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Biomedical subjects

T N James

Publications and source records attributed to T N James.

At least 127 records · Page 7Linked to original sources
PubMed1980

Analysis of sympathetic discharges during cardiogenic hypertensive chemoreflex.

Serotonin activates a cardiogenic hypertensive chemoreflex. During this reflex, sympathetic efferent neural discharges were examined in 10 anesthetized dogs. Thoracic nerves were identified, severed distally, and placed across electrodes. The efferent neurogram was recorded along with an electrocardiogram and blood pressure and stored on tape. Neurograms were later analyzed by a Lab 8/e computer with a Schmitt trigger. The resting tone and the elicited discharges of the multifiber preparations were plotted as poststimulus histograms. The integrals of the histograms were normalized. During the reflex, sympathetic efferent discharges averaged 4.9 (+/- 0.8) s in duration and the total discharge frequency was 199 (+/- 16)% of control tone. The evoked peak blood pressure response averaged 221/171 mmHg. Following autonomic blockade, the attenuated blood pressure response averaged 125/96 mmHg. The sympathetic efferent discharges then lasted 5.2 (+/- 0.7) s (NS). However, total discharge frequency (268 +/- 37% of control tone) was significantly greater (P less than 0.01) that before autonomic blockade. These data suggest that baroreceptors influence the rate of discharge and the total amount of neural traffic, but not the duration of the sympathetic response evoked by the cardiogenic hypertensive chemoreflex.

Animals↗
PubMed1980

Quantitative difference in "critical" stenosis between right and left coronary artery in man.

Coronary artery stenoses that limit blood flow below demand are considered critical. In this comparative study we investigated whether the same degree of stenosis in either the proximal third of the right coronary artery (RCA) or the proximal third of the left anterior descending artery (LAD) causes critical flow reduction. Lesions were quantified from 35-mm cinefilms in multiple projections using a vernier caliper. These morphometric measurements were correlated with various manifestations of critical flow reduction, such as angina pectoris, development of collateral vessels and segmental wall motion abnormalities. In 13 patients with anginal pain and isolated RCA stenosis, the mean degree of obstruction was 63% area stenosis, which was significantly lower (p < 0.05) than that measured in 17 symptomatic patients who had isolated obstructions of the LAD (77% area stenosis). In patients with an identical degree of obstruction (78%) in either the LAD or RCA, collateral vessels were angiographically demonstrable in 53% of the RCA stenoses but in only 29% of the LAD stenoses. Furthermore, when the stenoses were less than 63% in the RCA and LAD, regional wall motion abnormalities were more frequently (p < 0.05) associated with RCA than with LAD stenoses. These observations indicate that a significantly smaller percent area of stenosis is critical in the RCA than in the LAD.

Arterial Occlusive Diseases↗
PubMed1980

Paroxysmal ventricular arrhythmias and familial sudden death associated with neural lesions in the heart.

A high school athlete with history of syncopal attacks died suddenly. Paroxysmal ventricular arrhythmias had been documented many times, as had at least one episode of ventricular fibrillation. A brother with similar history also had died suddenly and unexpectedly at about the same age. Except for the syncope and arrhythmias, they were both considered to be in good health. At postmortem examination, no significant extracardiac abnormalities were found, and the heart was normal on gross examination. The cardiac conduction system was the subject of special study. Focal inflammatory degeneration of small nerves and ganglia was found in various sites within the heart, including atrioventricular node, but were especially prominent in and around the sinus node. There was epicardial edema and thickening of the pericardium in that vicinity, but all of the pericardium elsewhere was normal. Some persistent fetal dispersion of the atrioventricular node was present. Ways are discussed in which these neural lesions may have contributed to the pathogenesis of paroxysmal arrhythmias and eventually sudden death. The possible etiology of the neural disease and the basis for its familial occurrence are considered.

Adolescent↗
PubMed1980

Selective effects of clonidine on the canine sinus node.

The direct and indirect chronotropic effects of clonidine (0.001--10 micrograms/ml) were studied by selective perfusion of the sinus node artery of 20 pentobarbital anesthetized dogs. Concentrations of 0.1, 1.0 and 10 migrograms/ml produced dose-related reductions in sinus rate of 3.7 +/- 0.9 (P less than .005), 6.9 +/- 1.8 (P less than .005) and 15.8 +/- 2.3 (P less than .0001) beats/min, respectivel. Sinus acceleration after right stellate ganglion stimulation at 16 and 32 Hz was significantly (P less than .05) inhibited by intranodal clonidine (0.1 microgram/ml). The positive chronotropic effect of norepinephrine (0.1 microgram/ml, sinus node artery) was not significantly affected by prior administration of clonidine. Atropine (1 mg/kg i.v. or 10 micrograms/ml, selectively perfused into the sinus node artery) had no effect on the sinus slowing produced by clonidine. Clonidine had an inconsistent effect on the response to vagal stimulation. Clonidine had an inconsistent effect on the response to vagal stimulation. Clonidine inhibits the heart rate increase after sympathetic nerve stimulation without affecting the heart rate response to norepinephrine infusion. The findings are consistent with previous observations that clonidine can inhibit norephinephrine release and demonstrate that this mechanism of action may occur within the sinus node.

Animals↗
PubMed1980

Persistent fetal dispersion of the atrioventricular node. Association with the Wolff-Parkinson-White syndrome.

Symptomatic supraventricular tachycardias developed in a 58-year-old man not long before he also was found to have metastatic cancer. During electrophysiological studies, type A Wolff-Parkinson-White syndrome was defined and at least four different forms of supraventricular tachycardias were documented. When he died of his cancer, autopsy studies included special examination of his heart and its conduction system. There was a slender connection between the left atrium and left ventricle posterior to the margo obtusus, composed of ordinary working myocardial cells. There was also persistent fetal dispersion of the atrioventricular (AV) node within the central fibrous body, forming a suitable anatomical substrate for reentrant tachycardias originating entirely there. The anatomical and electrophysiological findings are discussed relative to the question of surgery in such patients, since cutting the lateral AV connections might eliminate the delta wave but not the supraventricular tachycardias.

Atrioventricular Node↗
PubMed1979

Experimental studies on the pathogenesis of asystole after verapamil in the dog.

The effect of verapamil on automaticity and conduction in the atrioventricular (A-V) junctional region was studied in anesthetized dogs. In five normal dogs verapamil, 10 microgram/ml, was selectively perfused into the A-V nodal artery and caused first degree heart block, which progressed to second degree heart block in three of the five. Higher concentrations of verapamil, 25 microgram/ml, caused complete heart block in three of five other dogs, but no episodes of asystole (defined as a ventricular pause of 10 or more seconds). In six other dogs after beta receptor blockade with propranolol, 20 microgram/ml, perfused into the A-V nodal artery, verapamil, 10 microgram/ml, regularly caused second degree heart block; in four of the six dogs there was a transient episode of third degree A-V block, and in two of these there was a period of asystole. In each of the 10 dogs pretreated with reserpine, verapamil, 10 microgram/ml, caused third degree A-V block; in seven of these there was a period of asystole with ventricular standstill up to 30 seconds. Concentrations of verapamil that do not produce high grade heart block in the normal heart thus readily cause both high grade block and prolonged ventricular standstill after elimination of adrenergic influences in the A-V junction.

Adrenergic beta-Antagonists↗
PubMed1979

Fine structure of cells and their histologic organization within internodal pathways of the heart: clinical and electrocardiographic implications.

The fine structure of the normal internodal pathways was studied in 1 human and 2 canine hearts and correlated with histologic observations on more than 100 human and 10 canine hearts. From the electron microscopic studies six different kinds of myocardial cells were classified from two locations: the Eustachian ridge (posterior internodal pathway) and the Bachmann bundle (anterior internodal pathway). Five of the six kinds of cells (working myocardial cells, Purkinje-like cells, either broad or slender transitional cells and P cells, all previously described) were present in both locations. A sixth cell, pleomorphic and dark in appearance, with a special intertwined relation to P cells, is newly designated as an ameboid cell. It was found solely in the Eustachian ridge. In the same area a rare direct contact between a nerve and a myocardial cell was observed. The importance of these different kinds of cells, their respective cell connections, and their topographic locations inside the internodal pathways are discussed relative to certain functions such as rapid conduction and subsidiary pacemaking. The possible influence of these factors on clinical electrocardiographic changes is considered.

Animals↗
PubMed1979

Dysautonomia in mitral valve prolapse.

Many of the clinical features of patients with mitral valve prolapse can logically be attributed to abnormal autonomic neural function. Accordingly, we have studied heart rate and blood pressure response to a standardized Valsalva maneuver and postural test in 44 untreated patients with demonstrated mitral valve prolapse. Fifteen healthy subjects of similar age served as controls. The directional changes of blood pressure and heart rate were similar in control subjects and patients in both tests, but patients differed from control subjects by their widely oscillating heart rate during the upright posture, and their exaggerated and prolonged bradycardia during the recovery phase of the Valsalva maneuver and following their return to recumbency in the postural test. This bradycardia persisted for 30 to 90 seconds after blood pressure returned to control values. Patients also showed a greater respiratory variation of R-R interval, which became especially marked during the adjustment to changes of posture. We postulate an abnormal central modulation of baroreflexes as the best explanation for the dysautonomic responses of symptomatic patients with prolapsed mitral valves.

Adolescent↗
PubMed1979

Correlative electrophysiological and anatomical studies concerning the site of origin of escape rhythm during complete atrioventricular block in the dog.

Complete heart block was produced in eight dogs by the selective perfusion of physostigmine or neostigm into the atrioventricular (AV) node artery. A characteristic escape AV junctional rhythm emerged in each dog. After reversal of the cholinesterase paralysis with atropine, in each dog partial heart block was produced by an incision into the AV nodal region. In three of these eight dogs, a second incision placed slightly more anteriorly produced complete AV block which was followed by the emergence of an escape AV junctional rhythm similar to the one produced pharmacologically. Hearts of these three dogs were examined histologically with serial sections to determine the exact location of the incisions and their relationship to the AV node and His bundle. In each dog the incision that produced complete heart block passed directly through the junction of AV node with His bundle. In this region previous studies had demonstrated numerous P cells, which are thought to be the site of origin of normal cardiac automaticity. In each of the three hearts there were abundant P cells in continuity with the His bundle distal to the cut producing heart block. Significance of these findings is discussed relative to the locus of action of acetylcholine within the AV junction, the site of origin of AV junctional rhythm, and sme aspects of the experimental and therapeutic production of heart block.

Animals↗