PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “GENERAL ADAPTATION SYNDROME”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1994

[Scientific bases of health].

The usefulness of the change of paradigm, which treats health as a passive process, for the concept of activity, is substantiated: health is the ability of active self-protection... . The concept is worked out as a computer database, it generalizes the laws of self-smoothing, homeostasis, phylogenetic and ontogenetic regulating, following, compensation, self-disposing, systematic genesis and equilibration. The research work has shown that collection of mistakes does not make a barrier on the way of improving and does not limit the duration of health; the research work has also allowed to divide general regularities and individual affairs: the reactions' individuality is dropped by general adaptation syndrome, but because of non-typical situations the changes have an individual character and they cannot be generalized. The last idea gives specific requires on the control technology, if individuality (situationality) of conditions, state and abilities were taken into account. These regulations are hard to be done, but they do not have principle limitations. The author makes a conclusion: the perspective of using the models, uniting in the real time the abilities of men and the abilities of global computer networks, for the control and improvement of individual health, which adapt to the owner, is determined.

Computer Simulation↗
PubMedDate not supplied

[The pathophysiological significance of the low triiodothyronine syndrome with increased clearance in cancer of the stomach and large intestine].

Investigations designed to study T3 pharmacokinetics under malignant tumors of the stomach and large intestine showed an augmented total T3 clearance, which fact is indicative of enhancement of the processes of 5-monodeiodezing of thyroid hormones. It is to be thought that intensification of T3 metabolism and rise in inverse T3 produced through peripheral conversion of T4 underlie the pathogenesis of that low triiodothyronine syndrome to be encountered in malignant tumors. Since the above mechanism of development of low T3 syndrome has been identified in traumata and infectious diseases, the changes in question might be considered to be one of the links in the general adaptive syndrome directed towards satisfaction of the phagocytosing leucocytes' requirements in the biocydic substrate iodine and augmentation of the production of the fat-mobilizing factor inverse T3.

Adult↗
PubMedDate not supplied

[Thyroid morphofunctional changes in various types of experimental chronic stress].

Structural and functional parameters of the thyroid were studied in mature rabbits, inducing stress by stimulating the ventromedial nucleus of the hypothalamus or by exposing the animals to electrocutaneous irritations. Morphometric and radioimmunoassay results have revealed thyroid activation during the adaptation syndrome. Prolonged intensive stress was shown to cause a decrease in thyroid secretory activity, reflecting change of a stage of stable resistance by a phase of depletion of compensatory resources. However the nature of changes in the blood levels of thyroid and thyrotropic hormones in experimental animals have some characteristic features. A conclusion was made of the correlation between pathogenesis of the general adaptation syndrome and a methodological approach to simulation of a body tension reaction.

Adaptation, Physiological↗
PubMedDate not supplied

[The irritable bowel syndrome and chronic colitis--different diseases or stages of a single process? (debatable problems of pathogenesis)].

Morphofunctional state was studied of intestinal enteroendocrine cells in biopsies obtained during fibrocolonoscopy using Grimelius's argyrophil reaction, as was immune status, condition of vegetative nervous system, together with the psychological examination being conducted. Most of the systems examined showed alterations peculiar to the stage of resistance of the general-adaptation syndrome. Dependence was found out between the morphofunctional state of endocrinocytes and type of disorder in the motor function of the intestine, parameters characterizing the vegetative regulation. Statistical analysis of the results obtained showed that most of the studied parameters of different systems have come in a single-modal distribution of variants (sequences), which fact suggests that pathologic processes in irritable colon syndrome (ICS) and chronic non-infectious undefined colitis (ChNIUC) might be uniform. Based on the above results the authors believe ICS and ChNIUC to be different stages of the same pathologic process. It can be asserted, to the authors' thinking, that ICS and ChNIUC are dystrophic, disregenerative, rather than inflammatory processes, as to their pathogenetic mechanisms.

Biopsy↗
PubMed2004

The overtraining syndrome in athletes: a stress-related disorder.

Physical exercise is a type of allostatic load for several endocrine systems, notably the hypothalamic-pituitary-adrenal (HPA) axis. Athletes undergoing a strenuous training schedule can develop a significant decrease in performance associated with systemic symptoms or signs: the overtraining syndrome (OTS). This is a stress-related condition that consists of alteration of physiological functions and adaptation to performance, impairment of psychological processing, immunological dysfunction and biochemical abnormalities. Universally agreed diagnostic criteria for OTS are lacking. The pituitary-adrenal response to a standardized exercise test is usually reduced in overtrained athletes. This HPA dysfunction could reflect the exhaustion stage of Selye's general adaptation syndrome. The most attractive hypothesis that accounts for the observed neuro-endocrine-immune dysregulation is the Smith's cytokine hypothesis of OTS. It assumes that physical training can produce muscle and skeletal trauma, thus generating a local inflammatory reaction. With the excessive repetition of the training stimulus the local inflammation can generate a systemic inflammatory response. The main actors of these processes are the cytokines, polypeptides that modulate HPA function in and outside the brain at nearly every level of activity. It is hoped that future research will focus on endogenous risk factors for morbidities related to the neuro-endocrine-immune adaptation to exercise.

Adaptation, Physiological↗
PubMed2000

Cytokine hypothesis of overtraining: a physiological adaptation to excessive stress?

Overtraining syndrome (OTS) is a condition wherein an athlete is training excessively, yet performance deteriorates. This is usually accompanied by mood/behavior changes and a variety of biochemical and physiological alterations. Presently, there is no global hypothesis to account for OTS. The present paper will attempt to provide a unifying paradigm that will integrate previous research under the rubric of the cytokine hypothesis of overtraining. It is argued that high volume/intensity training, with insufficient rest, will produce muscle and/or skeletal and/or joint trauma. Circulating monocytes are then activated by injury-related cytokines, and in turn produce large quantities of proinflammatory IL-1beta, and/or IL-6, and/or TNF-alpha, producing systemic inflammation. Elevated circulating cytokines then co-ordinate the whole-body response by: a) communicating with the CNS and inducing a set of behaviors referred to as "sickness" behavior, which involves mood and behavior changes that support resolution of systemic inflammation: b) adjusting liver function, to support the up-regulation of gluconeogenesis, as well as de novo synthesis of acute phase proteins, and a concomitant hypercatabolic state; and c) impacting on immune function. Theoretically, OTS is viewed as the third stage of Selye's general adaptation syndrome, with the focus being on recovery/survival, and not adaptation, and is deemed to be "protective," occurring in response to excessive physical/physiological stress. Recommendations are made for potential markers of OTS, based on a systemic inflammatory condition.

Acute-Phase Proteins↗
PubMed1991

[The endocrine stress reaction in anesthesia and surgery--origin and significance].

Stress can be defined as a "reaction by living beings to any relevant impairment". The effect of anaesthesia on endocrine function is closely related to the actual stress concept based on the works by Cannon and Selye. Cannon described the role of catecholamines in stress and characterised the fight-flight reaction. Selye emphasised the role of the adrenocortical reaction defining the "general adaptation syndrome", which evolves in three stages ("alarm reaction", "stage of resistance", "stage of exhaustion"). Later, Henry postulated the dual stress concept. The sympathetic-adrenomedullary system is activated during the fight-flight reaction, thus representing an active role of the organism. The pituitary-adrenocortical system is activated during loss of control, submission and depression, especially in a social context. Main valid parameters of this endocrine stress response are adrenaline, noradrenaline, ADH, ACTH and cortisol. In the perioperative period, both pathways are "stressed". The most important factors are patient, operation, and anaesthesia. Anaesthesia can influence the stress response by afferent blockade (local anaesthesia), central modulation (general anaesthesia) or peripheral interactions with the endocrine system (etomidate). Up to now, a total peripheral blockade of the nociceptive system is impossible, due to surgical technique (destruction of nerve fibres) and release of mediator substances. With regard to reduction of endocrine stress response, inhalation anaesthesia with volatile anaesthetics and nitrous oxide may be less effective than neuroleptic, spinal or epidural anaesthesia. Immediately after extubation, rapid increases of endocrine parameters are observed. In addition to central modulation of pain and stress, both halothane and enflurane inhibit catecholamine release from the adrenal medulla. Neuroleptic anaesthesia and total intravenous anaesthesia are very potent and sufficient to control the increases in endocrine parameters even during major surgery, due to their central effects. Spinal and epidural anaesthesia alone as well as in combination with general anaesthesia can reduce the endocrine stress response more than necessary. This is due to the sympathetic blockade, combined with an afferent blockade of central cord fibers which modulate the pituitary-adrenocortical system. Only few data are available concerning the stress response during infiltration anaesthesia or nerve block, but additional sedation seems to be beneficial. Peripheral interactions with the endocrine system like blockade of the adrenal cortex by etomidate is dangerous and has caused a high mortality in intensive-care patients if the substance was admitted for a longer period. Assessment of endocrine stress response in anaesthesia and surgery is controversial.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthesia↗
PubMed2002

Genetic determinants of the stress response in cardiovascular disease.

Originating from Hans Selye's general concept, the biological notion of the stress response implicates neuroendocrine and endocrine pathways as well as their cellular mediators as components of the general adaptation syndrome and its consequences. A highly variable degree of response to psychological and physical stresses has been noted in experimental animals and in human populations. Some stressors, such as the "cold pressor test," have been developed as tools for disease prediction. They apply to variable conditions, from hypertension to insulin resistance, but mostly in relation to cardiovascular outcomes. Other environmental factors, including the degree of salt intake, potentiate the stress response in animals and humans. Our group has undertaken to explore the genetic determinants of the stress response in inbred strains, recombinant congenic and congenic strains, as well as founder human populations. We have succeeded, initially, in linking increased body temperature, a major phenotypic response to stress, to the quantitative trait loci (QTL), one at myh3 on chromosome (Chr) 10, one at hsp27 on Chr 12, and one on Chr Y in the rat. The expression of several stress proteins is under the dominant influence of hstf1 at the rat Chr 7 locus (Mit3). The high prevalence of cardiovascular diseases with traits of enhanced stress responsiveness is discussed here in the context of a paradigm, such as hypertension, in the general population.

Animals↗
PubMed1987

The phenomenon of stress: concepts and mechanisms associated with stress-induced responses of the neuroendocrine system.

'Stress', 'stressors' and the 'stress response' are terms which represent concepts rather than being precisely definable. No single theory of stress has been universally accepted. Selye's General Adaptation Syndrome of stress remains the primary theory for the basis of stress research in food-producing animals; however, other concepts and theories have been developed. This paper reviews current theories and suggests that the complexity of research on stress in food-producing animals can be attributed to the lack of concrete theories and concepts regarding identifiable stressors, the endocrine responses stimulated by potential stressors and the complex and integrated biological changes in the neuro-endocrine system resulting from exposure to hypothesized stressors.

Animals↗
PubMedDate not supplied

Biological basis of the stress response.

Chronic, as well as acute emotional arousal, is a consequence of various types of social interaction, i.e., those between mother and infant and between controlling dominant and less effective subordinate. The neurohumoral accompaniments of this social stress include the sympathetic adrenal medullary and hypothalamic pituitary adrenal responses. A common ensuing pathophysiological state involves a chronic increase of blood pressure. Although Selye's General Adaptation Syndrome presupposed the same response to a variety of stimuli; recent work shows that specific perceptions of control result in different patterns of neuroendocrine activation. A challenge perceived as easy to handle will elicit an active coping response and release of the neurosympathetic system's norepinephrine. Testosterone will rise as the subject savors success. With increasing anxiety this active coping shifts to a more passive mode and the behavior becomes less assured as the animal loses control. The norepinephrine/epinephrine ratio decreases as epinephrine, prolactin, renin and fatty acids rise. As the outcome becomes still less certain and distress grows, adrenocorticotropic hormone and cortisol levels arise. Thus, the effort required on the one hand and the degree of frustration conflict and uncertainty on the other, determine the ratio of catecholamines to corticoids. With severe emotional trauma, brain dysfunction may occur. These effects can be lasting, and corticoids paradoxically return to normal as the behavior changes to that of post-traumatic stress disorder. Repression and denial set in and the organism responds with decreased concern of impaired attachment and increased irritability.

Animals↗
PubMed1991

Stress--mechanisms of immunosuppression.

Stress, a term commonly used to describe varied phenomena, should be restricted to describe an adaptive response by an animal to threats to homeostasis. The threats to homeostasis are called stressors. Stressors include a variety of physical, psychological, chemical, or infectious causes that are modified by intrinsic and extrinsic factors. Examples of modifiers include stressor severity, duration, novelty, host genetics and immune status. What may be a stressor to an animal in one situation, when modified, may not be a stressor in another situation. Mechanisms of stress once thought to involve a single pathway described by Seyle as the General Adaptation Syndrome, have been rejected. Four pathways, some incompletely defined, have been implicated in modulation of the immune system. They include autonomic nervous system, the hypothalamic adrenal axis, extra-adrenal pathways involving neuropeptides and neurotransmitters and neuroimmunological mediators. The mechanisms of stress-induced immunosuppression resistance are poorly defined in domestic fowl and will require careful experimentation linking defined stressors with altered physiological responses that affect specific immune function and result in increased disease susceptibility.

Adaptation, Physiological↗
PubMed2005

Metal stress consequences on frost hardiness of plants at northern high latitudes: a review and hypothesis.

This paper reviews the potential of trace/heavy metal-induced stress to reduce plant frost hardiness at northern high latitudes. The scientific questions are first outlined prior to a brief summary of heavy metal tolerance. The concepts of plant capacity and survival adaptation were used to formulate a hypothesis, according to which heavy metal stress may reduce plant frost hardiness for the following reasons: (1) Heavy metals change membrane properties through impaired resource acquisition and subsequent diminution of the cryoprotectant pool. (2) Heavy metals change membrane properties directly through oxidative stress, i.e. an increase of active oxygen species. (3) The involved co-stress may further increase oxidative stress. (4) The risk of frost injury increases due to membrane alterations. An opposite perspective was also discussed: could metal stress result in enhanced plant frost hardiness? This phenomenon could be based on the metabolism (i.e. glutathione, polyamines, proline, heat shock proteins) underlying a possible general adaptation syndrome of stress (GAS). As a result of the review it was suggested that metal-induced stress seems to reduce rather than increase plant frost hardiness.

Adaptation, Physiological↗