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Biomedical subjects

T N James

Publications and source records attributed to T N James.

At least 91 records · Page 5Linked to original sources
PubMed1983

Studies of changes in breathing and blood pressure accompanying a cardiogenic hypertensive chemoreflex compared in conscious and anesthetized dogs.

Serotonin activates a cardiogenic hypertensive chemoreflex characterized by sudden hypertension. This study in 16 awake and 12 anesthetized dogs was conducted to examine the influence of changes in breathing or heart rate as they may influence the reflex hypertension. In all 28 dogs, either anesthetized or awake, there is a variable but brief initial reflex bradycardia and in all dogs there is transient ventilatory stimulation, but the response in every dog was characterized by hypertension within at most 10 seconds after administering serotonin. Treatment with atropine regularly eliminated the reflex bradycardia and caused the hypertension to appear soon (average of 6 seconds to maximal level). Atropine did not alter the reflex stimulation of breathing. Since atropine eliminated any transient bradycardia (and associated hypertension) but did not prevent reflex changes in breathing, we do not believe that breathing alteration plays any significant hemodynamic role in this reflex.

Afferent Pathways↗
PubMed1983

Influence of atrial mechanoreceptors upon the sympathetic efferent activity elicited during a cardiogenic chemoreflex in the dog.

Two different cardiogenic reflexes were studied for their effects upon the activity recorded from the thoracic cardiac nerves of 7 chloralose-anesthetized dogs. Sympathetic efferent activity in 5 right and 7 left anterior ansa multifiber preparations was quantitatively analyzed. A cardiogenic hypertensive chemoreflex was induced by administration of serotonin (100 micrograms/ml, 2 ml) into the left atrium before, during and after inflation of balloons in the right and/or left atrial appendages. Balloon inflations alone resulted in heart rate increases of 5-20 bpm but arterial blood pressure, pulse pressure and end diastolic pressure were not significantly affected. Control serotonin-induced efferent discharges were 174 +/- 10% (mean +/- S.E.M.) of resting activity with a duration of 5.2 +/- 0.4 s. During inflation of both atrial balloons, the serotonin-induced efferent discharges were 165 +/- 14% (N.S.) of resting activity with a duration of 7.8 +/- 0.7 s (P less than 0.01). Following release of the balloons, the serotonin-induced discharges were 152 +/- 17% (N.S.) of resting activity with a duration of 4.9 +/- 0.4 s (N.S.). These results suggest that afferent signals from atrial mechanoreceptors can act to increase the duration but not the total intensity of the efferent sympathetic discharges elicited during a cardiogenic chemoreflex.

Animals↗
PubMed1983

Chance and sudden death.

An aura of mystery has always surrounded the subject of sudden unexpected death. Part of the explanation is an absence of a single or unusual explanation, although electrical instability of the heart does serve as a unifying concept for the final common pathway. In this review, emphasis is placed on the random aggregation of a wide variety of contributing factors in the pathogenesis of sudden death. Such factors include coronary disease, platelet aggregation, neural control of the heart, apoplexy of the heart, normal and abnormal variations in the structure of the atrioventricular junction, lessons from certain rare cardiac tumors and the nature of ventricular fibrillation. Useful thinking about these and related causes should employ both a horizontal (concurrence of events) and vertical (sequence of events) matrix, in all of which chance plays a major role. One impediment to understanding sudden death associated with coronary disease is the prevalent assumption that one is due to the other without proper examination of the other factors involved, some of which may be more susceptible to intervention or modification. The multifactorial nature of the pathogenesis of sudden death and the recognition that chance is a major determinant of which factors convene and when they will aggregate in the victim are essential elements to consider if more effective means of treatment and prevention are to be obtained.

Animals↗
PubMed1983

Primary and secondary cardioneuropathies and their functional significance.

For most functions of the heart its nerves are as important as its coronary arteries, but this is particularly true concerning cardiac rhythm, conduction and repolarization. It is thus paradoxical that postmortem correlative studies of sudden death virtually always include careful scrutiny of the coronary arteries but only rarely of the cardiac nerves or ganglia. In this review, abnormalities of the cardiac nerves and ganglia, collectively termed cardioneuropathies, are examined from the dual standpoint of their structural appearance and functional significance. Some cardioneuropathies are found in the absence of any other significant structural abnormality detectable in the heart and these are designated as primary cardioneuropathies. A viral etiology or some heritable disorder must rank high among possible causes. Secondary cardioneuropathies are those observed in association with almost every disease that can affect the heart; examples include myocardial infarction, infections, amyloidosis and cancer, but there are many others. Because abnormalities of the heart's nerves and ganglia not only have their own unstabilizing influence on cardiac electrical activity but can also profoundly alter a patient's responses to pharmacologic treatment, it is hoped that future clinicopathologic examinations will more often include their careful study and thereby add to our meager knowledge about these important structures.

Cardiomyopathies↗
PubMed1983

Thrombi in antrum atrii dextri of human heart as clinically important source for chronic microembolisation to lungs.

In many cases of chronic microembolic pulmonary hypertension the source of the emboli is unknown. Disease or injury to the sinus node is usually accompanied by thrombus formation within the antrum atrii dextri, and this region is not often inspected carefully during necropsy. In the present study the hearts of 14 patients with right ventricular hypertrophy or documented pulmonary hypertension showed disease or injury in the sinus node, and each had both old and recent thrombosis in the antrum atrii dextri. In all 14 cases both lungs were available for histological examination. The group included six cases of rheumatic heart disease with mitral stenosis, four cases of disseminated lupus erythematosus, and four cases of so-called primary pulmonary hypertension. Every lung contained both new and old microemboli, as well as a wide variety of other histological abnormalities narrowing the small pulmonary arteries. Many of these narrowing lesions were recognisable as the consequence of prior microembolisation. For future postmortem examination of cases of chronic microembolic pulmonary hypertension, mural thrombi within the antrum atrii dextri should be considered as one important potential source for recurring microembolisation to the lungs.

Adult↗
PubMed1983

Effects of gamma-aminobutyric acid on neural regulation of the canine sinus node.

The direct effects of gamma-aminobutyric acid (GABA) on the sinus node and its neural regulation were studied by selective perfusion of the sinus node artery (SNA) in 26 open-chest pentobarbital-anesthetized dogs. GABA (1-1,000 micrograms/ml, 2 ml, SNA) produced no direct effect on intrinsic sinus rate, but in several experiments (at 1 microgram/ml) it produced an inconsistent augmentation of the sinus tachycardia due to right stellate stimulation. At all other concentrations tested (10-1,000 micrograms/ml), GABA did not significantly alter the sinus node response to stellate stimulation. Local alpha-receptor blockade with phentolamine or muscarinic receptor blockade with atropine through the SNA prior to the perfusion of GABA did not change the sinus node responses. GABA (10-1,000 micrograms/ml, 2 ml, SNA) significantly attenuated (by 45-80% of control) the sinus bradycardia due to stimulation of the right vagosympathetic trunk. The sinus node response to selective perfusion of norepinephrine or acetylcholine (0.01 micrograms/ml, 2 ml, SNA) was not affected by GABA. The stellate augmentation (when present) and vagal attenuation were both antagonized by perfusion of picrotoxin (1,000 micrograms/ml, 2 ml, SNA). It is concluded that GABA does not exert any direct effect on the sinus node but may indirectly influence sinus rate by an effect on local nerves or ganglia.

Animals↗
PubMed1983

Acute effects of amiodarone upon the canine sinus node and atrioventricular junctional region.

Amiodarone was selectively perfused into the sinus node artery and atrioventricular node artery of 51 dogs. Amiodarone had an immediate negative chronotropic and dromotropic effect. Threshold concentration was 2.5 micrograms/ml. 25 and 50 micrograms/ml of amiodarone injected into the sinus node artery slowed the heart by 25.6 +/- 3.1 and 33.7 +/- 2.6 beats/min (mean +/- 1 SEM), respectively. Amiodarone 25 and 50 micrograms/ml injected into the AV node artery during AV junctional rhythm slowed the AV junctional pacemaker by 12.2 +/- 1.8 and 17.4 +/- 1.7 beats/min, respectively. Injections of amiodarone into the AV node artery during sinus rhythm regularly increased AV conduction time sometimes causing 2 degrees AV block at the highest concentration used. Impaired conduction was exclusively measured at the level of the A-H interval in the His electrogram. Neither atropine nor propranolol prevented the negative chronotropic effects of amiodarone. Amiodarone had no significant effect on sinus node response to either stellate stimulation or intranodal administration of norepinephrine. The negative chronotropic action of amiodarone was significantly enhanced when amiodarone was administered in a perfusate containing low (0.6 mM) instead of normal calcium. Taken collectively these observations indicate that amiodarone has immediate depressant electrophysiologic effects on both the sinus node and the AV junction and that these early effects might involve the blockade of the slow channel.

Amiodarone↗
PubMed1982

Histologic and fine-structural anatomy of the adrenorenal portal vessels in the dog.

Reflex vasoconstriction that occurs in the kidney of the dog can be the result of activation of catecholamine flow reaching the kidney directly from the adrenal medulla via adrenorenal portal vessels. This study was undertaken to learn more about the histologic and fine-structural anatomy of these unusual vessels. We found that they are thin-walled vessels (200-500 micrometers) which are accompanied by many capillaries. These portal vessels have distinctive valves and have sparse, longitudinally arranged musculature which is denser at the base of the valves. The valves in the portal vessels are arranged to permit flow in the direction from the adrenal gland toward the kidney. Smooth muscle at the base of the valve is in close proximity to non-myelinated nerve fibers, suggesting that the opening of these valves may in part be neurally mediated. These unique anatomical features distinguish the adrenorenal portal vessels from other blood vessels and likely have functional importance in control of the adrenorenal circulation.

Adrenal Medulla↗
PubMed1982

Structure and function of specific regions in the canine atrioventricular node.

The functional subregions of the rabbit atrioventricular (AV) node have been examined in detail, but it has not been possible to subject the normal canine AV node to such rigorous scrutiny. Arterial perfusion and beveled microelectrodes have now allowed us to explore the anatomic and functional regions of the isolated canine AV node. The atria and AV junctional tissues of 20 young dogs were excised and selectively perfused with physiological solution through the nutrient arteries to the sinus node, AV node, and His bundle. AV node action potentials had shapes similar to those of the rabbit AV node and were conducted slowly (56 +/- 7 mm/s); slowest conduction (16 +/- 14 mm/s) was observed in the distal AV node where diastolic depolarization was always recorded and where maximum upstroke velocity of the action potential was slowest. From subsequent anatomic studies of the same preparations we found that the proximal region of the canine AV node was predominantly composed of interwoven slender transitional cells and that the distal region contained bundles of transitional cells and small but conspicuous aggregations of P-cells. The proximal portion of the canine AV node appeared to be organized for triage of atrial input during sinus rhythm. Electron microscopic examinations revealed numerous relatively long (greater than 1.0 micrometers) gap junctions between proximal AV node cells. The large gap junctions may provide an anatomic basis for electrotonic interaction during summation and conduction of AV node inputs. The distal AV node is the site of slowest AV conduction and also where most forms of AV junctional rhythm originate.

Action Potentials↗