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Biomedical subjects

T N James

Publications and source records attributed to T N James.

At least 145 records · Page 8Linked to original sources
PubMed1979

Mechanism of postarrhythmic renal vasoconstriction in the anesthetized dog.

The mechanism of postarrhythmic renal vasoconstriction was studied in 28 dogs anesthetized with pentobarbital sodium (30 mg/kg i.v.). Rapid atrial or ventricular pacing or induction of atrial fibrilation were used to produce at least 20% prompt decrease in cardiac output and mean arterial blood pressure. Return to control cardiac output and blood pressure occurred within 3 minutes after cessation of the arrhythmia, but renal blood flow remained significantly decreased (26%) with gradual recovery by 17.7 +/- 6.6 min. Infusion of phentolamine (0.25 mg/min) into the renal artery, intravenous hexamethonium (l mg/kg), adrenal demedullation, or cooling the cervical vagi prevented postarrhythmic renal vasoconstriction. In contrast, renal denervation, intravenous bretylium (10 mg/kg), intravenous atropine (0.5 mg/kg) or intrarenal SQ 20881 (0.20 mg/min) has no effect on postarrhythmic renal vasoconstriction. Intravenous propranolol (0.5 mg/kg) intensified postarrhythmic renal vasoconstriction. These data suggested that the postarrhythmic renal vasoconstrictive response required intact vagi and was due to alpha adrenergic stimulation by adrenal catecholamines. However, femoral arterial catecholamine levels were not elevated above control during postarrhythmic renal vasoconstriction. We therefore sought local vascular pathways by which catecholamines might reach the kidneys. An adrenorenal vascular network was found in each dog. Collection of catecholamines from these vessels during postarrhythmic renal vasoconstriction in six dogs revealed catecholamine concentrations threefold higher than simultaneously collected femoral arterial catecholamines levels. Because ligation of these vessels abolished postarrhythmic renal vasoconstriction in each dog, we conclude that postarrhythmic renal vasconstriction is due to adrenal catecholamines reaching the kidneys through an adreno-renal vascular network and that the response requires intact vagi.

Adrenal Glands↗
PubMed1979

Chronotropic and dromotropic effects of histamine on the canine heart.

The actions of 2-methylhistamine (H1 agonists), 4-methylhistamine (H2 agonist), and histamine were studied by selective perfusion of the sinus node artery and atrioventricular node artery in 75 dogs anesthetized with pentobarbital sodium. 2-Methylhistamine and histamine had variable and inconsistent effects on the sinus rate. 4-Methylhistamine (100 microgram/ml) produced acceleration of the sinus rate from 158 +/- 4 to 173 +/- 5 beats per minute (P less than 0.05) when perfused via the sinus node artery. The effects of the histamine agonists on atrioventricular junctional rhythms were similar to the effects on sinus rhythm. The response of the sinus node to vagal stimulation was attenuated by selective perfusion with histamine; however, the direct negatively chronotropic action of acetylcholine was not affected by histamine. Neither 2-methylhistamine nor 4-methylhistamine affected the response of the sinus node to vagal stimulations. Both 4-methylhistamine and histamine (but not 2-methylhistamine) attenuated (P less than 0.05) the response of the sinus node to stimulation of the right stellate ganglion. The positively chronotropic effects of directly perfused norepinephrine were unaffected by histamine or 4-methylhistamine. These results suggest a neural depressing action of histamine on autonomic efferent fibers. In the atrioventricular junction, both histamine and 2-methylhistamine (but not 4-methylhistamine) had negatively dromotropic effects. Cimetidine (an H2 antagonist) had no significant direct effects on the sinus rate or atrioventricular conduction and failed to prevent the acceleration of the sinus rate produced by local perfusion with 4-methylhistamine.

Acetylcholine↗
PubMed1979

Cardiac ganglionitis associated with sudden unexpected death.

In a postmortem study of the hearts of two young women who died suddenly and unexpectedly, we found a remarkably similar and distinctive ganglionitis, predominantly in the region of the sinus node. Both women had ventricular fibrillation at the time of collapse. Vesicular neuritis and older neural degeneration were present in other regions of the heart. Except for focal fibromuscular dysplasia of the sinus node artery and atrioventricular node artery of one heart, there was no other significant anatomic abnormality in either heart. The functional significance of this cardiac ganglionitis is unclear, but its location in and around the conduction system makes it a possible cause of the fatal electrical instability. Recognition that ganglionitis of the heart may be associated with sudden death should stimulate a number of additionally useful studies.

Adult↗
PubMed1979

Effects of verapamil on automaticity and conduction with particular reference to tachyphylaxis.

Verapamil delivered via the sinus node artery exerted a dose-related, exclusively negative chronotropic action at all concentrations studied. Perfusion through the AV node artery during AV junctional rhythm also caused a dose-related negative chronotropic response, but the concentrations required to depress this pacemaker were ten times higher than those required to depress sinus node automaticity. Verapamil administered into the AV node artery during sinus rhythm impaired AV conduction. His bundle electrograms demonstrated that depressed A-V conduction was exclusively located at the A-H level. In 5 out of 10 dogs verapamil (5 to 10 mg) delivered into the septal artery caused an abrupt onset of ventricular fibrillation without premonitory dysrhythmias. Verapamil (except at very high concentrations) did not alter the responsiveness of the sinus node and the AV junction to acetylcholine or norepinephrine, whether administered selectively into the sinus node artery or the AV node artery or released by neural stimulation. Serial injections of verapamil were associated with tachyphylaxis for the direct chronotropic and dromotropic properties of the drug.

Acetylcholine↗
PubMed1979

Termination of "ventricular" arrhythmias from digoxin by selective production of complete atrioventricular block with physostigmine in the dog.

In previous studies we have come to doubt that ventricular rhythms of an automatic nature will arise spontaneously from the peripheral Purkinje system. In 20 anesthetized dogs, digoxin was administered i.v. (0.1-1.0 mg/kg) and in 12 dogs by selectively perfusing the atrioventricular (AV) node artery (2 ml; 40 microgram/ml). We obtained the following results. First, selective pharmacological production of complete AV block (acetylcholine or physostigmine) interrupts the "ventricular" arrhythmias considered characteristic of digitalis intoxication.Second, digitalis arrhythmias are difficult to produce when this type of complete heart block had been previously established. Third, abolition of ventricular arrhythmias by selective pharmacological production of heart block can be reversed (i.e., the arrhythmia restored) with atropine. Fourth, rapid pacing of the ventricles during complete heart block in dogs poisoned with digitalis can eventually induce ventricular arrhythmias, but not quickly. We interpret that these digitalis arrhythmias originated within the acetylcholine-sensitive portion of the AV node-His bundle region.

Acetylcholine↗
PubMed1979

Morphological changes in the right ventricular septomarginal trabecula (false tendon) during maturation and ageing in the dog heart.

Right ventricular septomarginal trabeculae ('false-tendons') from puppies, young adult, and older adult dogs were examined by light and electron microscopy. The connective tissue of the trabeculae obtained from the puppies and the young adult dogs had few elastic fibres, but this component was well developed in the connective tissue of the adult dogs. The trabeculae of older dogs also showed scattered foci of extracellular fat droplets, and their junctional regions nearest to the ventricular wall were often heavily laden with fat. The Purkinje cells were uniform in each group, but differed from one group to another: in the puppies they resembled typical conducting cells, being predominantly cuboidal with few, poorly developed myofibrils, whilst in the adults the Purkinje cells resembled working myocytes, being elongated with a well developed complement of longitudinally arranged myofibrils. The cells of all age groups showed a complete absence of T-tubules, simply arranged interculated discs, and frequent dilatations of the sarcoplasmic reticulum. The cells of older dogs showed separations of the undifferentiated regions of most discs. Membrane degenerations and the presence of numerous fat droplets also were common. The fine structural cytology of Purkinje cells therefore appears to change considerable with age in the right ventricular septomarginal trabeculae ('false-tendons') of the dog heart.

Aging↗
PubMed1978

The effect of aging on ventricular contractile performance.

The effects of aging on mechanical performance of isolated canine right ventricular trabeculae were studied in two age groups. The first group was comprised of nine dogs, about 9 months of age. The second group was composed of seven dogs over 8 years of age. Aging had no significant effect on developed force. Extent of shortening tended to decrease. There was a significant decrease in both the rate of rise of tension and the velocity of shortening (20%). THis reduction was primarily due to an increased duration of contraction. Twitch duration increased by as much as 40% during aging but most of this prolongation was due to a profound slowing of relaxation. Aging caused a significant increase in passive stiffness since equivalent changes in muscle length brought about twice as much increase in resting tension in the aged muscle as in the young muscle. On the other hand, aging caused a significant shift of Lo to the right. Taken collectively, these results indicate that aging is associated with increased passive stiffness and decreased speed of contraction without changes in strength.

Aging↗
PubMed1978

Characterization of atrial fibrillation in man: studies following open heart surgery.

The nature of localized atrial activation during atrial fibrillation was characterized in 34 patients following open heart surgery. Bipolar atrial electrograms (AEG) recorded in each patient with atrial fibrillation exhibited a myriad of sizes, shapes, polarities, amplitudes, and beat-to-beat intervals. On the basis of the AEG morphology and the nature of its baseline, we have classified the recordings into four Types. Type I was characterized by discrete AEG complexes separated by an isoelectric baseline free of perturbation, Type II by discrete AEG complexes but with perturbations of the baseline between complexes, Type III by AEGs which failed to demonstrate either discrete complexes or isoelectric intervals, and Type IV in which AEGs of Type III alternated with periods characteristic of Type I and/or Type II. In 22 patients, the AEGs were recorded a second time, and in 11 of these patients the type of atrial fibrillation changed between the first and second recording period. An atrial flutter-fibrillation pattern in the ECG was associated with a relatively ordered atrial activation pattern and a relatively slow atrial rate. Human atrial fibrillation is not an electrophysiologically homogeneous process when compared among different patients or ad seriatim in the same patient.

Adult↗
PubMed1978

Progressive postnatal changes in sinus node response to atropine and propranolol.

Postnatal development of autonomic control of heart rate was evaluated in the sinus nodes of isolated, perfused right atria obtained from 21 sibling puppies in three different litters between 3 and 11 wk postpartum. Age-related changes in response to autonomic blockade indicated that propranolol administered after atropine had its most profound direct depressive effect on less mature atrial cells. In the youngest sinus nodes the familial antimuscarinic action (increase in sinus rate) of atropine was regularly preceded by a brief period of cholinomimetic action (a marked slowing of sinus rate) in the youngest sinus nodes. These two opposing effects of atropine underwent a developmental change during the 2-mo study. The cholinomimetic action diminished, whereas the antimuscarinic action increased as a function of age.

Aging↗
PubMed1978

Neural pathways of a cardiogenic hypertensive chemoreflex.

Excitation of a cardiac chemoreceptor with 5-hydroxytryptamine (serotonin) produces a complex autonomic reflex which includes hypertension, changes in heart rate and contractile force, and disturbances of AV conduction. This study examines the afferent and efferent neural pathways of this autonomic reflex in 60 anesthetized dogs. We used cooling and sectioning techniques in 40 of these, and in 20 others recorded afferent neurograms. The most common afferent pathways for the reflex were found in the left and right recurrent cardiac nerves. No preferential efferent routes to the heart were found, although the nature of the reflex cardiac response could be altered by specific nerve interruption. Cyproheptadine (1 mg/kg iv) regularly abolished both the reflex and the chemoreceptor afferent neural traffic, but injection of a 10 times higher concentration of serotonin (1 mg/ml) readily surmounted the blockade and restored the chemoreceptor neural traffic. Thus cyproheptadine interdicts the reflex at the site of its initiation.

Afferent Pathways↗
PubMed1978

De subitaneis mortibus. XXVIII. Apoplexy of the heart.

Apoplexy of the heart can be responsible for sudden and for recurring instability of cardiac rhythm and conduction, and for the clinical counterparts of syncope and sudden death. Every pathophysiological mechanism which produces cerebral apoplexy has its counterpart in apoplexy of the heart. Among the mechanisms documented are thrombosis, embolism and rupture of those special vessels supplying the sinus node, atrioventicular (A-V) node and His bundle. Apoplexy of the heart can occur either with or without significant or recognizable ventricular myocardial infarction. Acute vascular accidents within the critical centers of cardiac impulse formation and conduction deserve more frequent consideration in the explanation of unusual cases of "epilepsy", of seizure disorders of the elderly, of neurologic manifestations (which may be secondary as well as primary) of systemic diseases such as lupus erythematosus or thrombotic thrombocytopenic purpura, and indeed of every case of otherwise unexplanined syncope or sudded death at any age.

Arterial Occlusive Diseases↗
PubMed1978

De subitaneis mortibus. XXIX. Randomly distributed focal myocardial lesions causing destruction in the His bundle or a narrow-origin left bundle branch.

Most focally destructive lesions of the heart (e.g., myocarditis) have an essentially random distribution. Any mechanical significance of such diseases depends primarily on there being a very large number of foci. However, single even very small lesions can have profound electrophysiological significance if appropriately located within the cardiac conduction system. Two cases of sudden unexpected death are here reported which had destructive lesions involving the His bundle and a narrow-origin left bundle branch. Not much is known of the electrical or mechanical effects of acute left branch block which is due to complete anatomical transection of that structure in the human heart, and some possible consequences (including sudden unexpected death) are considered. Myocarditis or any other focally destructive disease in the heart may be of little functional importance if it is not widespread, unless some of the lesions happen to damage any of several small but crucially important sites in the cardiac conduction system. Studies to determine the presence or absence of this precise type of damage should be done especially in cases of sudden unexpected death.

Adolescent↗
PubMed1978

De subitaneis mortibus. XXX. Observations on the pathophysiology of the long QT syndromes with special reference to the neuropathology of the heart.

Eight patients (different families) with syncopal attacks and a long QT interval in the ECG died suddenly. Five heard normally and three were born deaf. At postmortem examination of all eight hearts the single consistent abnormality was focal neuritis and neural degeneration within the sinus node, A-V node, His bundle and ventricular myocardium. Although the etiology of this intracardiac neural disease is uncertain, a chronic viral infection or some noninfectious degenerative process are among the plausible causes discussed. If intracardiac neuritis and neural degeneration prove to be a prevalent finding among other victims dying from the long QT syndromes, further consideration should be given to whether there is any genuine hereditary component in the pathogenesis. Because of the asymmetrical and focal distribution of the cardioneural lesions, the response to present forms of medical or surgical treatment of the lung QT syndromes may vary from benefit to harm. Until more is known of the true etiology of the neural disease, treatment will probably remain empirical in nature and should be conducted with cautious clinical observation.

Adolescent↗
PubMed1978

Hemodynamic components of a cardiogenic hypertensive chemoreflex in dogs.

The mechanical and hemodynamic components of a cardiogenic hypertensive chemoreflex were studied in 50 dogs. Within 6 seconds after a single injection of serotonin (100 microgram/ml) into the left atrium, mean pressure (mm Hg) rose in the aorta from 103 to 197 and in the pulmonary artery from 21 to 34. Left ventricular dp/dt virtually doubled. There was an increase (75%) in peripheral vascular resistance that returned to control within 10 seconds. There was no significant change in pulmonary vascular resistance. Aortic and pulmonary arterial hypertension were associated with a profound depression (82%) in atrial force. Atropine transformed this negative inotropic effect on the atria into a positive inotropic action that averaged 65%. In contrast, ventricular force was always sharply increased, more in the right (95%) than in the left ventricle (50%). Bilateral stellectomy did not eliminate the reflex but it completely abolished the initial increase of cardiac contractility; a delayed increase in contractility persisted and was due exclusively to release of catecholamines from the adrenal glands. This cardiogenic hypertensive chemoreflex uses the vagus for its afferent neural traffic and both the sympathetic and the vagus nerves for its efferent route. The brief and intense systemic vasoconstriction concomitant with an increase in cardiac contractility might represent a kind of "aortic cough." Some possible clinical implications are discussed.

Adrenal Medulla↗