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Results for “GENERAL ADAPTATION SYNDROME”

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PubMed2003

Response of skeletal muscle mitochondria to hypoxia.

This review explores the current concepts relating the structural and functional modifications of skeletal muscle mitochondria to the molecular mechanisms activated when organisms are exposed to a hypoxic environment. In contrast to earlier assumptions it is now established that permanent or long-term exposure to severe environmental hypoxia decreases the mitochondrial content of muscle fibres. Oxidative muscle metabolism is shifted towards a higher reliance on carbohydrates as a fuel, and intramyocellular lipid substrate stores are reduced. Moreover, in muscle cells of mountaineers returning from the Himalayas, we find accumulations of lipofuscin, believed to be a mitochondrial degradation product. Low mitochondrial contents are also observed in high-altitude natives such as Sherpas. In these subjects high-altitude performance seems to be improved by better coupling between ATP demand and supply pathways as well as better metabolite homeostasis. The hypoxia-inducible factor 1 (HIF-1) has been identified as a master regulator for the expression of genes involved in the hypoxia response, such as genes coding for glucose transporters, glycolytic enzymes and vascular endothelial growth factor (VEGF). HIF-1 achieves this by binding to hypoxia response elements in the promoter regions of these genes, whereby the increase of HIF-1 in hypoxia is the consequence of a reduced degradation of its dominant subunit HIF-1a. A further mechanism that seems implicated in the hypoxia response of muscle mitochondria is related to the formation of reactive oxygen species (ROS) in mitochondria during oxidative phosphorylation. How exactly ROS interfere with HIF-1a as well as MAP kinase and other signalling pathways is debated. The current evidence suggests that mitochondria themselves could be important players in oxygen sensing.

Adaptation, Physiological↗
PubMed1996

Explaining fatigue in congestive heart failure.

Fatigue is a prominent symptom in patients with chronic heart failure, limiting physical activity and impairing quality of life. Although the underlying mechanisms are not clearly identified, alterations associated with peripheral adaptation in heart failure appear to play an important role, including a variably impaired peripheral perfusion during exercise, reduced oxidative capacity of skeletal muscle, impaired muscle strength, and possibly reflex mechanisms associated with alterations in the metabolism of skeletal muscle. Exercise training can, in part, reverse these peripheral alterations, improve exercise capacity, and alleviate fatigue.

Activities of Daily Living↗
PubMed1980

The stress response.

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Adaptation, Physiological↗
PubMed1984

Physiological functions of glucocorticoids in stress and their relation to pharmacological actions.

Almost any kind of threat to homeostasis or stress will cause plasma glucocorticoid levels to rise. The increased levels have traditionally been ascribed the physiological function of enhancing the organism's resistance to stress, a role well recognized in glucocorticoid therapy. How the known physiological and pharmacological effects of glucocorticoids might accomplish this function, however, remains a mystery. A generalization that is beginning to emerge is that many of these effects may be secondary to modulation by glucocorticoids of the actions of numerous intercellular mediators, including established hormones, prostaglandins and other arachidonic acid metabolites, certain secreted neutral proteinases, lymphokines, and a variety of bioactive peptides. These mediators participate in physiological mechanisms--endocrine, renal, immune, neural, etc.--that mount a first line of defense against such challenges to homeostasis as hemorrhage, metabolic disturbances, infection, anxiety, and others. Contrary to the traditional view that glucocorticoids enhance these defense mechanisms, however, it has become increasingly clear that glucocorticoids at moderate to high levels generally suppress them. This paradox, which first emerged when glucocorticoids were discovered to be antiinflammatory agents, remains a major obstacle to a unified picture of glucocorticoid function. We propose that stress-induced increases in glucocorticoid levels protect not against the source of stress itself but rather against the body's normal reactions to stress, preventing those reactions from overshooting and themselves threatening homeostasis. This hypothesis, the seeds of which are to be found in many discussions of particular glucocorticoid effects, immediately accounts for the paradox noted above. Furthermore, it provides glucocorticoid physiology with a unified conceptual framework that can accommodate such apparently unrelated physiological and pharmacological effects as those on carbohydrate metabolism, inflammatory processes, shock, and water balance. It also leads us to suggest that some of the enzymes rapidly induced by glucocorticoids, such as glutamine synthetase, detoxify mediators released during stress-induced activation of primary defense mechanisms. These mediators would themselves lead to tissue damage if left unchecked.

Animals↗
PubMed2002

Endocrine stress response in jugular-vein cannulated rats upon multiple exposure to either diethyl-ether, halothane/O2/N2O or sham anaesthesia.

The main objective of this study was to assess the endocrine stress response to multiple anaesthesia followed by sham anaesthesia in order to detect any memory effects. For this purpose, jugular-vein cannulated rats were subjected to either sham, diethyl-ether or halothane/O2/N2O anaesthesia, and their plasma ACTH, corticosterone, glucose, adrenaline and noradrenaline levels measured. The study had three separate experiments, each consisting of a control and treatment group. In two experiments, the rats were exposed to high or low concentrations (40-15%) of diethyl ether, using either a jar containing cotton soaked in diethyl ether or a vaporizer. In the third experiment, rats were exposed to halothane/O2/N2O. Control animals underwent sham anaesthesia. Blood samples were taken 6 min before and at 5, 15 and 55 min after starting the exposure (t = 0 min). For each variable, the dt5 (level at t = 5 min minus that at t = -6 min) and the cumulative levels over the one-hour period as determined by the area under the curve (AUC) were calculated. Further, the peak levels (Cmax) were determined. The mean time needed to induce anaesthesia was 68, 121 and 55 s for exposure to high and low concentrations of diethyl ether and to halothane/O2/N2O, respectively. Increased noradrenaline and adrenaline dt5 levels were observed only after the first exposure to the high concentration of diethyl ether. Multiple anaesthesia sessions using either diethyl ether or halothane/O2/N2O did not clearly influence adrenaline and noradrenaline levels. Diethyl ether induced a sharp rise in plasma ACTH and glucose levels, irrespective of the concentration used. The response of the ACTH and glucose was similar for single and multiple exposure. An increased response of ACTH, corticosterone and glucose to sham anaesthesia following multiple induction of anaesthesia was observed for the high concentration of diethyl ether only. Halothane/O2/N2O raised plasma glucose without differences between single and multiple anaesthesia sessions. Upon sham anaesthesia following multiple exposures to halothane/O2/N2O, glucose levels were significantly increased. This study indicates that repeated anaesthesia in rats can elicit an increased stress response during subsequent handling and change of environment.

Adrenocorticotropic Hormone↗
PubMed1985

Use and misuse of an imprecise concept: alternative methods in animal experiments.

The concept of inhumanity of Russell & Burch in 1959 with proposals for human procedures in experiments on animals by way of replacement, reduction and refinement (the 3 R's) and the revival of these by Smyth (1978) as alternatives to animal experiments are presented. Since then under the name 'alternative methods', replacement of in vivo by in vitro methods has found great public attention and promotion. It is argued that alternative methods are a fallacy, because in the progress of research a continual control and reinvestigation of findings on each system level is required until knowledge is complete, which makes in vivo experiments irreplaceable. True alternatives exist only for refinement within a system level. On the level of the organism, refinement would be in the care of animals and experimental procedure through alleviation of stress. The possibilities which refinement offers for animal welfare have been nearly forgotten and need promotion among researchers, animal technicians and attendants.

Animal Testing Alternatives↗
PubMed1976

[Dynamics of adaptation and maladaptation phenomena in rats exposed to weak chronic stimulation].

Experiments were carried out with rats to study the influence of disturbing artifical light-dark regimens. The findings are consistent with the definition of "relatively weak stress-stimuli" which, according to R. BAUMANN, can be essential in causing regulation diseases. Disturbances in the circadian patterns of spontaneous motor activity are described as an inversion of normal activity maxima and minima, as periodicity step-down and as a dissolution of the day-periodical order. Their occurrence is proportional to the magnitude of the disturbing effect. As vegetative disturbing effects there occurred transient hypertensive derangements, the extent of which is inversely proportional to the magnitude of the stressing stimulus. These differences are discussed basing on a hypothesis of differently synthetized cerebro-visceral regulation mechanisms.

Animals↗
PubMed1999

[Adamantane derivatives enhancing body's resistance to emergencies].

A total of 329 novel adamantane derivatives have been synthesized and pharmacologically studied. Among them, the compounds containing halogen-containing aromatic radicals in the second position show the most pronounced effect on animal resistance to the emergencies induced by its habitat and performance. N-(2-adamantyl)-N-(para-bromphenyl)amine (bromantane) possesses a low toxicity, a high ability to enhance the physical and operant working maintenance of animals, to accelerate its recovery in developed fatigue, in hyperthermia and hypoxia in particular. 2-(para-chlorobenzoylamine)adamantane (chlodantane) has the processes of a rapid-action adaptogenic agent by enhancing the resistance of animals to various physical and toxically chemical noxious agents. The two compounds have immunostimulating effects in secondary stress-induced immunodeficiencies whose mechanism of action is a membranous protective activity.

Adamantane↗
PubMed1999

[Ongoing conflict situations and physical disease].

In most cases psychosomatic patients are not vitally threatened. Nevertheless almost half of the emergency patients have got psychical disturbances (e.g. neurotic heart disease, states of hyperventilation or vertigo). A reason is not only the personal development of early childhood. More often the problems are to be found within strained relations. The physical illness can be conceived as an (unconscious) attempt to master a conflict or loss, as narcissistic reparation, as adaption-effort or even as self destruction Selye's theory of stress presents the linkage between the organ pathology and the influence of the psychosocial situation. Examples of medical cases explain these correlations.

Adaptation, Psychological↗