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Biomedical subjects

B H Natelson

Publications and source records attributed to B H Natelson.

At least 145 records · Page 8Linked to original sources
PubMed1983

Ultradian rhythms in cognitive functions and their relationship to visceral processes.

Visceral and behavioral data were repeatedly sampled over time in 7 men performing tests of eye-hand coordination and of recall. Spectrum analysis of behavioral data showed peaks in the ultradian range which for the group were significantly different from white noise. Relations between visceral and behavioral data were not striking. However, relations between (a) epinephrine and indices of sympathetic tone (i.e., norepinephrine or heart rate) and (b) ongoing performance were positive and the highest of all tested.

Activity Cycles↗
PubMed1983

Stress, predisposition and the onset of serious disease: implications about psychosomatic etiology.

Based on the author's own work and a review of the literature, the hypothesis is made that potentially lethal disease does not usually occur in healthy animals or people but does so when covert or overt disease exists or when a predisposition for disease exists. The author supports this hypothesis in his assessment of the human literature on sudden death. Further support for the hypothesis is presented from 2 animal models being studied in his laboratory--stress-induced heart failure in the cardiomyopathic hamster and stress-induced sensitization of digitalis-toxic ventricular arrhythmias. This analysis suggests a different view from the classical one of what a psychosomatic disease might be.

Angina Pectoris↗
PubMed1983

Stress-induced heart failure.

Stress produced heart failure in cardiomyopathic hamsters (CMHs) with subclinical heart disease. CMHs exhibited a variety of peripheral manifestations of heart failure including subcutaneous edema, fluid in the abdominal and thoracic cavities, and increased organ weight. In contrast, stress did not produce heart failure in healthy hamsters. These data indicate that the presence of covert heart disease can dramatically alter the pathogenic consequences of stress.

Animals↗
PubMed1983

Role of luminal acidity in the pathogenesis of stress-induced gastroduodenal disease.

Infusion of progressively more acidic fluids into the stomachs of rats stressed by immobilization had disparate effects on gastric erosive disease despite their producing a stepwise fall in venous pH. At the highest concentration infused, disease was exacerbated. However, at lower concentrations, disease was ameliorated. The acidity of the infusate altered the incidence but not the magnitude of the duodenal disease that accompanies stress. When bicarbonate was given parenterally, systemic pH was normalized but gastric disease still developed. Thus the level of mucosal pH does not reliably predict whether or not gastric disease will develop. When a series of progressively more basic fluids was infused into the stomachs of stressed rats, gastric disease was lessened in only those rats infused with the highest concentration of bicarbonate. Increasing the pH of the infusate in a stepwise fashion produced a stepwise diminution of duodenal disease incidence with no effect on duodenal disease severity. When the stressed rat's mucosa was stimulated to secret acid by the parenteral injection of secretagogues, gastric disease severity was the same as in control animals given saline. Although secretagogue infusion did not affect the incidence of stress-induced duodenal disease, it significantly exacerbated the magnitude of the elicited disease. These experiments suggest that luminal acid plays a negligible role in the onset of stress-induced gastric disease but may be important in determining the severity of the gastric disease once it has begun. Conversely the amount of luminal acid correlates with the incidence of stress-induced duodenal disease but does not seem to play a role in determining the severity of the duodenal disease after it has begun.

Animals↗
PubMed1983

Roles of stress and adaptation in the elicitation of face-immersion bradycardia.

Thirteen young healthy human volunteers immersed their faces in warm or cold water on one day while breathing through a snorkel and on another day while breath holding. The magnitude of the elicited bradycardia was most prominently due to water temperature, with apnea playing a less important role. Perceived stress could affect the magnitude of the response, but it was less important than the other variables. Thus statistically significant nonparametric correlations were found for the group but not for most individuals between a scoring technique that assessed perceived stress and heart rate. In contrast to animals, these data indicate that bradycardia may be reliably elicited in humans by face immersion in cold water and that stress is neither necessary nor sufficient to produce this phenomenon. Adaptation did not seem to play a role in the development of this physiological response.

Adaptation, Physiological↗
PubMed1982

Vertebral artery injection of ouabain does not hasten arrhythmogenesis.

Cats were infused with ouabain into either their vertebral artery or their femoral vein, and latencies to early and late ventricular arrhythmia and death were determined. No significant differences were found between the 2 groups. These data question the likelihood that the area postrema is, as has been recently proposed, the primary site of action for digitalis-induced cardiac arrhythmias.

Animals↗
PubMed1982

Effect of linoleic acid on digitalis cardiotoxicity.

Adult male guinea pigs were anesthetized, catheterized and i.v. infused with either saline and then ouabain or with linoleic acid salt and then ouabain. The linoleic acid pretreatment produced a significant delay until the onset of digitalis induced cardiac arrhythmias.

Animals↗
PubMed1981

The role of shock predictability during aversive conditioning in producing psychosomatic digitalis toxicity.

Guinea pigs were subjected to Pavlovian fear conditioning (signaled shock) and then infused with a fast acting digitalis preparation on a day when all experimental stimuli except shock were delivered. A significant shortening in latency to the onset of life-threatening digitalis toxicity was found when comparisons were made to control pigs that had never been shocked. This effect was not found in other guinea pigs infused with ouabain after exposure to sessions of unsignaled shock. These experiments indicate that psychological factors, when divorced form physical factors, may produce lethal digitalis toxicity in an organism that would otherwise by asymptomatic. The data from these experiments suggest that the intense arousal associated with a signal that had previously been paired with shock is sufficient to precipitate cardiac arrhythmias in an animal with a predisposition to cardiac automaticity such as is produced by digitalis. Conversely, the less intense arousal associated with unsignaled shock is inadequate to produce this effect. This interpretation indicates that the state of an animal's health will affect its psychosomatic response to signaled or unsignaled shock.

Animals↗
PubMed1981

Ultradian rhythm of plasma norepinephrine in rats.

This study examined the possibility that laboratory rats exhibit ultradian plasma catecholamine rhythms. Four rats were prepared with chronic venous cannulas. After recovery, blood was sampled every 15 min for 8 h. Spectrum analysis revealed ultradian norepinephrine rhythms with spectral peaks around 80-90 min and around 40 min. However, no reliable ultradian rhythms were found for epinephrine. Ultradian norepinephrine rhythms appeared to be synchronized across three of the four rats, suggesting that the rhythm can be synchronized by some environmental stimulus. Thus, rats exhibit ultradian norepinephrine rhythms similar to those found in humans and in rhesus monkeys, indicating (a) that laboratory rats can be used to study the biological mechanisms of ultradian rhythms and (b) that ultradian oscillations of sympathetic function are a common property of mammalian systems.

Animals↗
PubMed1981

Cholinergic activation produces psychosomatic digitalis toxicity.

The purpose of this study was first to develop an animal model for stress-induced digitalis toxicity in such a way that physical and psychological factors might be kept separate. The other purpose was to begin an analysis of the mechanism of this psychosomatic effect. To do this, free-ranging guinea pigs were subjected to repeated sessions of signaled shock (Pavlovian fear conditioning) or to signal alone. On a probe day in which signals were delivered as usual but shock was not administered, guinea pigs were infused i.v. with ouabain after an i.p. injection of either saline, atropine sulfate or atropine methylbromide. Saline-treated guinea pigs with prior fear conditioning became digitalis toxic at a significantly lower dose of the drug than control guinea pigs that had not had exposure to signaled shock. This effect was blocked by both atropine salts, indicating a cholinergic effector on the blood side of the blood-brain barrier responsible for early arrhythmogenesis in the fear-conditioned animals.

Animals↗