfusion PVCs was also significantly reduced (10 +/- 5 PVCs/h, P less than 0.02 compared with saline-treated dogs). However, peak reactive hyperemia was reduced similar to that in saline-treated dogs. Myocardial infiltration and capillary plugging by leukocytes in the reperfused regions was also similar in the U63,557A- and saline-treated dogs. These results indicate that treatment with U63,557A decreases reperfusion arrhythmias and preserves myocardial function. However, coronary reperfusion-induced deterioration in reactive hyperemia is not affected.(ABSTRACT TRUNCATED AT 250 WORDS)

VENTRICULAR FIBRILLATION INDUCED BY CORONARY OCCLUSION DURING HYPOTHERMIA IN DOGS AND THE EFFECTS OF QUINIDINE, QUINACRINE, AND OXYTOCIN

1963 ◽  
Vol 41 (2) ◽  
pp. 511-517 ◽  
Author(s):  
D. R. Varma ◽  
K. I. Melville
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Left Coronary Artery ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Surface Cooling ◽  
Normal Body Temperature ◽  
Oesophageal Temperature ◽  
Consistent Method

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.

Diazepam administered prior to coronary artery occlusion increases latency to ventricular fibrillation

Life Sciences ◽  
1991 ◽  
Vol 49 (8) ◽  
pp. 587-594 ◽  
Author(s):  
Judith M.B. Pinto ◽  
Debra A. Kirby ◽  
David A. Johnson ◽  
Bernard Lown
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion

Vagal reflexes and survival during acute myocardial ischemia in conscious dogs with healed myocardial infarction

1991 ◽  
Vol 261 (1) ◽  
pp. H63-H69 ◽  
Author(s):  
G. M. De Ferrari ◽  
E. Vanoli ◽  
M. Stramba-Badiale ◽  
S. S. Hull ◽  
R. D. Foreman ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Rate ◽  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Myocardial Ischemia ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Acute Myocardial Ischemia ◽  
Acute Ischemia ◽  
Control Test

The role of vagal tone and reflexes in the genesis of life-threatening arrhythmias was investigated in a clinically relevant animal model for sudden cardiac death. Forty-five dogs with a healed anterior myocardial infarction in which transient myocardial ischemia during exercise did not induce malignant arrhythmias were utilized for the study. They underwent a further exercise and ischemia test in which atropine (75 micrograms/kg) was injected before coronary artery occlusion. Novel occurrence of ventricular arrhythmia, or worsening of the type of arrhythmia present in the control test, occurred in 23 of 45 dogs (51%) and ventricular fibrillation occurred in 11 of 45 (24%, P = 0.001). Analysis of heart rate response to acute ischemia in the control test indicates that these 11 animals had powerful vagal reflexes during coronary artery occlusion, compared with the 34 survivors (-32 +/- 35 vs. +2 +/- 27 beats/min, P = 0.003). This study indicates that approximately 75% of animals resistant to ventricular fibrillation are characterized by weak sympathetic reflexes in response to acute myocardial ischemia. In the remaining 25% powerful vagal reflexes counteract concomitant reflex sympathetic hyperactivity, decrease heart rate, and are essential for survival.

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