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Biomedical subjects

R L Verrier

Publications and source records attributed to R L Verrier.

At least 19 recordsLinked to original sources
PubMed1992

Behavioral states and sudden cardiac death.

Remarkable progress has been made both experimentally and clinically in defining the influence of behavioral states on susceptibility to life-threatening arrhythmias. Biological models have been developed to emulate anger and fear and have permitted detailed study of the intermediary mechanisms involved in stress-induced ischemia and ventricular fibrillation. The studies highlight the importance of adrenergic factors and the pathological significance of the poststress state. Clinically, the role of daily stresses in inducing silent myocardial ischemia and arrhythmias has been extensively characterized, and standardized behavioral stress tests have become available. Certain sleep states have been found to provoke ischemic episodes and arrhythmias. In particular, phasic rapid eye movement (REM) sleep has been shown both in animals and humans to conduce to perfusion abnormalities and propensity to fibrillation. Episodic surges in sympathetic nervous system activity appear to be the underlying basis. These conceptual and practical advances illustrate the promise of behavioral cardiology in the diagnosis and treatment of individuals at risk for sudden cardiac death.

Anger↗
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↗
PubMed1977

Acute blood pressure elevation and ventricular fibrillation threshold during coronary occlusion and reperfusion in the dog.

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.

Animals↗
PubMed1977

Effect of stellectomy and vagotomy on ventricular refractoriness in dogs.

The influence of tonic sympathetic and parasympathetic nervous system activity on ventricular refractory period duration was studied in 13 mongrel dogs. Strength-interval curves were obtained from the apex of the right ventricular endocardium with a transvenous bipolar catheter. The effects of sympathetic activity were assessed by unilateral and bilateral stellectomies and tonic vagal effects were studied by inducing cholinergic blockade with atropine (0.2 mg/kg) and by sectioning the cervical vagi bilaterally. Right stellectomy shifted the strength-interval curve 3-5 msec earlier (P less than 0.005). In contrast, left stellectomy shifted the strength-interval curve 4-7 msec later (P less than 0.001). Thus, right and left unilateral stellectomy produced opposite effects. However, when the contralateral ganglion was removed, right and left stellectomy produced qualitatively similar effects, increasing refractoriness. The net effect of bilateral stellectomy was to shift the strength-interval curve 8-10 msec later (P less than 0.001) and this was primarily dependent on left stellectomy. Blockade of vagal efferent activity with atropine shifted the strength-interval curve 3-6 msec earlier (P = .001). Removal of vagal afferent activity by vagotomy during atropine blockade shifted the strength-interval curve 2-3 msec earlier (P = 0.03). It is concluded that both stellate ganglia exert qualitatively similar effects on cardiac refractoriness; however, the left ganglion dominates and unilateral right stellectomy produces a paradoxical decrease in refractoriness. The sympathetic effects are tonically antagonized by vagal activity.

Animals↗
PubMed1976

Effect of vagus nerve stimulation upon excitability of the canine ventricle. Role of sympathetic-parasympathetic interactions.

The effect of vagus nerve stimulation on ventricular excitability was studied in 28 dogs under various conditions of adrenergic neural tone. Strength-interval curves were delineated from the apex of the right ventricular endocardium with a transvenous bipolar catheter. Vagus nerve stimulation in both closed chest and open chest dogs shifted the strength-interval curve 6 to 8 msec later into electrical diastole (P less than 0.001). Left stellate ganglion stimulation shifted the strength-interval curve 9 to 11 msec earlier into diastole (P less than 0.001). The effect of simultaneous left stellate ganglion and vagus nerve stimulation was not significantly different from that of left stellate ganglion stimulation alone. The influence of vagus nerve stimulation on the strength-interval curve under basal conditions was abolished by acute beta adrenergic blockade with propranolol. It is concluded that vagus nerve stimulation affects ventricular excitability as well as vulnerability by opposing the effects of sympathetic neural tone.

Adrenergic beta-Antagonists↗