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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine alterations in myocardial metabolism and and hemodynamics that occur within the first 30 minutes after coronary arterial occlusion, before the onset of ventricular fibrillation, measurements were compared in two series of dogs. Series A, 90 dogs that did not manifest ventricular fibrillation after coronary occlusion, were considered a control group. Series B consisted of 28 dogs that had ventricular fibrillation within 30 minutes after occlusion. All had similar comprehensive measurements completed preceding the onset of ventricular fibrillation. The animals in series B (subseuqnt fibrillation) had significantly higher heart rates before and after coronary occlusion. In this series cardiac metabolism of the occluded segment judged by transmyocardial lactate extraction, potassium balance, sodium/potassium ratio and blood pH because grossly more abnormal after coronary occlusion than in series A. In 5 animals whose measurements were obtained within 5 minutes of the onset of ventricular fibrillation, a sudden massive lactate production, potassium loss and increased acidosis of the occluded portion supervened minutes before the onset of the fatal arrhythmia. Animals with ventricular fibrillation had higher intracoronary S-T segment elevation that persisted until the onset of ventricular fibrillation. Measurements of abnormal hemodynamic function (left ventricular end-diastolic pressure, peak systolic pressure and first derivative of left ventricular pressure [DP/dt]) were not associated with an increased incidence of ventricular fibrillation. The study indicates that animals that manifest ventricular fibrillation within 30 minutes after coronary occlusion have higher preocclusion heart rates, a more severe metabolic disorder of the coronary occluded segment and more persistent intracoronary S-T segment elevation compared with animals that do not manifest ventricular fibrillation.
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PMID:Derangements of myocardial metabolism preceding onset of ventricular fibrilliation after coronary occlusion. 1 79

The effect of nitroglycerin on vulnerability to ventricular fibrillation was examined in 44 chloralose-anesthetized dogs. In 19 animals ventricular fibrillation threshold was measured before and during a 10 minute period of occlusion of the left anterior descending coronary artery followed by abrupt release of occlusion. Fibrillation threshold was determined using the single stimulus and train of stimuli methods. The influence of nitroglycerin on vulnerability was assessed with and without prevention of the drug's hypotensive effect by intravenous injection of phenylephrine. In the nonischemic myocardium, infusion of nitroglycerin alone or in combination with phenylephrine did not alter the ventricular fibrillation threshold. However, during both coronary occlusion and reperfusion, administration of nitroglycerin alone afforded partial protection against vulnerability to ventricular fibrillation. Nearly complete protection was imparted by combined administration of nitroglycerin and phenylephrine. The incidence of spontaneous ventricular fibrillation during reperfusion was significantly reduced by combined administration of nitroglycerin and phenylephrine. It is concluded that infusion of nitroglycerin decreases susceptibility to ventricular fibrillation during both acute myocardial ischemia and reperfusion and that this beneficial action is substantially enhanced when the drug's hypotensive effect is prevented.
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PMID:Effect of nitroglycerin on vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion. 10 8

Continuously recorded bipolar electrograms were obtained simultaneously from epi-, endo-, and mid-myocardial regions of the ischemic and normal zones of cat left ventricle in vivo after coronary occlusion, analyzed by computer, and compared to regional cyclic AMP levels. Regional cyclic AMP content was used as an index of the combined local effects of: (a) efferent sympathetic nerve discharge; (b) release of myocardial catecholamines due to ischemia; and (c) circulating catecholamines. Ischemia resulted in a progressive increase in pulse width and rise time and a decrease in rate of rise of voltage (dV/dt) of the local electrograms from ischemic zones reaching a maximum within 2.4+/-0.3 min (mean+/-SE) at the time of onset of severe ventricular dysrhythmias, all of which returned toward control before the cessation of the dysrhythmia (33.5+/-1.5 min after coronary occlusion). Increases in cyclic AMP in ischemic zones preceded corresponding increases in the frequency of premature ventricular complexes (PVCs). Propranolol inhibited the increases in cyclic AMP and reduced the frequency of PVCs in animals without ventricular fibrillation. In animals with ventricular fibrillation, cyclic AMP was significantly elevated in normal and ischemic zones compared to animals with PVCs only. Electrical induction of PVCs or ventricular fibrillation in ischemic and nonischemic hearts failed to increase cyclic AMP. The results suggest that the changes in regional adrenergic stimulation of the heart may contribute to perpetuation of ventricular dysrhythmia and the genesis of ventricular fibrillation early after the onset of myocardial ischemia.
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PMID:Mechanisms contributing to malignant dysrhythmias induced by ischemia in the cat. 20 67

The effects of methylprednisolone (50 mg.kg-1) on the incidence of ventricular tachycardia and fibrillation and on ventricular fibrillation threshold were studied during acute coronary occlusion in anaesthetised dogs. Ventricular tachycardia and/or ventricular fibrillation occurred in 11 of the 16 animals (69%) both before and after methylprednisolone pretreatment. The mean ventricular fibrillation threshold of 10 dogs was 10.1 +/- 1.8 mA before methylprednisolone and it increased slightly to 13.3 +/- 2.3 mA after the drug. This difference was not statistically significant (P greater than 0.2).
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PMID:Effects of methylprednisolone on ventricular arrhythmias during acute myocardial ischaemia. 44 31

Extracellular potassium activity before and after coronary occlusion was measured in the canine heart by means of potassium-selective surface electrodes. In the ischaemic myocardium potassium activity rapidly increased from a preocclusion value of 3.2 +/- 0.3 mmol.litre-1 to 10 +/- 0.6 mmol.litre-1 within the first 5 min and to about 11.3 +/- 0.5 mmol.litre-1 after 10 min of ischaemia (range from 9.5 to 14.5 mmol.litre-1). Following the initial 10 min of ischaemia no further increase was measured. In the non-ischaemic area potassium activity remained constant. Acute beta-blockade significantly attenuated the initial rate of increase in potassium activity; however, beta-blockade did not influence maximal values of extracellular potassium activity measured after occlusion. Lowering of heart rate by vagal stimulation did not modify the pattern of increase in potassium during acute ischaemia. Following ventricular fibrillation, a slow but continuous rise in potassium activity was found. These results demonstrate that extracellular potassium activity in the acutely ischaemic myocardium is considerably higher than indicated by the technique of coronary vein sampling and is in the range necessary for the development of re-entrant arrhythmias in the early phase after coronary occlusion.
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PMID:Extracellular potassium activity changes in the canine myocardium after acute coronary occlusion and the influence of beta-blockade. 47 50

The risk of instantaneous death due to ventricular fibrillation was compared in resting and exercised dogs. Three weeks before testing, all dogs had bipolar left ventricular stimulating electrodes implanted and a reversible snare was placed around the anterior descending coronary artery. The dogs were randomly assigned to either an exercise (13 dogs) or a control (12 dogs) group. We measured ventricular fibrillation thresholds (VFTs) in all dogs before and after inducing ischemia by tightening the snare while the dogs stood at rest. The next day, nonischemic and ischemic VFTs were redetermined for control dogs at rest and for the exercise group during a treadmill run. No statistically significant changes were noted within and between groups in nonischemic or in ischemic VFTs at rest. In five exercise dogs, spontaneous ventricular fibrillation occurred during the first 8 minutes of the ischemic run, For the eight other exercise dogs, running increased the mean drop in VFTs during coronary occlusion by 23% (p less than 0.01). These data suggest that moderate dynamic exercise may greatly enhance the risk of ventricular fibrillation and sudden death in the presence of myocardial ischemia. In the absence of ischemia, exercise does not appear to increase vulnerability to ventricular fibrillation.
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PMID:Effect of submaximal exercise on vulnerability to fibrillation in the canine ventricle. 47 84

Acute occlusions of the left circumflex coronary artery were performed in open-chest dogs. A control group (n = 19) was compared with three groups (total n = 17) pretreated once daily with different doses of the cardioselective beta-blocking drug atenolol (ICI 66 082) given by mouth for 5 days. Only animals without coronary collateral vessels were examined, having a mortality rate of 100% in the control group. Arrhythmias and ventricular fibrillation during the first 30 min after coronary occlusion showed a biphasic distribution in time (phase 1a and 1b). A lower degree of beta-adrenoceptor blockade reduced the incidence of arrhythmias and ventricular fibrillation in phase 1a, but fibrillation occurred in all animals during phase 1b. A higher dose of the beta-blocking drug protected the animals from ventricular fibrillation, and arrhythmias in phase 1a were greatly reduced. At all times the ventricular fibrillation threshold in the group pretreated with atenolol was significantly higher than in the control group. In both groups a significant decrease in ventricular fibrillation threshold was found only during phase 1a. The greater sensitivity of phase 1a arrhythmias to beta-blockade and the lack of a decrease in ventricular fibrillation threshold during phase 1b might indicate differences in the genesis of arrhythmias and fibrillation in phases 1a and 1b.
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PMID:Prophylaxis of ventricular fibrillation after acute experimental coronary occlusion by chronic beta-adrenoceptor blockade with atenolol. 51 61

To study the action of aspirin upon the myocardium per se, independent of thrombosis, coronary occlusion with a balloon catheter was induced in 53 anesthetized dogs divided into two groups. One group (N = 20) was treated daily with aspirin (600 mg/dog) for seven days and another (N = 33) was untreated. Left ventricular hemodynamics and precordial ECG mapping were used to assess the influence of myocardial ischemia over a four hour period. There were no significant differences in left ventricular function or extent of injury as judged by ECG mapping between the two groups. However, there was a significant decrease in the incidence of ventricular fibrillation in the treated dogs (5% vs 39%). Serial plasma samples for free fatty acid determination showed a significant rise in the untreated group. Aspirin blocked the FFA increment in the treated animals. Tissue samples from the ischemic area of left ventricle exhibited a significant reduction of the sodium and water increments, as well as a lesser potassium loss in the treated animals compared to the controls and may have been the basis for the lower incidence of arrhythmias. Since infusion of 51Cr labelled platelets showed no myocardial accumulation of platelets in either group, microthrombi did not appear to contribute to the observed differences.
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PMID:Antiarrhythmic effects of aspirin during nonthrombotic coronary occlusion. 63 Jun 76

This study examined nonuniform postganglionic cardiac sympathetic neural discharge as a possible mechanism involved in the production of coronary occlusion or ouabain-induced arrhythmias. After acute occlusion of the left anterior descending coronary artery in 12 cats, anesthetized with alpha-chloralose and pretreated with atropine, arrhythmia occurred within 3 min in eight animals; three of these died in ventricular fibrillation. In recordings from 15 nerves in the eight animals with arrhythmia, spontaneous discharge increased in nine nerves, decreased in five nerves, and showed no change in one nerve. This nonuniform neural discharge was associated with the development of arrhythmia after occlusion. In four of the cats, neural discharge did not change within the first 3 min after coronary artery occlusion and arrhythmia did not occur. Development of ouabain-induced arrhythmia was accompanied by a nonuniform pattern in the neural discharge (13 cats). This discharge may alter ventricular excitation and conduction to produce arrhythmia.
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PMID:Nonuniform cardiac sympathetic nerve discharge: mechanism for coronary occlusion and digitalis-induced arrhythmia. 63 25

The sequence of localized changes in ventricular repolarization time during and after temporary coronary artery occlusion was studied in 10 open chest dogs. Immediately after the onset of coronary occlusion functional refractory periods (FRPs) prolonged slightly in the ischemic area, then shortened with continued occlusion. Within the first minute following release of occlusion, FRPs underwent a further brief decrease in duration. By varying the period of occlusion from 1 1/2 to 6 1/2 min, evidence was obtained that the post-release shortening of RFPs was temporally related to release of the clamp and not to the onset of occlusion. Ventricular fibrillation occurred in 2 dogs, in each instance soon after release of the coronary artery occlusion. The possible relationship of these experimental FRP changes to waveform abnormalities and arrhythmias in ischemic heart disease is discussed.
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PMID:Changes in ventricular recovery properties during and after temporary coronary artery occlusion. 69 Dec 76


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