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Biomedical subjects

T N James

Publications and source records attributed to T N James.

At least 73 records · Page 4Linked to original sources
PubMed1986

Degenerative lesions of a coronary chemoreceptor and nearby neural elements in the hearts of victims of sudden death.

A coronary chemoreceptor and its neighboring nerves and ganglia were studied by serial section from the hearts of 11 victims of sudden unexpected death. Either focal or extensive inflammatory destruction was present in the chemoreceptors of 10 of the 11 hearts, and similar abnormalities of local nerves and ganglia were present in all 11 hearts. Because an identical coronary chemoreceptor in the dog has previously been shown to be the site of origin of a powerful reflex with major influence on the electrical activity of the heart, the functional significance of the neural abnormalities found in these 11 human hearts may include important distortion of cardiac rhythm, conduction or repolarization. Future studies are needed to determine the prevalence of such lesions in the hearts of other victims of sudden death and among control subjects, as well as to determine the etiology of this special neuropathology of the heart.

Adolescent↗
PubMed1986

Differential modulation of autonomic activity by ethmozin and ethacizin (analog of ethmozin) on the canine sinus node and atrioventricular junction.

The chronotropic and dromotropic actions of ethmozin and its diethylamine analog ethacizin were studied in the presence and absence of combined muscarinic, beta- and alpha-adrenoreceptor blockade in the intact canine heart in situ (n = 38). Injections of ethacizin, 5, 10 and 25 micrograms/ml, into the sinus node artery caused an immediate and significant (p less than 0.001) sinus bradycardia of 2, 6 and 11%, respectively. Injection of 25 and 50 micrograms/ml of ethacizin into the atrioventricular (AV) node artery significantly (p less than 0.001) prolonged AV conduction time with occasional second degree heart block. Conduction delay was located exclusively during the AH interval of the His bundle electrogram. Autonomic blockade did not alter the negative chronotropic or negative dromotropic effects of ethacizin. Ethacizin, 25 micrograms/ml, injected into the sinus node artery immediately reduced the sinus node response to vagal stimulations by 30% and the effect of acetylcholine, 0.1 micrograms/ml, injected into the sinus node artery by 50%. Ethacizin, 25 micrograms/ml, injected into the AV node artery immediately reduced the duration of complete AV block elicited by vagal stimulation or intranodal acetylcholine, 0.5 micrograms/ml, by 90%. Ethacizin caused a minor reduction in sinus node response to right stellate stimulations without, however, altering the sinus node response to intranodal norepinephrine. Ethmozin injections of up to 50 micrograms/ml into the sinus and AV node arteries had no chronotropic or dromotropic effects. Ethmozin had a minor and variable vagolytic action but significantly (p less than 0.05) reduced the sinus node response to sympathetic nerve stimulation. Hence, ethacizin, in contrast to ethmozin, has a direct depressing action on both the sinus node and the AV junction.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1986

Serial production of controlled periods of temporary heart block used to unmask and assess latent ventricular automaticity during experimental acute myocardial ischemia.

This study examined the onset, time course of development and response to overdrive stimulation of ventricular tachycardia in 10 dogs that underwent a Harris two-stage ligation of the left anterior descending coronary artery. Transient (12 +/- 3 minutes) complete atrioventricular (AV) block was produced 2, 3, 4, 5, 8, 12, 16, 20 and 24 hours after onset of infarction through selective injection of physostigmine salicylate into the AV node artery. Seven of the 10 dogs had early transient arrhythmic episodes that occurred within 20 to 40 minutes after coronary occlusion but none of the dogs had any spontaneous ventricular tachycardia in the ensuing 2 hours. Two hours after left anterior descending coronary artery ligation, complete AV block unmasked in every dog a slow (37 +/- 9 beats/min) AV junctional rhythm readily suppressed by overdrive. Three hours after coronary ligation, AV block revealed a monomorphic ventricular tachycardia (106 +/- 10 beats/min) in 3 of the 10 dogs. Four and five hours after coronary ligation, five and eight dogs, respectively, had ventricular tachycardia during AV block and in three the tachycardia was polymorphic. The two remaining dogs did not develop ventricular tachycardia during the 24 hours of observation. Ventricular tachycardia always began abruptly, first with brief and then longer bursts. Soon after onset the rate of tachycardia began to increase to reach a plateau 2 to 3 hours later at frequencies 21 +/- 9% greater than the initial tachycardia rate. Concomitant with this increase in rate there was a steady decline of overdrive suppressibility and during the plateau phase there was little or no overdrive suppression.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Degenerative lesions of a coronary chemoreceptor and nearby neural elements in the hearts of victims of sudden death.

A coronary chemoreceptor and its neighboring nerves and ganglia were studied by serial sections of tissue taken from the hearts of sixteen victims of sudden unexpected death. Either focal or extensive inflammatory destruction was present in the chemoreceptors of 13 of the 16 hearts, and similar abnormalities of local nerves and ganglia were present in all 16 hearts. Since an identical coronary chemoreceptor in the dog has previously been shown to be the site of origin of a powerful reflex with major influence upon the electrical activity heart, the functional significance of the neural abnormalities found in these 16 human hearts may include important distortion of cardiac rhythm, conduction or repolarization. Future studies are needed to determine the prevalence of such lesions in the hearts of other victims of sudden death and among control subjects, as well as to determine the etiology of this special neuropathology of the heart.

Adolescent↗
PubMed1985

Crib death.

Explore the source record for details and available documents.

Atrioventricular Node↗
PubMed1985

Anatomy of the crista supraventricularis: its importance for understanding right ventricular function, right ventricular infarction and related conditions.

During careful studies of the human cardiac conduction system the anatomy of the crista supraventricularis is an inescapable concomitant demonstration. For the purpose of this report the observations from about 1,000 human hearts were combined with special additional studies of 75 human hearts (50 adults, 25 infants), 30 dogs and 5 chickens. The crista supraventricularis is similar in human and canine hearts. Avian hearts differ from mammal hearts in that they contain only a muscular right atrioventricular valve which replaces the crista supraventricularis. In addition to dividing the inflow and outflow pathways of the right ventricle, the crista supraventricularis is crucially located to join the interventricular septum and left ventricle to much of the right ventricular free wall, thereby playing an important role in emptying the right ventricle and closing the tricuspid valve. On the basis of these observations, the function of the crista supraventricularis is examined relative to right ventricular systole, right ventricular infarction, various electrophysiologic problems, the performance of cardiac surgery and new questions in cardiac imaging.

Adult↗
PubMed1985

Function of the atrioventricular node considered on the basis of observed histology and fine structure.

From the hearts of 20 young dogs, the region of the atrioventricular (AV) node was studied in vitro utilizing direct perfusion of the AV node artery. Intracellular impalement with microelectrodes provided records of local transmembrane action potentials in all 20 dogs. These were correlated with serial section histologic studies in 7 of the 20 dogs to characterize a smaller region that served as an anatomic guide for electron microscopic examination in 4 other dog hearts. This report describes the variety of specific cells found, including their intracellular content and organization, as well as the nature of their intercellular junctions. On the basis of these findings, AV nodal cells were arbitrarily divided into two types, transitional cells and P cells, although three somewhat different groups of transitional cells were identified. The first group, found principally at the outer margin of the AV node, has long and slender cells that exhibit large profiles of gap junctions or nexuses. The second and third groups of transitional cells, which constitute most of the body of the AV node, are oblong or oval and contain fewer and smaller gap junctions. P cells of the AV node resemble those more abundantly present in the sinus node; they are found principally at the junction of the AV node and His bundle. On the basis of these fine structural features and the histologic organization and transmembrane action potentials observed, clinical and experimental aspects of the local electrophysiologic events are discussed.

Action Potentials↗
PubMed1985

Normal variations and pathologic changes in structure of the cardiac conduction system and their functional significance.

The rarity with which the cardiac conduction system is carefully examined in cases of sudden unexpected cardiac death is deplorable. Whatever the reasons for this failure, it is clearly one of the major lost opportunities for improving our understanding of a major national heart problem. To illustrate some of the morphologic changes found in such cases, two categories are discussed: normal variations (which may themselves promote electrical instability) and changes due to disease. During normal postnatal morphogenesis of the atrioventricular (AV) node and His bundle, there are a variety of derangements that may cause malfunction of those critical structures. In addition to large vessel coronary disease and platelet disorders, narrowing of small coronary arteries may also lead to ischemic damage in the conduction system. Certain intracardiac tumors and systemic diseases of an infiltrative or inflammatory nature may also involve elements of the conduction system, leading to arrhythmias or conduction disturbances with their clinical counterparts of syncope and sudden death. How any of these and many related anatomic changes may participate in the pathogenesis of electrical instability of the heart deserves much more careful study, but an essential requirement will be the wider practice of making careful clinicopathologic correlations.

Adult↗
PubMed1985

Negative chronotropic and parasympatholytic effects of alinidine on canine sinus node and AV junction.

The direct effects of alinidine (N-allyl-clonidine) on the sinus node and atrioventricular (AV) junction were studied in 18 anesthetized dogs. Stimulus frequency-response curves to right stellate ganglion and right cervical vagus stimulations as well as responses to norepinephrine or acetylcholine were determined before and after selective perfusion of alinidine into the sinus node artery. Alinidine (1 microgram/ml) had no effect on spontaneous sinus rate [148 +/- 5 (SE) beats/min]. However, alinidine concentrations of 5, 10, and 25 micrograms/ml produced significant (P less than 0.05) sinus slowing to 138, 127, and 121 beats/min, respectively. Recovery to control rate was dose dependent and took from 4 to 33 min. Sinus rate increases with right stellate stimulations were not affected by alinidine. However, sinus rate decreases with right vagal stimulations were significantly (P less than 0.01) attenuated by alinidine. The negative chronotropic effects of acetylcholine were not influenced by alinidine. Alinidine (1-100 micrograms/ml into AV node artery) had no effect on the A-H interval of the His bundle electrogram. However, alinidine (10 and 25 micrograms/ml) diminished the AV block produced by stimulation of the left vagus in electrically paced hearts but not the negative dromotropic actions of directly administered acetylcholine. Thus alinidine has direct negative chronotropic effects, no effect on sinus node responses to sympathetic stimulation, ability to diminish sinus node and AV junctional responses to vagal stimulations without interference at the cholinergic muscarinic receptor, and 4) no effect on AV nodal conduction.

Acetylcholine↗
PubMed1985

Multifocal Purkinje-like tumor of the heart. Occurrence with other anatomic abnormalities in the atrioventricular junction of an infant with junctional tachycardia, Lown-Ganong-Levine syndrome, and sudden death.

A 13-month-old boy with intermittent preexcitation (Lown-Ganong-Levine type) and paroxysmal tachycardias of 280 to 300 beats per minute died suddenly with cardiac arrest. At necropsy the only abnormalities were in the heart. There were multifocal Purkinje cell tumors in the conduction system, including one directly at the bifurcation of the His bundle. In addition, a fault in the central fibrous body was filled with an accessory communication between the mid-portion of the atrioventricular node and both the interventricular septum and the His bundle. This accessory communication connected with the Purkinje cell tumor. Although an atrioventricular nodal bypass was thus present and could account for the preexcitation and for reentrant tachycardias, there is also the anatomic basis for an automatic arrhythmia originating within one or more of the Purkinje cell tumors, particularly the one directly within the His bundle. Dispersion of elements of the conduction system within the central fibrous body resembled the normal fetal pattern. Whether this persistence of fetal dispersion of the atrioventricular node and His bundle within the central fibrous body is causally related to the presence of multifocal Purkinje cell tumors or is only coincidence merits further consideration.

Arrhythmias, Cardiac↗
PubMed1985

Testicular lesions in Whipple's disease.

In two patients with Whipple's disease a variety of abnormalities were found in the testis. In both there was a thickened tunica albuginea containing macrophages filled with Schiff-positive bacilli, and both exhibited Whipple bacilli alone or in small clumps within the tunica media of the testicular arteries. One patient had focal inflammatory lesions among the Leydig cells. The most prominent abnormality in each was the abundance of Whipple bacilli within the epithelium of the seminiferous tubules. Some of these bacilli (which were free rather than within macrophages) appeared to be being shed into the tubular lumen; there was no associated inflammation. In some areas macrophages filled with bacilli appeared to migrate from the arterial adventitia toward the seminiferous tubules. Potential significance of these findings is discussed relative to a variety of testicular and prostatic diseases, as well as the possible (and arguable) relationship to the acquired immune deficiency syndrome.

Arteries↗
PubMed1984

No electrical instability after intracoronary streptokinase administered into sinus node or AV node of dogs.

Intracoronary streptokinase (SK) is being used to treat acute myocardial infarction. Complications including atrioventricular (AV) block and both supraventricular and ventricular arrhythmias have been described. Selective cannulation of the nutrient arteries of the sinus node and AV node in the pentobarbital-anesthetized dog provides a model to study the specific pharmacologic effects of drugs administered directly to these structures. Selective perfusion of 2 ml normal saline into the sinus node artery of five dogs resulted in a transient 38.6% decrease in heart rate (148 +/- 9.6 to 91 +/- 12.7 bpm). This control response is typical of the method. Administration of 100, 500, 1000, 2000, and 4000 IU of SK/ml in these same dogs resulted in similarly brief bradycardias of 41.2%, 40.2%, 39.4%, 41.2%, and 40.3% (p = NS) below the control rate, respectively. The tachycardia induced by 0.0125 and 0.025 micrograms/ml of norepinephrine (24.2% and 31.4% sinus acceleration) was unaffected by the simultaneous administration of 500, 1000, and 2000 IU SK/ml. AV conduction was unchanged by selective perfusion of 1000, 2000, and 4000 IU SK/ml into the AV node artery of seven dogs, respective AV intervals being 111, 114, and 116 msec, with the control interval being 109 msec. Thus after selective perfusion of either the sinus node or AV node with SK in clinically used concentrations, we found no significant chronotropic or dromotropic effect in the dog.

Animals↗
PubMed1984

Parasympathetic and sympathetic efferent traffic during a cardiogenic hypertensive chemoreflex.

Activation of a cardiac chemoreceptor with serotonin elicits a reflex which includes changes in heart rate, contractile force, regional blood flow and hypertension. In six anaesthetised dogs we simultaneously recorded parasympathetic and sympathetic efferent traffic elicited during this cardiogenic reflex. The parasympathetic fibres were confirmed by reciprocal frequency changes with changes in blood pressure. The sympathetic fibre activity (anterior ansa subclavia) was attenuated or eliminated by ganglionic blockade or by clonidine. Whereas the phasic sympathetic multifibre discharge was only followed by a quiet period, the parasympathetic multifibre discharge was both preceded and followed by a quiet period. The sympathetic discharge preceded the parasympathetic discharge by 683 +/- 170 ms. These autonomic efferent discharges were not elicited by administration of serotonin into the carotid artery, but were abolished by pretreatment with the serotonin antagonist, cyproheptadine. Cyproheptadine blockade could be overcome by increasing the serotonin concentration tenfold. This remarkable neural asynchrony has important implications concerning the electrical stability of the heart.

Animals↗
PubMed1984

Vascular lesions of the gastrointestinal system in Whipple's disease.

In five cases of Whipple's disease the vessels in several organs of the gastrointestinal system were carefully examined for PAS-positive bacilli. Bacilli were particularly abundant in the arteries of the small intestinal serosa and the liver, but they were also present in stomach, colon, gallbladder and mesenteric lymph nodes. The predominant site of involvement was the arterial tunica media. In addition to focal degeneration and fibrosis in the tunica media, other local reactions included arteritis and intimal proliferation. Within the tunica media and less often the endothelium the bacilli were found alone or in small clumps, but in the tunica adventitia they were usually present within macrophages. The possible significance of this Whipple's arteriopathy is considered relative to unexplained gastrointestinal bleeding, focal ischemia due to arterial narrowing, and some role in the further dissemination of bacilli being shed from the endothelium.

Adult↗
PubMed1984

Whipple bacilli within the tunica media of pulmonary arteries.

In the lungs of two patients dying with Whipple's disease, we found Schiff-positive bacilli within the tunica media of many pulmonary arteries. Tissue was examined from all five lobes of the lungs in both cases. There were no pulmonary emboli and no alveolar lesions of Whipple's disease. Focal degeneration of the tunica media was conspicuous in areas where bacilli were present, and at some sites there was some overlying intimal proliferation. Little inflammatory response was present. All the bacilli within the tunica media were free as single organisms or small clumps, and there were none within macrophages. Macrophages containing bacilli were occasionally found within the adventitia of the pulmonary arteries. The possible role of these lesions in the pathogenesis of chronic pulmonary arterial disease merits consideration.

Humans↗