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PubMed1999

ATP as a source of interstitial adenosine in the rat heart.

The contribution of neuronal ATP to interstitial adenosine levels was investigated in isolated perfused rat hearts. Ventricular surface transudates, representing interstitial fluid, were analyzed for norepinephrine, ATP, and adenosine. Exocytotic release of norepinephrine was induced by electrical stimulation of cardiac efferents emanating from the stellate ganglion. Ganglion stimulation increased contractility, interstitial norepinephrine, ATP, and adenosine. Interstitial adenosine was 11- to 27-fold higher than interstitial ATP, suggesting that the released ATP is unlikely the only source of adenosine. In the presence of AOPCP (alpha,beta-methyleneadenosine 5'-diphosphate), an ecto-5'-nucleotidase inhibitor, the ganglion-stimulated increase in interstitial ATP and adenosine reached levels similar to those in the absence of AOPCP, also suggesting that adenosine does not derive from extracellular ATP. The perfusate Ca2+ was raised from 1 to 4 mM to determine the importance of the enhanced contractile function on the levels of norepinephrine, ATP, and adenosine. The results were increases in contractility and interstitial norepinephrine, ATP, and adenosine, which were not suppressed with atenolol, indicating a norepinephrine-independent release of ATP and adenosine. Reserpine treatment and administration of guanethidine depleted the catecholamine stores and diminished the catecholamine release, respectively. However, neither agent altered Ca2+-induced increases in ATP and adenosine. It is concluded that the amount of neuronal-derived ATP is low and most likely does not contribute significantly to interstitial levels of adenosine. Furthermore, elevations in interstitial norepinephrine, ATP, and adenosine are associated with neuronal-independent increases in contractile function.

Adenosine↗
PubMed2005

Blunted functional responses to pre- and postjunctional sympathetic stimulation in hibernating myocardium.

Regional reductions in norepinephrine-tracer uptake are found in pigs with hibernating myocardium. Clinical studies would suggest that this is evidence for denervation; however, the functional responses to sympathetic stimulation have not been evaluated, and our previous studies with beta-adrenergic stimulation have not suggested denervation hypersensitivity. Therefore, pigs were chronically instrumented to produce hibernating myocardium characterized by chronic regional dysfunction and histological viability. Open-chest studies were performed to determine changes in regional function in response to both pre- and postjunctional stimulation. Regional segment shortening was reduced at rest in hibernating myocardium compared with controls (13 +/- 3% vs. 27 +/- 3%, P = 0.004). During stellate ganglion stimulation, regional function increased in both groups of animals (P = 0.008 vs. baseline), but the increase in hibernating myocardium was blunted compared with controls (Delta%, 3 +/- 2% vs. 8 +/- 3%, P = 0.04). Similar results occurred with intracoronary tyramine (10 mug/kg). Functional improvement during intravenous epinephrine infusion (0.35 mug.kg(-1).min(-1)) was also blunted in hibernating myocardium compared with controls (Delta%, 7 +/- 1% vs. 15 +/- 2%, P = 0.04). Even when the improvement in function was expressed relative to the reduced baseline, there was no evidence for catecholamine-mediated hypersensitivity in hibernating myocardium. We therefore conclude that functional responses to both pre- and postjunctional sympathetic stimulation are blunted in pigs with hibernating myocardium. In contrast to previous studies of infarcted, denervated, and acutely stunned myocardium, there is no catecholamine-induced hypersensitivity in hibernating myocardium. These data suggest a downregulation in functional responses to stimulation that would protect hibernating myocardium from demand-induced ischemia at the expense of contractile reserve during sympathetic stimulation.

Animals↗
PubMed2002

Epinephrine in the heart: uptake and release, but no facilitation of norepinephrine release.

BACKGROUND: Several studies have suggested that epinephrine augments the release of norepinephrine from sympathetic nerve terminals through stimulation of presynaptic receptors, but evidence pertaining to this mechanism in the heart is scarce and conflicting. Using the microdialysis technique in the porcine heart, we investigated whether epinephrine, taken up by and released from cardiac sympathetic nerves, can increase norepinephrine concentrations in myocardial interstitial fluid (NE(MIF)) under basal conditions and during sympathetic activation. METHODS AND RESULTS: During intracoronary epinephrine infusion of 10, 50, and 100 ng/kg per minute under basal conditions, large increments in interstitial (from 0.31+/-0.05 up to 140+/-30 nmol/L) and coronary venous (from 0.16+/-0.08 up to 228+/-39 nmol/L) epinephrine concentrations were found, but NE(MIF) did not change. Left stellate ganglion stimulation increased NE(MIF) from 3.4+/-0.5 to 8.2+/-1.5 nmol/L, but again, this increase was not enhanced by concomitant intracoronary epinephrine infusion. Intracoronary infusion of tyramine resulted in a negligible increase in epinephrine concentration in myocardial interstitial fluid (EPI(MIF)), whereas 30 minutes after infusion of epinephrine an increase of 9.5 nmol/L in EPI(MIF) was observed, indicating that epinephrine is taken up by and released from cardiac sympathetic neurons. Although 68% to 78% of infused epinephrine was extracted over the heart, the ratio of interstitial to arterial epinephrine concentrations was only approximately 20%, increasing to 29% with neuronal reuptake inhibition. CONCLUSIONS: Our findings demonstrate epinephrine release from cardiac sympathetic neurons, but they do not provide evidence that epinephrine augments cardiac sympathoneural norepinephrine release under basal conditions or during sympathetic activation.

Adrenergic Uptake Inhibitors↗
PubMed2000

Treating electrical storm : sympathetic blockade versus advanced cardiac life support-guided therapy.

BACKGROUND: Electrical storm (ES), defined as recurrent multiple ventricular fibrillation (VF) episodes, often occurs in patients with recent myocardial infarction. Because treating ES according to the Advanced Cardiac Life Support (ACLS) guidelines yields a poor outcome, we evaluated the efficacy of sympathetic blockade in treating ES patients and compared their outcome with that of patients treated according to the ACLS guidelines. METHODS AND RESULTS: Forty-nine patients (36 men, 13 women, mean age 57+/-10 years) who had ES associated with a recent myocardial infarction were separated into 2 groups. Patients in group 1 (n=27) received sympathetic blockade treatment: 6 left stellate ganglionic blockade, 7 esmolol, and 14 propranolol. Patients in group 2 (n=22) received antiarrhythmic medication as recommended by the ACLS guidelines. Patient characteristics were similar in the 2 groups. The 1-week mortality rate was higher in group 2: 18 (82%) of the 22 patients died, all of refractory VF; 6 (22%) of the 27 group 1 patients died, 3 of refractory VF (P<0.0001). Patients who survived the initial ES event did well over the 1-year follow-up period: Overall survival in group 1 was 67%, compared with 5% in group 2 (P<0.0001). CONCLUSIONS: Sympathetic blockade is superior to the antiarrhythmic therapy recommended by the ACLS guidelines in treating ES patients. Our study emphasizes the role of increased sympathetic activity in the genesis of ES. Sympathetic blockade-not class 1 antiarrhythmic drugs-should be the treatment of choice for ES.

Adrenergic beta-Antagonists↗
PubMed1976

The effect of adrenergic enhancement on overdrive excitation.

The effect of adrenergic enhancement (stimulation of a stellate ganglion or administration of norepinephrine) on arrhythmias induced by ventricular overdrive ("overdirve excitation") was studied in dogs with complete atrioventricular block. The following results were obtained. (1) Adrenergic enhancement may lead to abnormal ventricular rhythms. (2) A brief drive during adrenergic enhancement induced or enhanced fast ventricular rhythms. (3) The induced rhythms were characterized by an abrupt onset, a fast rate of discharge, and a moderate degree of slowing before an abrupt cessation. (4) The induced rhythms were accelerated by further drive. (5) Increasing the duration of overdrive during adrenergic enhancement resulted in overdrive suppression and not in overdrive excitation. (6) Prolonged drive could induce a few beats (instead of suppression) but at a rate below control ("inhibited excitation"). (7) The arrhythmogenic effects of overdrive and adrenergic enhancement were potentiated by the simultaneous administration of calcium. It is concluded that interventions which increase the inward calcium current (overdrive, adrenergic enhancement and higher [Ca]o) favor the onset and the maintenance of overdrive excitation.

Animals↗
PubMed1980

Ultrastructure of HRP-identified sympathetic preganglionic neurons in cats.

Electron microscopic studies were conducted on cat sympathetic preganglionic neurons which were labeled using retrograde transport of horseradish peroxidase from the injection site in the stellate ganglion to somas in the thoracic spinal cord. Based on size, the identified somas were divided into two groups: large multipolar somas (25-35 micron), usually having three dendrites with a mean diameter of 8 micron, and small fusiform somas (12-24 micron), with two primary dendrites with a mean diameter of about 4 micron. The ultrastructures of the perikarya and dendrites were similar to other spinal neurons. Three types of terminals were identified: 1) round asymmetric terminals, 2) pleomorphic symmetric terminals, and 3) round symmetric terminals. On the soma, pleomorphic terminals were more numerous than round asymmetric terminals. On the dendrites, the density of round asymmetric terminals was similar to pleomorphic symmetric terminals. Round symmetric terminals represent only a small percent on either the soma or dendrites. Because of the greater total density of terminals on the dendrites than soma, pleomorphic symmetric and round asymmetric terminals are primarily located on the dendrites. Very few dense-core vesicles characteristic of monomamine terminals were observed, perhaps due to the fixative used.

Animals↗
PubMed1986

Autonomic responses of the isolated, innervated trachea of the guinea-pig: interaction with autonomic drugs, histamine and 5-hydroxytryptamine.

Intraluminal pressure was measured in the isolated, fluid-filled trachea of the guinea pig, with autonomic innervation on the right side intact. Increases or decreases in intraluminal pressure reflected excitatory or inhibitory responses respectively, in the tracheal smooth muscle. Stimulation of the cervical vagus nerve evoked a cholinergic excitatory response. After cholinergic blockade with atropine, a non-adrenergic, non-cholinergic inhibitory response was obtained. Stimulation of the cervical sympathetic trunk, or stellate ganglion, evoked beta-adrenergic inhibitory responses. In the presence of propranolol, sympathetic stimulation evoked alpha-adrenergic excitatory responses which were of low amplitude (less than or equal to 5% of cholinergic excitatory responses). In the presence of phentolamine but not prazosin, beta-adrenergic inhibitory responses were potentiated. Neostigmine potentiated responses to vagal stimulation, increasing the amplitude and duration of response. At higher concentrations neostigmine (i) raised intraluminal pressure, a response blocked by atropine, and (ii) attenuated sympathetic inhibitory responses, an effect largely blocked by atropine. Histamine increased intraluminal pressure and this response was attenuated by atropine. In the presence of histamine, vagal excitatory responses were attenuated. Sympathetic inhibitory responses at low frequencies of stimulation (up to 10 Hz) were inhibited by histamine. 5-Hydroxytryptamine (5-HT) increased intraluminal pressure also, an effect partially blocked by atropine. 5-HT had no effect on vagal excitatory responses. Like histamine, 5-HT attenuated sympathetic inhibitory responses at lower frequencies of stimulation.

Adrenergic alpha-Agonists↗
PubMed1985

The effect of antiarrhythmic drugs on life-threatening arrhythmias induced by the interaction between acute myocardial ischemia and sympathetic hyperactivity.

Transient myocardial ischemia, with attendant sympathetic hyperactivity, seems to play a major role in sudden cardiac death among patients with ischemic heart disease. Ventricular tachycardia (VT) and fibrillation (VF) are consistently and repeatedly elicited in cats by the interaction between a 2-minute occlusion of the left descending coronary artery and a 30-second stimulation of the left stellate ganglion. When three consecutive trials yield almost identical results, time alone will not modify the response and a given drug can be injected to test its efficacy with an internal control analysis. In 90 cats the efficacy of the following drugs was assessed: lidocaine (n = 11), mexiletine (n = 12), propafenone (n = 12), propranolol (n = 19), prazosin (n = 10), amiodarone (n = 14), and verapamil (n = 12). Class I antiarrhythmic drugs completely failed to afford protection and worsening of arrhythmia was observed in several instances. Propranolol and prazosin showed efficacy in approximately 80% and 60% of the animals, respectively. Amiodarone and verapamil completely prevented the onset of VT and VF. Protection from arrhythmias seems to be related to the combined presence of a noncompetitive adrenergic blockade associated with salutary effects on coronary circulation. These findings correlate with and help to explain the results of clinical trials in postmyocardial infarction patients. This model may help to provide a rational choice of antiarrhythmic drugs to be tested in clinical trials.

Amiodarone↗
PubMed1992

Prevention of life-threatening arrhythmias by pharmacologic stimulation of the muscarinic receptors with oxotremorine.

The potential antiarrhythmic efficacy of pharmacologic parasympathetic activation is still controversial. This study assessed the antiarrhythmic effect of saline solution (n = 9) and of the muscarinic agonist oxotremorine (1.5 micrograms/kg administered intravenously) (n = 17) in a feline animal model in which malignant arrhythmias were reproducibly elicited by the combination of acute myocardial ischemia and left stellate ganglion stimulation. Although saline solution had no effect, oxotremorine significantly decreased heart rate, blood pressure, the incidence of ventricular fibrillation from 47% to 0% (p = 0.004), and the incidence of malignant arrhythmias (either ventricular tachycardia or ventricular fibrillation) from 88% to 12% (p less than 0.001). When reduction in heart rate was prevented by means of atrial pacing (n = 15), the incidence of malignant arrhythmias was still significantly reduced from 87% to 27% (p = 0.001). Arrhythmias were also graded as follows: 0 = no premature ventricular contractions; 1 = 1 to 10 premature ventricular contractions; 2 = 11 to 50 premature ventricular contractions; 3 = ventricular tachycardia; 4 = ventricular fibrillation. Arrhythmia severity was 3.29 +/- 0.16 (SEM) in the control trials and was reduced to 0.76 +/- 0.26 (p less than 0.001) by oxotremorine and to 1.53 +/- 0.34 by oxotremorine and pacing (p = 0.002). Therefore a muscarinic agonist can significantly reduce malignant arrhythmias during acute myocardial ischemia and may represent a novel approach to the prevention of sudden cardiac death.

Animals↗
PubMed1990

The epistellar body and what followed from its discovery.

The sequence of discoveries that has followed the investigation of this small yellow spot shows the value of studies begun out of "mere curiosity". The spot occurs on the stellate ganglion of octopods. It proved to be an enclosed sac, perhaps a gland. The search for it in squids and cuttlefishes led to the discovery of the giant nerve fibres. At first they were thought to be veins but we soon showed that they were nerve fibres concerned with jet propulsion. Their action potentials, membranes and synapses have been used for thousand of studies, including those that led to the Hodkin Huxley equations. They have been the basis of much of modern neuroscience. The epistellar body itself proved not to be a gland but a photoreceptor. Comparable photosensitive vesicles are especially large in the heads of deep-sea squids. In the mesopelagic ones they allow the squid to conceal itself by counterillumination, matching its own light output to the light coming from above. In bathypelagic squids the vesicles are enormous and probably keep the animals in the dark, where they breed. The function of the epistellar body, lying within the mantle of octopods is still unknown. It may act in the transparent larval stage to trigger the ejection of luminous plankton, which would be a hazard.

Animals↗
PubMed1975

Cytochemical localization of cholinesterase activity at the giant synapse of the squid.

The giant synapse of squid stellate ganglion is a chemical synapse where the transmitter substance is not known. The components of the ACh-system are present in squid nervous tissue in large quantities. However externally applied cholinergic drugs have no effect on junctional transmission. Using the Copper thiocholine method for electron microscopic cytochemistry the reaction product was found at the axolemmal surface, in the cisternae of the endoplasmic reticulum of neurons and occasionally between the infoldings of the sheat cells surounding the axons. Abundant deposits of end product are observed in the extracellular space in the proximity to junctional region. However, the localization of the cytochemical end product at the junctional region proper was observed frequently, but not consistently. Radiometric measurements of enzyme activity have revealed that neither specific inhibitors nor specific substrates generaly used for differentiation of cholinesterases in mammalian nervous tissue can be employed for differentiation of squid enzymes. Considering the permeability barriers imposed for external acetylcholine by cytoplasmic processes and the high enzyme activity of structures surrounding the giant synapse, the possibility that acetylcholine may still be a candidate for the missing transmitter is discussed.

Animals↗
PubMed2000

Inactivation of one copy of the mouse neurotrophin-3 gene induces cardiac sympathetic deficits.

Whether two copies of the neurotrophin-3 (NT3) gene are necessary for proper development of cardiac sympathetic innervation was investigated in mice carrying a targeted inactivation of the NT3 gene. Heterozygous (+/-) and null (-/-) mutant mice had fewer stellate ganglion neurons than did wild-type (+/+) mice at postnatal day 0 (P0 or birth), and this deficit was maintained between adult (P60) +/- and +/+ mice. The sympathetic innervation of the heart matured postnatally in +/+ and +/- mice. Tyrosine hydroxylase (TH)-positive axons were restricted largely to the epicardium at P0, were concentrated around large blood vessels in the myocardium at P21, and were present among cardiac myocytes at P60. Cardiac norepinephrine (NE) concentrations paralleled the growth of the sympathetic axons into the heart. NE concentrations were equivalent among +/+, +/-, and -/- mice at birth, but differences between +/- and +/+ mice increased with age. Adult +/- mice also exhibited lower resting heart rates and sympathetic tonus than +/+ mice. Thus deletion of one copy of the NT3 gene translates into anatomical, biochemical, and functional deficits in cardiac sympathetic innervation of postnatal mice, thereby indicating a gene-dosage effect for the NT3 gene.

Aging↗
PubMed1998

[Regional cerebral blood flow and oxygenation following cervicothoracic sympathetic block].

Stellate ganglion block (SGB) is considered to increase blood flow to the governing area, but recent studies have shown the decrease of common carotid arterial blood flow in the unblocked side following SGB. We investigated the influence of SGB on bilateral cerebral blood flow and oxygenation using a regional oxygen saturation (rSO2) monitor, TOS-96 (TOSTEC, Japan). The changes of blood volume (hemoglobin index: Hb I) and rSO2 were measured in twenty adult patients who underwent SGB at the transverse process of the C 6 vertebra. Prior to the investigation, two sensors were calibrated and placed on either side of each patient's forehead in order to see the difference. There were significant increases in rSO2 and Hb I in the blocked side and decreases in rSO2 and Hb I in the contralateral side. These results suggest that blood flow in the blocked side following SGB increases with decreased blood flow in the unblocked side. Patients with cerebral vascular disease undergoing SGB might be at risk of a decrease in cerebral blood flow in the unblocked area.

Adult↗
PubMed1984

Tracing of afferent and efferent pathways in the left inferior cardiac nerve of the cat using retrograde and transganglionic transport of horseradish peroxidase.

Retrograde and transganglionic transport of horseradish peroxidase (HRP) was used to trace afferent and efferent pathways in the left inferior cardiac nerve of the cat. Cardiac efferent and afferent neurons were located, respectively, in the stellate ganglion (average cell count per experiment:2679) and in the ipsilateral dorsal root ganglia (DRG) from C8 to T9 (average cell count per experiment:213). Labeled cardiac afferent projections to the spinal cord were most dense in segments T2-T6 where they were located in Lissauer's tract and in lamina 1 on the lateral border of the dorsal horn. Labeled afferent axons extended ventrally through lamina 1 into lamina 5 and the dorsolateral region of lamina 7 in proximity to the intermediolateral nucleus. A weak projection was noted on the medial side of the dorsal horn. These sites of termination are similar to projections by other sympathetic afferent pathways (i.e. renal, hypogastric and splanchnic nerves) to the lower thoracic and lumbar spinal cord, indicating that visceral afferents may have a uniform pattern of termination at various segmental levels. This pattern of termination in regions of the gray matter containing spinothalamic tract neurons and neurons involved in autonomic mechanisms is consistent with the known functions of sympathetic afferent pathways in nociception and in the initiation of autonomic reflexes.

Animals↗
PubMed1989

[Localization of heart-innervating sympathetic neurons].

Localization, amount, form of the bodies and maximal diameter of horseradish peroxidase (HP)-labelled neurons in the right stellate ganglion (SG) in the cat spinal cord have been investigated. HP application has been performed on the central parts of the SG connective branch with vagus nerve, or with the caudal cardiac nerve. In the neurons HP has been revealed after Straus or Mesulam method. In the SG, regardless the HP application place, the labelled neurons arrange in the zone, adjoining the place, where the caudal cardiac nerve and the connective branch get to the vagus nerve. In the spinal cord, when HP is applied on the connective branch, the labelled neurons are revealed in the lateral horns of the TI-TVI segments. The amount of the labelled neurons decreases in the rostro-caudal direction. Their greatest amount is revealed in the TI-TIII segments. When HP is applied on the central part of the caudal cardiac nerve, a small amount of the labelled neurons has been found in TI-TIII segments of the spinal cord only in one experiment. Thus, in the connective branch of the SG with the vagus nerve much more amount of the preganglionar fibers run than in the caudal cardiac nerve.

Animals↗
PubMed2002

The neurochemical characterisation of hypothalamic pathways projecting polysynaptically to brown adipose tissue in the rat.

The identification of leptin and a range of novel anorectic and orexigenic peptides has focussed attention on the neural circuitry involved in the genesis of food intake and the reflex control of thermogenesis. Here, the neurotropic virus pseudorabies has been utilised in conjunction with the immunocytochemical localisation of a variety of neuroactive peptides and receptors to better define the pathways in the rat hypothalamus directed polysynaptically to the major thermogenic endpoint, brown adipose tissue. Infected neurones were detected initially in the stellate ganglion, then in the spinal cord followed by the appearance of third-order premotor neurones in the brainstem and hypothalamus. Within the hypothalamus these were present in the paraventricular nucleus, lateral hypothalamus, perifornical region, and retrochiasmatic nucleus. At slightly longer survival times virus-infected neurones appeared in the arcuate nucleus and dorsomedial hypothalamus. Neurones in the retrochiasmatic nucleus and in the adjacent lateral arcuate nucleus which project to the brown adipose tissue express cocaine- and amphetamine-regulated transcript, pro-opiomelanocortin and leptin receptors. Neurones in the lateral hypothalamus, a site traditionally associated with the promotion of feeding, project to brown adipose tissue and large numbers of these contained melanin-concentrating hormone and orexin A and B. These data provide part of an anatomical framework which subserves the regulation of energy expenditure.

Adipose Tissue, Brown↗
PubMed1976

Mechanical stimuli exciting type A atrial vagal receptors in the cat.

The activity of type A right atrial vagal receptors was recorded from the right cervical vagus in cats anesthetized with sodium pentobarbital, immobilized with gallamine, and with their chests open. Nerve impulses initiated by receptor activation were recorded simultaneously with instantaneous right atrial pressure and dimensional changes under various hemodynamic conditions. Atrial volume changes induced by infusion of saline, bleeding, and occlusion of the inferior vena cava did not alter consistently the systolic activity of the receptors. Electrical stimulation of the right stellate ganglion significantly increased the frequency of discharge during systole, whereas electrical stimulation of the left thoracic vagus significantly reduced the frequency of discharge. These inotropic interventions produced similar effects when the heart was paced at a fixed rate. Pacing the right atrial appendage increased the systolic discharge of the receptors only when at high rates the atrium contracted against closed atrioventricular valves. To investigate the influence of tonic efferent sympathetic activity on spontaneous receptor discharge, three receptors were studied before and after bilateral surgical stellectomy, and in cats with their chest closed three receptors were studied before and after infusion of propranolol. Both of these interventions markedly reduced the systolic activity. In addition to having effects on systolic activity, injection of saline, vagal stimulation, and sympathetic "denervation" always activated the receptors during filling. Our results indicate that: (1) the systolic discharge of type A receptors is a function of the active tension developed by atrial muscle during contraction; and (2) the pattern of discharge of the receptors during the atrial cycle depends on both the degree of atrial distention and the state and extent of contraction.

Animals↗
PubMed2000

Colocalization of tenascin and sympathetic nerves in a canine model of nerve sprouting and sudden cardiac death.

INTRODUCTION: Sympathetic nerve sprouting after myocardial infarction (MI) may contribute significantly to the occurrence of ventricular arrhythmia and sudden cardiac death. Tenascin-X (TnX), a matrix protein known to be associated with nerve growth in central and peripheral nerves, also may play a role in cardiac nerve sprouting after MI. METHODS AND RESULTS: Immunocytochemical staining techniques were used to identify nerves in 5-microm serial sections from 6 normal dogs and 11 dogs with MI. Among the dogs with MI, 4 also received nerve growth factor infusion to the left stellate ganglion. The time between MI to tissue harvest averaged 35.7 +/- 14.4 days. Tyrosine hydroxylase (TH) stain was used to identify sympathetic nerves, and growth-associated protein-43 (GAP-43) was used to identify growing nerves. Polyclonal antibody was obtained for use in identifying TnX. Nerves were evident in both the infarcted and noninfarcted areas. Many nerves were found around blood vessels. A total of 181 nerves in 69 slides were examined: 89 were from noninfarcted myocardium, 4 from infarct, 13 from infarct border zone, and 75 from perivascular regions. Except in normal dogs, all nerves stained positive for TH also stained positive for GAP-43, indicating sympathetic nerve sprouting after MI. In all dogs, the nerves that stained positive for TH also stained positive for TnX. CONCLUSION: There is a colocalization of TnX, GAP-43, and TH in sprouted cardiac nerves. These results suggest that TnX is important not only in the existing normal myocardial nerve cells but also in cardiac sympathetic nerve sprouting after MI.

Animals↗