Abrupt Coronary Occlusion Research Articles

Spontaneous heart rate, propranolol, and ischaemia-induced ventricular fibrillation in the dog.

Abrupt coronary occlusion was performed in anaesthetised, open-chest dogs with pre-occlusion arterial blood PO2 ranging from 8.0 to 10.7 kPa (60 to mmHg). Ventricular fibrillation occurred in 15/19 dogs with high spontaneous heart rate (less than 155 beats.min-1) and in 0/8 dogs with low spontaneous heart rate (less than 155 beats.min-1). Dogs with low spontaneous heart rate fibrillated when paced at a fast rate (200.min-1) (4/5). In dogs with high spontaneous heart rate fibrillation occurred in 0/5 dogs when propranolol reduced spontaneous heart rate, but in 3/5 dogs when reduction in spontaneous heart rate in response to propranolol was prevented by pacing.

Pharmacologic and behavioral effects on arrhythmias that immediately follow abrupt coronary occlusion: A canine model of sudden coronary death

We have developed and studied a chronically instrumented canine model in which occlusion of a major coronary artery by an implanted balloon occluder promptly leads to arrhythmias that are reasonably reproducible on successive occlusions. Dogs were studied while conscious, and the electrocardiogram and electrograms from ischemic and nonischemic ventricular epicardium were recorded. Either the left anterior descending or circumflex coronary artery was occluded for up to 5.5 minutes. Experiments were performed in a carefully controlled environment at intervals sufficient for full recovery between occlusions. The arrhythmias that occurred were single or multiple premature ventricular depolarizations, runs of ventricular premature depolarizations or ventricular fibrillation. We measured the time from the onset of occlusion to the onset of arrhythmia (latency) and the severity of the arrhythmia (grade). Latency increased with successive occlusions in the same environment until no arrhythmia occurred during an occlusion of 5.5 minutes. In this state, addition of behavioral stress usually led to recurrence of arrhythmia. Stress decreased latency ( P < 0.02) and increased grade. We also studied the effects of tolamolol (a beta blocking agent), UM-272 (an analog of propranolol) and diazepam. Tolamolol increased latency ( P < 0.02) and tended to decrease grade. UM-272 had variable effects, but it clearly did not exert a protective action. The severity of arrhythmia was inversely related to latency, and latency decreased with increases in heart rate. The results obtained indicate that the model is useful for studies on arrhythmias that follow soon after the onset of ventricular ischemia, and they emphasize the relation between stress, enhanced sympathetic activity and ventricular arrhythmias.

Effect of stimulation of somatic nerves on the ventricular fibrillation threshold in dogs

Summary The data indicate that activation of somatic afferent fibers can produce a change in cardiac sympathetic activity which may influence development of arrhythmias under certain conditions. In this study, the VFT was lowered significantly by stimulation of somatic afferent fibers belonging to Groups II to IV. The decrease in VFT was probably due to increased sympathetic activity to the heart, since β-adrenergic blockade prevented the change in VFT during nerve stimulation. Recently, Theroux and associates 28 have shown that premedication of conscious dogs with morphine prevents the occurrence of ventricular fibrillation in the first few minutes following abrupt coronary artery occlusion. It was thought that morphine prevented the excitement reaction (which was characterized by marked agitation and struggling) in response to the ischemic pain associated with the coronary occlusion. According to the present study, morphine may have interrupted the somatosympathetic reflux associated with the pain and excitement and prevented the reflex increase in sympathetic activity to the heart. These observations deserve further, study, especially with regard to the effect of morphine on somatosympathetic reflexes. An alternate explanation is that morphine may have produced an increase in vagal efferent activity, which has been shown to antagonize the influence of the sympathetic nervous system on the heart 3 .

Temporary coronary occlusion in conscious dogs: collateral flow and electrocardiogram.

ARTICLESTemporary coronary occlusion in conscious dogs: collateral flow and electrocardiogramJE Chimoskey, M Szentivanyi, R Zakheim, and AC BargerJE Chimoskey, M Szentivanyi, R Zakheim, and AC BargerPublished Online:01 May 1967https://doi.org/10.1152/ajplegacy.1967.212.5.1025MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByA Servo-controlled Canine Model of Stable Severe Ischemic Left Ventricular Failure8 October 2009 | Cardiovascular Engineering, Vol. 9, No. 4Hyperosmotic mannitol and collateral blood flow to ischemic myocardiumJournal of Surgical Research, Vol. 47, No. 5Fatal myocardial infarct in a GreyhoundJournal of Small Animal Practice, Vol. 23, No. 8THE EFFECTS OF PROPRANOLOL AND ACEBUTOLOL ON LEFT VENTRICULAR FUNCTION AND CORONARY HAEMODYNAMICS IN THE CONSCIOUS DOG WITH MYOCARDIAL ISCHAEMIA19 July 2012 | British Journal of Pharmacology, Vol. 68, No. 3Radioautographic studies in experimental myocardial infarction: Profiles of ischemic blood flow and quantification of infarct size in relation to magnitude of ischemic zoneThe American Journal of Cardiology, Vol. 42, No. 1Pharmacologic and behavioral effects on arrhythmias that immediately follow abrupt coronary occlusion: A canine model of sudden coronary deathThe American Journal of Cardiology, Vol. 41, No. 6Influence of dobutamine on regional myocardial blood flow and ventricular performance during acute and chronic myocardial ischemia in dogs.Circulation, Vol. 53, No. 5Modification of ventricular fibrillation latency following coronary artery occlusion in the conscious pig.Circulation, Vol. 51, No. 4Magnetic determination of the relationship between the S-T segment shift and the injury current produced by coronary artery occlusion.Circulation Research, Vol. 36, No. 3Left ventricular function during acute ischemiaThe American Journal of Cardiology, Vol. 34, No. 7Reflex Blood Pressure Control during Acute Myocardial Ischemia in the Conscious DogCirculation Research, Vol. 34, No. 2Function of the hypoxic myocardiumThe American Journal of Cardiology, Vol. 32, No. 4Reflex Tachycardia Due to Temporary Coronary Occlusion in the Conscious DogCirculation Research, Vol. 32, No. 5Experimental myocardial infarctionThe American Journal of Cardiology, Vol. 31, No. 3Experimental Acute Myocardial InfarctionCirculation, Vol. 47, No. 3Hemodynamic Evidence of the Development of Coronary Collateral Circulation in Conscious DogsEffect of nitrate infusions on the systemic and coronary circulations following acute experimental myocardial infarction in the intact dogThe American Journal of Cardiology, Vol. 30, No. 4Pathophysiology of ischemic heart diseaseProgress in Cardiovascular Diseases, Vol. 14, No. 3Controlled Production of Left Ventricular Failure in Intact Calves Using Implanted Coronary OccludersThe Annals of Thoracic Surgery, Vol. 10, No. 6Experimental myocardial infarctionThe American Journal of Cardiology, Vol. 26, No. 4Sauerstoffdruck und Durchblutung im gesunden und koronarinsuffizienten Myokard des Hundes und ihre Beeinflussung durch koronarerweiternde PharmakaArchiv für Kreislaufforschung, Vol. 58, No. 3-4 More from this issue > Volume 212Issue 5May 1967Pages 1025-1032 Copyright & PermissionsCopyright © 1967 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1967.212.5.1025PubMed6023862History Published online 1 May 1967 Published in print 1 May 1967 Metrics