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Biomedical subjects

R L Verrier

Publications and source records attributed to R L Verrier.

At least 91 records · Page 5Linked to original sources
PubMed1981

Extra-adrenergic mechanisms responsible for the effects of glucose-insulin-potassium solution on vulnerability to ventricular fibrillation.

In 53 chloralose-anesthetized dogs, the actions of glucose (10 mg/kg per min), insulin (0.025 U/kg per min) and potassium (0.025 mEq/kg per min) on the ventricular fibrillation and repetitive extrasystole thresholds were examined. Measurements were initially made in the control state and then repeated at 30, 60 and 120 minutes of infusion of glucose-insulin-potassium solution at a constant rate of 1.23 ml/min. The dogs received on the average 36 g of glucose, 44 U of insulin and 44 mEq of potassium over a 2 hour period. In the nonischemic myocardium, the infusion raised the threshold for ventricular fibrillation and repetitive extrasystole to a peak of 94 and 61 percent, respectively, without significantly changing serum potassium or circulating catecholamine concentration. In the ischemic myocardium, the incidence of spontaneous ventricular fibrillation during 10 minutes of coronary occlusion was reduced from 83 percent in the control state to 17 percent with glucose-insulin-potassium infusion. However, the infusion did not alter the incidence of ventricular fibrillation associated with reperfusion. Because cardio-cardiac sympathetic reflexes are elicited in response to coronary occlusion, the effect of glucose-insulin-potassium infusion on ventricular vulnerability during left stellate ganglion stimulation and norepinephrine infusion was investigated. The infusion completely prevented the reduction in the vulnerable period threshold during stellate stimulation and norepinephrine infusion. Furthermore, the peak protection afforded by the infusion was greater than that achieved with beta adrenergic blockade and was still present in catecholamine-depleted hearts. It is concluded that infusion of glucose-insulin-potassium solution protects against ventricular fibrillation in the normal and ischemic canine heart but not during reperfusion. This protection may be due in part to antagonism of adrenergic activity; however, the primary influence of the solution is mediated by extra-adrenergic mechanism.

Animals↗
PubMed1981

Influence of autonomic nervous system stimulation on the protective zone.

The effect of sympathetic and parasympathetic stimulation on the vulnerable period threshold and the protective zone was studied in chloralose-anaesthetised dogs. Sympathetic stimulation substantially decreased the repetitive extrasystole threshold and shifted the timing of the protective zone earlier into diastole. Vagus nerve excitation exerted the opposite effect on both electrophysiological properties. During concurrent sympathetic nerve stimulation, the changes produced by vagal activation were accentuated. These findings suggest that parasympathetic influences on the protective zone are due, in part, to an antagonism of adrenergic effects on ventricular electrical properties.

Animals↗
PubMed1980

Protective effect of verapamil on vulnerability to ventricular fibrillation during myocardial ischaemia and reperfusion.

The effects of verapamil on vulnerability to ventricular fibrillation were studied in 55 chloralose-anaesthetised dogs. Ventricular fibrillation threshold was measured before and during a 10 min period of left anterior descending coronary artery occlusion and following abrupt release of occlusion. The action of intravenous verapamil (0.01 mg.kg-1.min-1, following a 0.1 mg.kg-1 bolus) on vulnerability to fibrillation was examined before and during coronary artery occlusion and reperfusion. While the infusion of verapamil did not alter the ventricular fibrillation threshold in the nonischaemic myocardium, the vulnerable period threshold was raised and the incidence of spontaneous ventricular fibrillation was reduced both after coronary artery occlusion and release. Since cardiocardiac sympathetic reflexes are elicited in response to coronary artery occlusion, the effect of verapamil on vulnerability during left stellate ganglion stimulation and during noradrenaline infusion was investigated. Verapamil completely prevented the reduction in vulnerable period threshold during sympathetic nerve stimulation or noradrenaline infusion. This study suggests that the antifibrillatory action of verapamil during coronary artery occlusion may be, in part, related to antagonism of enhanced adrenergic input to the heart, while the mechanism of protection during reperfusion is as yet uncertain.

Adrenergic Fibers↗
PubMed1979

Digitalis drugs and vulnerability to ventricular fibrillation.

The effect of acetylstrophanthidine (AS), a rapid-acting digitalis-like agent, on the ventricular fibrillation (VF) threshold was examined in normal and denervated chloralose-anesthetized dogs. In neurally intact dogs an intravenous bolus of AS (0.075 mg/kg) increased the VF threshold up to a maximum 50% (P less than 0.01) within 30 min after injection. The augmented VF threshold following intravenous administration of AS was not altered by vagotomy. Bilateral stellectomy in vagotomized dogs, as well as carotid sinus and aortic arch denervations, however, prevented the AS induced increase in VF threshold. In neurally intact dogs beta-adrenergic blockade with propranolol (0.25 mg/kg) precluded AS effects. These data suggest that the increase in the VF threshold resulting from AS administration in the normal canine ventricle is due to withdrawal of sympathetic tone mediated via the baroreceptor reflex. The direct effect of AS on the myocardium is to decrease the VF threshold.

Adrenergic beta-Antagonists↗
PubMed1979

Effect of nitroglycerin on vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion.

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.

Animals↗
PubMed1978

Effects of clonidine on vulnerability to fibrillation in the normal and ischemic canine ventricle.

Clonidine infusion (10 microgram/kg, i.v.) elicited a 30% increase in repetitive extrasystole (RE) threshold in 6 chloralose-anesthetized dogs. A reduction in heart rate and arterial blood pressure accompanied the increased threshold. Intracisternal injection of clonidine (2 microgram/kg) in 6 dogs caused similar alterations in these parameters. Bilateral vagotomy, performed in 6 dogs prior to intravenous clonidine, prevented the increase in RE threshold but did not prevent the drug-induced bradycardia. Atropine (0.2 and 0.6 mg/kg), however, did not attenuate the effect of clonidine on RE threshold. Clonidine administration did not prevent the reduction in ventricular fibrillation threshold associated with a 10 min occlusion of the left anterior descending coronary artery or following reperfusion. We conclude that: (1) clonidine reduces ventricular vulnerability in the normal but not the ischemic heart, and (2) its protective effect is mediated by enhanced afferent vagal input to midbrain cardiovascular regulatory centers. This central nervous system action causes a reduction in sympathetic tone to the heart.

Animals↗
PubMed1978

The effects of psychological stress and vagal stimulation with morphine on vulnerability to ventricular fibrillation (VF) in the conscious dog.

Ventricular vulnerability to fibrillation was assessed in 12 conscious dogs in aversive and nonaversive environments using the repetitive extrasystole (RE) threshold method. In the average environment, RE threshold was 45 per cent lower than in the nonaversive setting and heart rate and blood pressure were significantly elevated. This decrease in RE threshold occurred within 10 minutes of exposing the animals to stress. In contrast, the recovery in RE threshold in the nonaversive setting occurred over a 40 minute period. When morphine sulfate (MS) 0.25 mg./Kg was administered to dogs in the aversive environment, the RE threshold was significantly increased. Cholinergic blockade of vagal efferent activity with atropine (0.2 mg./Kg) annulled partially the effect of MS on RE threshold MS was without effect in the nonaversive environment. It is concluded that MS exerts a significant protective effect on increased ventricular vulnerability associated with psychological stress. This effect is mediated by the vagotonic and sedative actions of morphine.

Animals↗
PubMed1978

Precordial mechanical stimulation for exposing electrical instability in the ischemic heart.

Sequenital mechanical pulsing of the chest wall with three stimuli failed to induce arrhythmias in normal dogs. After coronary arterial occlusion, this technique evoked in 11 of 12 animals repetitive ventricular tachycardia in 2. These responses corresponded closely to those elicited by electrical testing. In four conscious animals after recovery from myocardial infarction, precordial pulsing induced repetitive ventricular arrhythmias. The type of arrhythmia produced depended on the degree of prematurity of the third pulse in the sequence. The use of precordial mechanical stimulation can perhaps be modified and adapted as a method of detecting persons at high risk for sudden cardiac death.

Animals↗
PubMed1978

Protective effect of the vagotonic action of morphine sulphate on ventricular vulnerability.

Administration of morphine sulphate to 16 anaesthetised dogs resulted in significant reduction in ventricular vulnerability to fibrillation. The repetitive extrasystole threshold was used as an index of vulnerability to ventricular fibrillation. In 14 dogs, atropine or vagotomy abolished this response. This suggests that central vagal activation by morphine sulphate may be protective against ventricular fibrillation.

Animals↗
PubMed1977

Neural and psychologic mechanisms and the problem of sudden cardiac death.

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.

Animals↗