Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042510 (ventricular fibrillation)
 10,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was designed to examine ventricular arrhythmias in the acute phase of experimental myocardial infarction in the pig and to evaluate possible antiarrhythmogenic influence of the beta-adrenergic blocking drug pindolol (Visken) and the calcium antagonist Ro 11-1781. Ventricular fibrillation (VF) occurred in 17 of 18 animals, in 4 almost immediately after coronary occlusion and in 12 with a delay of about 17 min. VF was almost always induced by episodes of ventricular tachycardia (VT) which were started by single ventricular premature beats (VPBs). VPBs occurred in 3 phases, whereas VT and VF coincided only with phase 1 and phase 3. The prematurity index QR/QT of single VPBs decreased significantly with time after coronary occlusion. The beta-adrenergic blocking drug pindolol and the calcium antagonist Ro 11-1781 did not prevent VT or VF.
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PMID:[Ventricular arrhythmias in the acute stage of experimental swine myocardial infarct; effect of the beta blocker pindolol and the calcium antagonist Ro 11-1781]. 71 14

Prostaglandin E2 and F1alpha infusions have been tested for their ability to reduce the arrhythmias associated with occlusion of the left descending coronary artery in the anaesthetised dog. At 1 microgram/kg/min both PGs reduced the incidence of premature ventricular contractions occurring during 25-min occlusions, while not reducing the incidence of ventricular fibrillation occurring on occlusion release. When infused for 5-min periods at 1 to 16 microgram/kg/min, neither PGE2 nor PGF1alpha effectively reduced the frequency of ventricular arrhythmias occurring 24 hr after a permanent coronary occlusion.
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PMID:The action of prostaglandin E2 and F1alpha on myocardial ischaemia-infarction arrhythmias in the dog. 74 80

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.
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PMID:Spontaneous heart rate, propranolol, and ischaemia-induced ventricular fibrillation in the dog. 75 78

Alterations of autonomic tone appear to have important effects on the electrical stability of the heart. Since altered electrical stability, ventricular fibrillation, is the cause of death in the majority of patients who die from ischemic heart disease, the effects of the autonomic nervous system on ventricular electrical stability have been examined. Increased vagal tone increases the electrical stability of the heart and reduces the incidence of spontaneous ventricular fibrillation after coronary occlusion. These salutary effects of increased cholinergic tone appear to be mediated by cholinergic innervation of the ventricular conducting system. Conversely, increased adrenergic tone decreases the electrical stability of the heart and increases the propensity of the heart to develop ventricular arrhythmias during coronary occlusion. The interaction of the adrenergic and cholinergic system during myocardial ischemia may be one of the important determinants of survival in patients with coronary artery disease and acute myocardial infarction.
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PMID:Neural basis for the genesis and control of arrhythmias associated with myocardial infarction. 78 2

Nitroglycerin (NTG) traditionally has bben avoided in the treatment of pain caused by acute myocardial infarction because of the belief that NTG-induced decrease in arterial pressure and concomitant reflex increase in heart rate might extend the ischemic process. However, recent experimental and clinical investigations cast doubt on this concept. For example, when the left anterior descending coronary artery is acutely occluded in normal dogs or in dogs when chronic coronary occlusions and extensive collaterals, NTG reduces ST-segment evevation (and presumably myocardial ischemia). This salutary effect occurs despite lowering of systemic arterial pressure, as long as excessive reflex tachycardia does not result; the magnitude of ischemia reduction is potentiated when methoxamine or phenylephrine are administered simultaneously to abolish the NTG -induced hypotension and reflex tachycardia. NTG and methoxamine treatment also results in 1) reduction of infarct size as (as assessed by gross morphologic examinations and myocardial CPK levels) in dogs subjected to 5 hours of coronary occlusion, and 2) increase in ventricular fibrillation (VF) threshold and reduction of the incidence of spontaneously occurring VF in dogs with acute coronary occlusion. Finally, the effectiveness of NTG during acute myocardial iinfarction (AMI) in man has been studied. Multiple precordial electrodes were used to measure changes in the degree of ST-segment elevation; these changes were used as an index of alterations in myocardial ischemic injury. Patients with normal pulmonary capillary wedge pressures ( less than 15 mm Hg) did not benefit consistently from NTG alone; however, when phenylephrine was administered with NTG (to abolish NTG-induced arterial pressure reduction and reflex increase in heart rate), ST-segment elevation diminished consistently. In patients with elevated wedge pressures ( greater than 15 mm Hg), NTG alone consistently reduced ischemia; addition of phenylephrine often partially reversed this benefit. Thus, administration of NTG, alone or with phenylephrine, appears to reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends upon the presence or absence of LV failure prior to treatment. These experimental and clinical results suggest this form of therapy may be use in reducing infarct size in man, although additional studies are necessary to determine the functional significance of these acute electrophysiologic alterations.
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PMID:Protection of ischemic myocardium by nitroglycerin: experimental and clinical results. 81 59

The effects of electrical stimulation of the vagus nerves and the administration of atropine on ventricular fibrillation threshold (VFT) were studied in open-chest hearts of 15 dogs anesthetized by alpha-chloralose. These studies were made in both normal and ischemic ventricles, i.e., before and during acute coronary occlusion. The ventricles were paces at a constant rate to eliminate rate-dependent changes and the minimal current required to induce ventricular fibrillation (or VFT) was determined by delivering a train of rapid rectanglular pulses (100 per second) to the venticle actoss the vulnerable period. In normal ventricles, VFT's were significantly increased by vagal stimulation (P less than 0.01) and decreased by atropine (P less than 0.05). Coronary occlusion markedly decreased VFT's (P less than 0.01), and vagal stimulation or atropine failed to alter VFT's significantly in these ischemic ventricles (P greater than 0.8). In additional 14 dogs, the effects of vagal stimulation and atropine were studied after the administration of propranolol. Propranolol alone increased VFT's significantly in boetreatment with propranolol, vagal stimulation and atropine failed to change VFT's significantly in both normal and ischemic ventricles (P greater than 0.8). These results indicate that the vagus nerves exert their effect on VFT by modifying the sympathetic nerve activity in normal ventricles, but such an effect is not significant enough to alter VFT in ischemic ventricles.
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PMID:Effects of vagal stimulation, atropine, and propranolol on fibrillation threshold of normal and ischemic ventricles. 83 12

Sympathetic discharges to the heart were recorded from the left inferior cardiac nerve of 16 dogs. Inferior cardiac nerve activity (ICNA) under normal conditions consisted of grouped discharges, synchronous with the cardiac cycle and modulated by respiration. After ligation of the circumflex branch of the left coronary artery, ICNA declined concomitant with a decline in heart rate and mean aortic pressure. After 30 minutes, when arterial pressure tended to recover toward control values (six dogs), ICNA remained low; in contrast, when arterial pressure dropped to shock levels (three dogs), ICNA increaed. When aortic pressure fell precipitously as a result of ventricular fibrillation, even during the first 30 minutes of ischemia (seven dogs), ICNA immediately increased greatly. The results of this study suggest that acute coronary occlusion produces a cardiocardiac depressor reflex with attenuation of sympathetic discharge to the heart. This reflex, under the experimental conditions studied, gives way to the baroreceptor reflex when aortic pressure drops to critically low levels.
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PMID:Attenuation of cardiac sympathetic drive in experimental myocardial ischemia in dogs. 83 14

The effect of acute elevation of arterial blood pressure on the ventricular fibrillation threshold was examined in 19 closed chest dogs anesthetized with chloralose during 10 minutes of occlusion followed by abrupt reperfusion of the left anterior descending coronary artery. Ventricular fibrillation threshold was determined using two methods of electrical testing: sequential R/T pulsing and the train of stimuli method. Blood pressure was increased with an intravenous injection of the alpha adrenergic stimulator phenylephrine. Acute hypertension significantly diminished the enhanced vulnerability associated with coronary occlusion. After denervation of the carotid sinus and aortic arch baroreceptors, elevation of blood pressure failed to affect vulnerability during occlusion. In both intact and denervated animals, the predisposition to ventricular fibrillation after reperfusion was unchanged by the increase in blood pressure. It is suggested that withdrawal of sympathetic tone mediated by the baroreceptor reflex is the basis for the protection against ventricular fibrillation resulting from elevation of blood pressure. The failure of acute hypertension to alter vulnerability during reperfusion suggests that the predisposition to ventricular fibrillation during reperfusion is due to mechanisms other than those operating during coronary occlusion.
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PMID:Acute blood pressure elevation and ventricular fibrillation threshold during coronary occlusion and reperfusion in the dog. 84 36

Brain stimulation can provoke a variety of arrhythmias and lower the ventricular vulnerable threshold. In the animal with acute myocardial ischemia such stimuli suffice to provoke ventricular fibrillation. Vagal neural traffic or adrenal catecholamines are not the conduits for this brain-heart linkage. Accompanying increases in heart rate or blood pressure are not prerequisites for the changes in cardiac excitability. Increased sympathetic activity, whether induced by neural or neurohumoral action, predisposes the heart to ventricular fibrillation. Protection can be achieved with surgical and pharmacologic denervation or reflex reduction in sympathetic tone. With acute myocardial ischemia, augmented sympathetic activity accounts for the early surge of ectopic activity frequently precipitating ventricular fibrillation. Asymmetries in sympathetic neural discharge may also contribute to the genesis of serious arrhythmias. The vagus nerve, through its muscarinic action, exerts an indirect effect on cardiac vulnerability, the consequence of annulment of concomitant adrenergic influence, rather than of any direct cholinergic action on the ventricles. There exist anatomic, physiologic as well as molecular bases for such interactions. Available experimental evidence indicates that environmental stresses of diverse types can injure the heart, lower the threshold of cardiac vulnerability to ventricular fibrillation and, in the animal with coronary occlusion, provoke potentially malignant ventricular arrhythmias. Available evidence indicates that in man, as in the experimental animal, administration of catecholamines can induce ventricular arrhythmia, whereas vagal activity exerts an opposite effect. Furthermore, in certain subjects diverse stresses and various psychologic states provoke ventricular ectopic activity.
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PMID:Neural and psychologic mechanisms and the problem of sudden cardiac death. 86 Jun 97

The time course of the ventricular fibrillation threshold (VFT) was studied in 10 open-chest mongrel dogs following acute occlusion of the left anterior descanding coronary artery (LAD). The VFT in the infarcted area was compared to a non-infarcted area of the left ventricle supplied by the circumflex coronary artery. Prior to coronary occlusion the mean VFT for the entire group of 10 animals was 14 ma. for the area supplied by the LAD and 17.6 ma. for the area of the left circumflex. Immediately after coronary ligation the VFT decreased in both areas. Within 90 to 120 minutes the VFT in the infarcted area was 27 ma. and after 6 hours of occlusion the VFT was 3 times the pre-ligation value. The VFT in the non-infarcted area remained near the pre-ligation values. The excitability of the infarcted area was markedly decreased after coronary occlusion and this accounted for the increase in the VFT in the infarcted area. In the non-ischemic area the excitability was unchanged during the entire six hour period following occlusion. The study stresses the importance of the location of the electrodes used for fibrillation and the natural course of the VFT in evaluating VFT's within the ischemic myocardium.
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PMID:Time course of ventricular fibrillation threshold in infarcted and non-infacted myocardium after acute coronary ligation. 88 67


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