Effects of unilateral stellate ganglion blockade on the arrhythmias associated with coronary occlusion

In anesthetized dogs the circumflex and/or the anterior descending coronary artery were briefly occluded (10 to 90 seconds) and ectopic beats occurring during the occlusion or for 60 seconds following release were counted. Control occlusions were alternated with occlusions performed during complete, reversible, unilateral blockade of either the right or the left stellate ganglion. This was achieved with thermodes through which coolant was circulated. In this way the shortcomings associated with stellectomy, which is irreversible, are avoided. Blockade of the right stellate ganglion increased the number of ectopic beats associated with coronary occlusion. The occurrence of episodes of ventricular tachycardia and fibrillation was also greater. By contrast, blockade of the left stellate ganglion reduced or abolished occlusion-induced arrhythmias. These effects are independent of changes in heart rate or vegal activity; they depend solely upon unilateral alteration in sympathetic tone, and are not demonstrable when such tone is low. We suggest that the right and left cardiac sympathetic nerves have a different influence upon cardiac excitability.     

Effect of narcotic analgesics on impulse conduction along the afferent pathways of visceral nerves]

Experiments were conducted on chloralose-anesthetized cats. The action of morphine and promedol upon the potentials of the cortical and subcortical structures occurring after the visceral nerve stimulation was studied. Morphine proved to depress the potentials evoked by stimulation of the inferior cardiac and vagus nerves, in the specific, associative and nonspecific structures of the brain; promedol produced an analogous effect. Morphine also inhibited the potentials occurring after the stimulation of the splanchnic nerve in the associative and nonspecific structures; depression of the responses in the specific pathways was less pronounced.     

Autonomic neural control of cardiac rhythm: the role of autonomic imbalance in the genesis of cardiac dysrhythmia

Cardiac dysrhythmias result from abnormalities in rate, regularity, or sequence of cardiac activation, and because of direct actions of the autonomic nervous system upon each of these properties, imbalance in this system may play an important role in the genesis of cardiac dysrhythmia. A canine model has been developed in which the extrinsic innervation of the heart is ablated with the exception of the ventrolateral cardiac nerve. This nerve is distributed primarily to the inferior atrial, AV junctional, and ventricular tissues. Following recovery from surgery, the animal is placed on a treadmill and required to perform strenuous exercise. In all of six animals which sustained repeated exercise testing over periods of 4-12 months, dysrhythmias of varying complexities were elicited. None appeared in parallel experiments conducted in control or sham-operated animals. The dysrhythmias consisted of supraventricular, AV junctional, or ventricular tachycardias with occasional premature atrial or ventricular systoles. The dysrhythmias were not influenced by atropine but were generally controlled by propranolol.     

Prolongation of ventricular action potential due to sympathetic stimulation

The changes of monophasic action potential durations due to stellate stimulation for the period of 3 sec were studied in dogs with suction electrodes from the anterior surface of the right ventricle and the posterior surface of the left ventricle. Prolongation of monophasic action potential duration was observed from the period of 2 to 3 sec during stimulation to that of 10 to 20 sec after the termination of stimulation. Prolongation of monophasic action potential duration due to right stellate stimulation was predominant in the right ventricle and that due to left stellate stimulation was predominant in the left ventricle. The transient T wave change in the surface electrocardiogram occurring immediately after the beginning of stellate stimulation could be explained by this local difference in prolongation of ventricle repolarization. Since the onset of prolongation of monophasic action potential duration preceded increase in blood pressure following stellate stimulation, this prolongation of monophasic action potential duration did not result from the hemodynamic changes and could be a primary effect of the sympathetic nerve stimulation.     

Significance of cardiac innervation on spontaneous ventricular arrhythmias elicited by left stellate ganglion stimulation in dogs 4 days after myocardial infarction: comparison of two experimental models

The effects of cardiac sympathetic overactivity on spontaneous arrhythmias and transmural left ventricular effective refractory period (LVERP) were assessed by left stellate stimulation (LSS) in 16 anesthetized dogs. The experiments were performed 4 days after proximal occlusion of the left anterior descending (LAD) coronary artery produced by either ligation (9 dogs) or embolization with histoacryl (7 dogs). The innervation of left ventricular myocardium was studied by light and electron microscopies. Synaptophysin (SYN)- and neuropeptide Y (NPY)-immunoreactive nerve fibers and terminals were thereby detected. In dogs subjected to ligation, LSS elicited negligible arrhythmias in spite of a decrease in LVERP by 6.9 +/- 2.2% (mean +/- SD, p < 0.001). However, dogs with intravascular occlusion were more susceptible to LSS, as indicated by development of sustained ventricular rhythms. In these animals, the LVERP decreased with LSS by 14.6 +/- 3.4% (p < 0.001). The innervation of the anterior left ventricular wall distal to the place of occlusion revealed a higher reduction of SYN- and NPY-immunoreactive nerves in infarcted myocardium and a more heterogeneous distribution of nerves in undamaged regions after ligation, compared to intravascular occlusion. Ultrastructurally, nerve terminals containing small agranular and large dense-core vesicles were found innervating ischemically damaged myocardiocytes. Our findings indicate a higher preservation of nerves in infarcted and noninfarcted myocardium of animals subjected to embolic occlusion of the LAD. Because LSS apparently elicited more arrhythmias in these animals, we suggested a proarrhythmic effect of intact myocardial innervation after infarction.     

A peptide binding motif for HLA-DQA1*0102/DQB1*0602, the class II MHC molecule associated with dominant protection in insulin-dependent diabetes mellitus

The central integration of signals from pulmonary vagal C-fibers (or type-J receptors) with those arising from cardiac, peripheral chemoreceptor, and baroreceptor afferents to neurons within the nucleus of the solitary tract (NTS) was studied in an arterially perfused working heart-brain stem preparation of adult mouse. Pulmonary vagal C-fibers were excited by right atrial injection of phenylbiguanide (PBG) while cardiac receptors were stimulated by left ventricular injection of veratridine (1-3 micrograms/kg) or mechanically by distension of the left ventricle (20-50 microl perfusate) using an indwelling cannula. Carotid body chemoreceptors were activated by aortic injection of Na cyanide, whereas baroreceptors were stimulated by increasing arterial perfusion pressure. Stimulation of pulmonary C-fibers and cardiac, chemo-, and baroreceptors all produced a reflex bradycardia (23-133 bpm). Central respiratory activity, as recorded from the phrenic nerve, was depressed by stimulating pulmonary C-fibers and cardiac and baroreceptors but enhanced in amplitude and frequency during chemoreceptor stimulation. Twenty-seven NTS neurons were excited and three were inhibited after pulmonary C-fiber stimulation displaying decrementing discharges with a peak firing frequency of up to 42 Hz (15 +/- 2.2 Hz, mean +/- SE) that lasted for 8.8 +/- 0.9 s. These responses occurred <1 s from the end of the PBG injection that was within the pulmonary circulation time. None of these cells responded to increases in right atrial pressure. All cells excited by PBG were also driven synaptically after electrical stimulation of the ipsilateral cervical vagus nerve at a latency of 32.9 +/- 3.2 ms (range 20-62 ms). None of these neurons had ongoing activity related to central respiratory activity. Convergence from cardiorespiratory afferents to 21 neurons driven by pulmonary C-fibers was tested. Twenty-five percent of cells were selectively excited by chemical stimulation of cardiac receptors alone, 19% were driven by peripheral chemoreceptors, and 38% responded to both cardiac and chemoreceptor activation. In contrast, only 13% of the cells activated by PBG injection responded to stimulation of baroreceptors and only 6% to cardiac mechanoreceptor stimulation. None of these neurons were activated by increasing right atrial pressure. The data indicate a high proportion of afferent convergence from pulmonary C-fibers, cardiac receptors, and peripheral chemoreceptors in the NTS. However, these neurons appear not to integrate inputs from cardiovascular mechanoreceptors. The significance of the data is discussed in relation to pathological disease states such as pulmonary congestion and cardiac failure.     

Common mutations in the fibroblast growth factor receptor 3 (FGFR 3) gene account for achondroplasia, hypochondroplasia, and thanatophoric dwarfism

A standard electrical stimulus applied to the posterior hypothalamus evoked cardiac arrhythmogenic responses in the spontaneously hypertensive rat. Isolated premature ventricular beats or doublets and nonsustained ventricular tachycardic salvos were observed. This effect was associated with a large rise in blood pressure (79 +/- 3 mm Hg). The same stimulus in normotensive Wistar-Kyoto rats produced no significant cardiac arrhythmias, and the rise in blood pressure was smaller (36 +/- 2 mm Hg). We investigated the influence of baclofen, a GABAB receptor agonist, and two N-methyl-D-aspartate receptor antagonists on the arrhythmogenic response to hypothalamic stimulation. Intravenous baclofen (3 mg/kg) had no effect in the normotensive Wistar-Kyoto rats, but in the spontaneously hypertensive rats it enhanced the adjusted mean value of the number of extrasystoles from 0.5 +/- 0.5 to 18 +/- 1 (P < .001). This value was also increased (from 3 +/- 1 to 17 +/- 1, P < .001) by an intracisternal injection of baclofen (1 micrograms/kg). This facilitatory effect of baclofen was prevented by treatment with atenolol (0.5 mg/kg). Two glutamate receptor antagonists, ketamine (7.5 mg/kg IV) and kynurenic acid (200 micrograms/kg intracerebroventricularly), prevented both the arrhythmogenic response to the hypothalamic stimulation and its facilitation by baclofen. The study confirms that hypothalamic stimulation facilitates the development of arrhythmias through a sympathetic drive and that these arrhythmias are easier to induce in spontaneously hypertensive rats than in normotensive Wistar-Kyoto rats. Both the central GABAergic and the glutamatergic systems are implicated in the development of these ventricular arrhythmias, since baclofen could disinhibit the glutamatergic central pathway. These results could account for the ability of the spontaneously hypertensive rats to develop ventricular arrhythmias of central origin.     

Hemodynamic benefits of right ventricular outflow tract pacing: comparison with right ventricular apex pacing

To assess optimal hemodynamics in relation to stimulation site during right ventricular pacing, 17 consecutive patients who underwent cardiac catheterization were studied. In all patients, right ventricular apex and right ventricular outflow tract stimulation was performed at 85, 100, and 120 beats/min. Cardiac index at both pacing sites was compared using the left ventricular outflow tract continuous wave Doppler technique. Comparison of the two stimulation sites demonstrated that right ventricular outflow tract pacing resulted in a higher cardiac index at 85 beats/min (2.42 +/- 1.2 vs 2.04 +/- 1.0 L/min per m2, P < 0.002) at 100 beats/min (2.78 +/- 1.4 vs 2.35 +/- 1.1 L/min per m2, P < 0.001) and 120 beats/min (3.00 +/- 1.5 vs 2.61 +/- 0.9 L/min per m2, P < 0.001). From a total of 51 paired observations, 45 showed an increase in cardiac index during outflow tract pacing as compared to apex pacing. Right ventricular outflow tract pacing at 120 beats/min resulted in a lower cardiac index than right ventricular apex pacing in patients with significant coronary artery disease and/or impaired left ventricular function (ejection fraction < or = 50%), whereas right ventricular outflow tract pacing produced higher cardiac indices in the absence of these abnormalities. Right ventricular outflow tract pacing resulted in higher cardiac indices as compared to apex pacing in all other subgroups at all other pacing sites tested. It is concluded that stimulation of the right ventricular outflow tract offers a significant hemodynamic benefit during single chamber pacing as compared to conventional apex pacing, particularly in the absence of significant coronary artery disease and/or left ventricular dysfunction.     

Neuroexcitatory effects of digoxin in the cat

The effect of intravenous injections of digoxin (20 mug/kg every 15 minutes) on spontaneously occurring activity in autonomic efferent nerves, motor nerves, afferent nerves, electrocardiogram and on arterial blood pressure was evaluated in chloralose-anesthetized cats. Administration of digoxin enhanced neural activity in pre- and postganglionic cardiac synpathetic nerves and this enhancement occurred near the time the disturbances in ventricular rhym were noted. Neural activity continued to increase during ventricular tachycardia and maximum enhancement was observed just proir to ventricular fibrillation. Similar results were observed when digoxin was administered to animals in which neural activity was recorded from preganglionic splanchnic and superior cervical nerves. Digoxin administration also increased discharge frequency from vagus (efferent fibers), phrenic and carotid sinus nerves. Denervation of cardiovascular reflexogenic areas prevented the increased discharge in vagus nerves, reduced it in phrenic nerves, but did not affect nerve discharge in sympathetic nerves. These results suggest that digoxin-induced hyperactivity in synpathetic nerves was related to a central nervous system effect of the drug, whereas the mechanism for the digoxin-induced hyperactivity in vagus nerves involved a peripheral reflex effect of the drug. Both sites were involved in the digoxin-induced hyperactivity in phrenic nerves. Enhancement of cardiac sympathetic nerve activity appeared to be responsible for the ventricular arrhythmias provoked by digoxin as 1) a temporal relationship was observed between augmented nerve activity and arrhythmia development, 2) a centrally acting sympathetic nervous system depressant drug, clonidine, converted the ventricular arrhythmia to normal rhythm, and 3) removal of sympathetic influence to the heart by spinal cord transection decreased the sensitivity of the heart to the arrhythmogenic effect of digoxin. These results suggest that digoxin partially responsible for its cardiotoxic effects.     

Comparative informative value of chromosome aberrations and sister chromatid exchanges in the evaluation of metals in the environment

The effects of met-enkephalin, leu-enkephalin, D-Ala2-metenkephalin, and somatostatin on Wenckebach arrhythmia and atrioventricular dissociation was investigated in experiments on anesthesized cats. Arrhythmias were induced by stimulation of the vagus with short repetitive bursts of pulses. Enkephalins evoked a protective effect in both arrhythmias whereas somatostatin had no antiarrhythmic properties. The protective effect of enkephalins persisted after blockage of mu-opiate receptors with naloxone (0.2 mg/kg), but in high doses (2 mg/kg), which blocked both mu- and delta-opiate receptors, antiarrhythmic effects was abolished. It is concluded that the protective effect of enkephalins against vagally induced arrhythmias may be due to the stimulation of delta-opiate receptors located on the presynaptic vagal endings. As a results, stimulation-evoked acetylcholine release is diminished, which prevent the arrhythmogenic effect of the vagus nerve.     

Vagal innervation of the gastrointestinal tract arises from dorsal motor nucleus while that of the heart largely from nucleus ambiguus in the cat

The origin of medullary cells that form the cardiac vagal branch and the vagal branches in the lower thorax innervating the gastrointestinal (GI) tract was studied using horseradish peroxidase (HRP), a retrograde transport tracer in the cat. The distributions of parasympathetic postganglionic neurons of the heart were studied with acetylcholinesterase histochemistry. Intracardiac ganglionic neurons were found mainly in the connective tissue surrounding the base of the pulmonary arteries and in an area in and dorsal to the interatrial septum. Following injection of HRP into the subepicardum where most of the cardiac postganglionic neurons reside, 91% of the labelled neurons were found bilaterally distributed in the nucleus ambiguus (NA). A small population of labelled neurons was found in the dorsal motor nucleus of the vagus (DMV) and an intermediate zone (IZ) between the two nuclei. When HRP was injected into the left or right cardiopulmonary vagus branch, labelled neurons were found exclusively in the ipsilateral NA, DMV and IZ with a predominance in the NA. In the thorax, after they course around the heart, the left and right thoracic vagus nerves divides into a left and a right branch, respectively. The left branch of the left thoracic vagus joins the left branch of the right thoracic vagus to form the anterior vagus nerve at 3 cm above the diaphragm. The right branch of the right thoracic vagus nerve joins the right branch of the left thoracic vagus to form the posterior vagus nerve. After application of HRP into the right or the left branch of the left thoracic vagus, HRP labelled cells were found in the left DMV. Similarly, after application of HRP into the left or the right branch of the right thoracic vagus, labelled cells were found in the right DMV. On the other hand, when HRP was injected into the anterior vagus, labelled neurons were found bilaterally in the DMV. This suggests that all rostral branches of the thoracic vagus have their origin in the ipsilateral DMV, and intermixing occurs only at the caudal level near the diaphragm. Findings of the present experiments suggest that parasympathetic preganglionic neurons innervating the GI tract are located exclusively in the DMV while those of the heart are located mainly in the NA. Within the DMV, GI vagal neurons were found medially from the level 0-2.5 mm rostral to the obex. In contrast, cardiac vagal neurons were found in the lateral edge of the DMV at the level 0-1 mm rostral to the obex.     

Signed value of monophasic action potential duration difference. A useful measure in evaluation of dispersion of repolarization in patients with ventricular arrhythmias

AIMS: To evaluate the usefulness of the signed value of monophasic action potential duration difference in analysing the cause of dispersion of ventricular repolarization. METHODS AND RESULTS: Monophasic action potentials were simultaneously recorded from the right ventricular apex and outflow tract during programmed stimulation in 36 patients with ventricular arrhythmias. The time difference between the ends of repolarization on the two monophasic action potentials was used as a measure of the dispersion of ventricular repolarization, and the signed value of the monophasic action potential duration difference was used to specify the contributions of the activation time difference and the monophasic action potential duration difference to the dispersion of ventricular repolarization. During right ventricular pacing, single and double programmed stimulation and at the induction of ventricular arrhythmias, the dispersion of ventricular repolarization and the signed value of monophasic action potential duration difference were markedly greater in the 11 patients with polymorphic ventricular tachycardia/ventricular fibrillation induced than in the 13 patients with monomorphic ventricular tachycardia induced, and in the 10 patients with clinical polymorphic ventricular tachycardia/ventricular fibrillation/cardiac arrest than in the 12 patients with sustained monomorphic ventricular tachycardia. This disclosed that the increased dispersion of ventricular repolarization was caused by increases in both the activation time difference and the monophasic action potential duration difference in the former, but mainly by an increased activation time difference in the latter groups. CONCLUSION: The signed value of monophasic action potential duration difference can specify whether an increased dispersion of ventricular repolarization is caused by inhomogeneous repolarization, inhomogeneous conduction or both, and thereby it is useful in study of the mechanism of ventricular arrhythmias.     

Brain blood flow alterations induced by therapeutic vagus nerve stimulation in partial epilepsy: I. Acute effects at high and low levels of stimulation

PURPOSE: Left cervical vagus nerve stimulation (VNS) decreases complex partial seizures (CPS) by unknown mechanisms of action. We hypothesized that therapeutic VNS alters synaptic activities at vagal afferent terminations and in sites that receive polysynaptic projections from these medullary nuclei. METHODS: Ten patients with partial epilepsy underwent positron emission tomographic (PET) measurements of cerebral blood flow (BF) three times before and three times during VNS. Parameters for VNS were at high levels for 5 patients and at low levels for 5. Resting BF measurements were subtracted from measurements during VNS in each subject. Subtraction data were averaged in each of 2 groups of 5 patients. t Tests were applied to BF changes in brain regions that receive vagal afferents and projections (significant at p < 0.05, corrected for repeated measures). RESULTS: In both the low- and high-stimulation groups during VNS, brain BF was (a) increased in the rostral, dorsal-central medulla; (b) increased in the right postcentral gyrus, (c) increased bilaterally in the hypothalami, thalami, and insular cortices, and in cerebellar hemispheres inferiorly; and (d) decreased bilaterally in hippocampus, amygdala, and posterior cingulate gyri. The high-stimulation group had greater volumes of activation and deactivation sites. CONCLUSIONS: Our findings suggest that left cervical VNS acutely increases synaptic activity in structures directly innervated by central vagal structures and areas that process left-sided somatosensory information, but VNS also acutely alters synaptic activity in multiple limbic system structures bilaterally. These findings may reflect sites of therapeutic actions of VNS.     

Differential effect of right and left vagal stimulation on right and left circumflex coronary arteries

In anasthetised, closed-chest dogs in complete heart block that were paced at a ventricular rate of 100 beats/min, vagal stimulation increased right coronary (RC) flow by 46% and conductance by 59%, but these increases were less than those measured in the left circumflex coronary (LCC) flow (66%) and conductance (80%). Both the right and left vagus nerves affected RC and LCC flow, the left vagus having the greater effect. The response to vagal stimulation is not limited at higher ventricular rates.     

Vagal, sympathetic and somatic sensory inputs to upper cervical (C1-C3) spinothalamic tract neurons in monkeys

1. Myocardial ischemia activates vagal and sympathetic cardiac afferent fibers. The purpose of this study was to determine a neuro physiological basis for cardiac pain referred to C1-C3 somatic dermatomes. We hypothesized that afferent fibers traveling in vagal or sympathetic nerves transmit nociceptive information to C1-C3 spinothalamic tract (STT) neurons. 2. Electrical stimulation of the left stellate ganglion to excite cardiopulmonary sympathetic afferent fibers increased extracellular activity of 44 of 77 C1-C3 STT neurons examined in 33 anesthetized male monkeys (Macaca fascicularis); responses increased as stimulus strength increased. Additionally, this stimulus inhibited 5 cells, increased/decreased activity of 2 cells, and did not affect 26 cells. 3. Electrical stimulation of the left (ipsilateral) thoracic vagus nerve excited 41 of 78 C1-C3 STT neurons, inhibited 4 neurons, increased/decreased activity of 2 neurons, and did not affect 31 neurons. Responses increased with increasing stimulus strength Contralateral vagal stimulation excited 7 of 39 cells tested, inhibited 4 cells and did not affect 28 cells. 4. Effects of stimulating one or more vagal branches were examined on 22 C1-C3 STT neurons excited by input from left thoracic vagus nerve. Stimulation of the cardiac branch excited 11 of 16 cells tested; stimulation of the recurrent laryngeal nerve excited 11 of 18 cells; stimulation of vagal fibers just rostral to the diaphragm excited 8 of 19 cells. 5. Excitatory somatic receptive fields ranged from small ipsilateral fields to large, sometimes bilateral or noncontinuous fields. Many fields included the ipsilateral neck and/or inferior jaw. Thirty-nine of 74 neurons examined were wide dynamic range (WDR), 21 were high threshold (HT), 6 were low threshold (LT), and 8 did not respond to brushing or noxious pinching of somatic tissues. Most (38 of 39) WDR cells responded to stimulation of the stellate ganglion or vagal fibers, as did 18 of 21 HT cells, 3 of 6 LT cells, and 2 of 8 cells unresponsive to brush or pinch stimuli. 6. Results of this study supported the concept that vagal and/ or sympathetic afferent activation of C1-C3 STT neurons might provide a neural mechanism for referred pain that originates in the heart or other visceral organs but is perceived in the neck and jaw region. Additionally, C1-C3 STT neurons processed sensory information from widespread regions of the body.     

Respiratory modulation of barareceptor and chemoreceptor reflexes affecting heart rate and cardiac vagal efferent nerve activity

1. Brief stimuli were delivered to the carotid chemoreceptors or baroreceptors in dogs anaesthetized with chloralose. Chemoreceptor stimulation was achieved by rapid retrograde injection of 0.2-0.5 ml. CO2 equilibrated saline through a cannula in the external carotid artery. Baroreceptor stimulation was achieved by forceful retrograde injection of 2-5 ml. air-equilibrated saline into the external carotid artery after first clamping the common carotid artery. 2. prompt decreases in heart rate were elicited by brief sudden chemoreceptor or baroreceptor stimuli when these were delivered during the expiratory phase of respiration. The stimuli did not modify the control heart rate pattern when delivered in the inspiratory phase of respiration. This respiratory modulation of reflex effectiveness persisted when the animals were completely paralysed and the phase of the respiratory cycle was monitored through a phrenic electroneurogram. 3. single cardiac vagal efferent nerve fibres were dissected from the cut central end of the right cervical vagus nerve. They were classified as cardiac efferents by their cardiac and respiratory rhythmicity, and by their increased activity in response to stimulation of a carotid sinus nerve or to mechanical elevation of the systemic arterial pressure. These efferent fibres increased their activity in response to brief chemoreceptor or baroreceptor stimuli delivered in expiration, but did not respond to stimuli delivered in inspiration. This respiratory modulation of both reflexes persisted after bilateral cervical vagotomy.     

Dietary treatment and growth of hyperchylomicronemic children severely restricted in dietary fat

BACKGROUND AND OBJECTIVES: A 9-year-old boy with a history of poorly controlled insulin-dependent diabetes mellitus was found at home unresponsive. QT prolongation was diagnosed on inspection of Holter monitoring performed immediately before episodes of ventricular fibrillation. METHODS: In spite of medical management with propranolol, esmolol, phenytoin, and diazepam, the patient continued to have episodes of QT prolongation followed by ventricular dysrhythmias that reverted to sinus rhythm only after cardiopulmonary resuscitation and cardioversion. RESULTS: A series of left stellate ganglion blocks with bupivacaine eradicated the dysrhythmias. The child was then referred to another institution for insertion of an automatic internal cardioverter defibrillator. CONCLUSIONS: This case report emphasizes the effectiveness of left stellate ganglion block with bupivacaine in a child with a variant of long QT syndrome.     

Posttraining electrical stimulation of vagal afferents with concomitant vagal efferent inactivation enhances memory storage processes in the rat

Peripherally administered or released substances that modulate memory storage, but do not freely enter the brain, may produce their effects on memory by activating peripheral receptors that send messages centrally through the vagus nerve. Indeed, vagus nerve stimulation enhances memory performance, although it is unclear whether this effect is due to the activation of vagal afferents or efferents. To eliminate the possible influence of descending fibers on memory storage processes, rats were implanted with cuff electrode/catheter systems along the left cervical vagus. Forty-eight hours following surgery, each animal received a 3. 0-microliter infusion (1.0 microliter/min) of either lidocaine hydrochloride (75.0 mM) or isotonic saline below the point of stimulation. Animals were then trained 10 min later on an inhibitory-avoidance task with a 0.75-mA, 1.0-s foot shock. Sham stimulation or vagus nerve stimulation (0.5-ms biphasic pulses; 20.0 Hz; 30 s; 0.2, 0.4, or 0.8 mA) was administered immediately after training. Memory, tested 24 h later, was enhanced by stimulation whether descending vagus nerve fibers were inactivated or not. Both lidocaine- and saline-infused groups showed an intensity-dependent, inverted-U-shaped pattern of retention performance, with the greatest effect observed for 0.4 mA (U = 9, p < .05, and U = 7, p < .01, respectively). Additionally, animals that received lidocaine infusions, but no vagus nerve stimulation, showed impaired memory compared to the performance of saline-infused control animals (U = 11, p < .05). Together, these findings suggest that vagal afferents carry messages about peripheral states that lead to the modulation of memory storage and that the memory-enhancing effect produced by vagus nerve stimulation is not mediated via the activation of vagal efferents.     

Coronary occlusion site as a determinant of the cardiac rhythm effects of atropine and vagotomy

We have previously demonstrated that atropine pretreatment increases the incidence of fatal ventricular arrhythmias induced by left anterior descending coronary artery (LAD) occlusion. The purpose of the present study was to determine whether the deleterious effect of atropine also applies to arrhythmias induced by right coronary artery (RCA) occlsusion. Occlusion of the RCA resulted in ventricular arrhythmias in all 20 animals studied, followed by ventricular fibrillation in three animals (15 per cent). Right coronary occlusion also resulted in bradycardia (-30.3 +/- 5.1 beats per minute) and hypotension (-23.1 +/- 4.9 mm. Hg). Pretreatment of 15 animals with atropine caused no significant increase in the incidence of ventricular fibrillation (i.e., 20 per cent). In addition, atropine pretreatment had no effect on the fall in heart rate and hypotension associated with RCA ligation. Sectioning the vagus nerves produced results similar to atropine pretreatment with the exception that a significant portion of the bradycardia was prevented. These results indicate that the increase in deaths after atropine observed in animals undergoing experimental LAD occlusion in not demonstrated with RCA occlusion. The results also indicate that the potential for deleterious effects of atropine in acute infarction might depend on the anatomic location of the involved myocardium.     

Effects of hypercapnea and of hypercapnea in combination with hypoxia on midbrain-induced cardiac dysrhythmias

Stimulation of the midbrain during acute combined arterial hypoxia and hypercapnea produces serious cardiac dysrhythmias which are not evoked when stimulation is elicited either with normal arterial blood gas tensions or with isolated mild hypercapnea. The cardiac dysrhythmias are mediated by both enhanced sympathetic and parasympathetic efferent discharge. The results support the concept that increased autonomic activity in combination with acute arterial hypoxia and hypercapnea contribute significantly to the exhibition of serious cardiac rhythm disturbances. Acute hypoxia appears to be the major determinant of such dysrhythmias.