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Adaptation to Stress and its Cardioprotective Effect in Stress, Ischemic, and Reperfusion Damage
Published in Felix Z. Meerson, Alexander V. Galkin, Adaptive Protection of The Heart: Protecting Against Stress and Ischemic Damage, 2019
Felix Z. Meerson, Alexander V. Galkin
It further turned out that the lack of blood corticosteroid elevation in response to heavy stress in adapted animals, i.e., “fading” of the adrenocortical link of the stress reaction, also does not result from exhaustion of the functional resources of the adrenal cortex. On the opposite, injected ACTH causes a much greater elevation of blood corticosterone in stress-adapted than in nonadapted animals.18 This is important evidence that adaptation involves (1) increased power of the adrenocortical link of the stress-effecting sympathoadrenal system and (2) altered organismic reaction to stress at the central level, i.e., at the level of releasing factors and ACTH. It is at this level that some mechanisms are actuated by adaptation and, despite the stress, hinder the output of releasing factors and tropic hormones, and prevent increased secretion of stress hormones and mediators (in this case corticosterone).
Nutritional Requirements in Extreme Sports
Published in Datta Sourya, Debasis Bagchi, Extreme and Rare Sports, 2019
Matthew Butawan, Jade L. Caldwell, Richard J. Bloomer
The human body has an incredible capacity to adapt to different types of stress. In 1936, Hans Selye proposed a model of the progression of any type of stressor, the General Adaptation Syndrome (GAS) (Selye 1936). In short, sympathoadrenal responses (alarm phase) to a stressor elicit metabolic and physiologic adaptations (resistance phase) until resolved or exhausted (exhaustion phase). Selye suggested the model could be applied to any type of stressor; for example, physical activity, exposure to toxins (illness), or enduring extreme temperatures.
Stress and Addiction
Published in Hanna Pickard, Serge H. Ahmed, The Routledge Handbook of Philosophy and Science of Addiction, 2019
The above brain stress responses coordinate our well-known “fight” or “flight” response, which produce stress sensations such as the heart beating faster, breathing faster, mobilizing energy stores and inflammatory responses, via the hypothalamic-pituitary-adrenal (HPA) axis that signals to produce cortisol, and the autonomic nervous system that mobilizes heart rate and blood pressure arousal, and also immune responses. These physiological arousal pathways signal the body and the brain to coordinate and modulate the behavioral, cognitive and learning aspects of the stress response. The HPA axis is stimulated by the corticotropin releasing factor (CRF), released from the paraventricular nucleus (PVN) of the hypothalamus, to stimulate the adrenocorticotrophin hormone from the anterior pituitary that initiates the secretion of cortisol/corticosterone from the adrenal glands. The autonomic nervous system includes the sympathetic nervous system that mobilizes the cardiovascular and immune arousal responses, and the parasympathetic nervous system that is involved in regulating the sympathetic arousal by providing the ‘brakes’ to the sympathetic arousal and in regaining homeostasis via the sympathoadrenal medulary (SAM) pathways. Recent evidence also indicates that the sympathetic pathways provide further modulation of the adrenal glands for release of cortisol as well as release of norepinephrine and epinephrine. These are the core stress pathways involved in stress arousal and mobilization of the body and brain to respond to stress and in regulation of stress so as to regain homeostasis.
Stress and social isolation, and its relationship to cardiovascular risk in young adults with intellectual disability
Published in Disability and Rehabilitation, 2023
Clara C. Zwack, Rachael McDonald, Ainura Tursunalieva, Shradha Vasan, Gavin W. Lambert, Elisabeth A. Lambert
Broadly speaking there are two kinds of stress, each with different physiological and psychological effects. Acute stress is when stress is experienced for a short period of time- for example an argument with a loved one, being stuck in a traffic jam or receiving criticism from an employer. Chronic stress results from repeated exposure to stressors such as a relationship break-down, job strain [15]1, loneliness and social isolation. Long-term chronic exposure to stress has been related to a 40–60% excess risk of incident coronary heart disease (CHD) [16]. Stress produces many physiological changes, some of which may contribute to the development of CVD. Stress reactivity to everyday events activates both the sympathetic nervous system (SNS), sympathoadrenal (SA) axis and the hypothalamic-pituitary-adrenocortical (HPA) axis. This in turn leads to mobilisation of stored energy, increased heart rate and peripheral vasoconstriction, and multiple other physiological effects [17].
Partial vs full glottic view with CMACTM D blade intubation of airway with simulated cervical spine injury: a randomized controlled trial
Published in Expert Review of Medical Devices, 2023
Chao Chia Cheong, Soon Yiu Ong, Siu Min Lim, Wan Zakaria Wan A., Marzida Mansor, Sook Hui Chaw
Sympathoadrenal response to laryngoscopy and tracheal intubation, which manifests as tachycardia and hypertension, can precipitate myocardial ischemia and intracranial hypertension in susceptible patients [27,28]. The mechanism of an exaggerated hemodynamic response during intubation is related to the strength and duration of upward lifting force applied to the laryngeal structure. Stronger and longer lifting force is needed to achieve full glottic view [29]. Therefore, we postulate that hemodynamic response would be attenuated by obtaining a POGO of < 50%. Contradictory to our postulation, there was no significant difference in hemodynamic changes between groups. One explanation could be that dosage of both hypnotic and opioid used in our study, are insufficient to attenuate hemodynamic response to laryngoscopy and intubation and therefore no differences were observed between the groups.
The neurobiology of childhood trauma—aldosterone and blood pressure changes in a community sample
Published in The World Journal of Biological Psychiatry, 2022
Jan Terock, Anke Hannemann, Johanna Klinger-König, Deborah Janowitz, Hans J. Grabe, Harald Murck
The renin-angiotensin-aldosterone-system (RAAS) is the key hormonal system for blood pressure regulation and sodium balance and specifically mediates the blood pressure response to stress exposure (Aguilera et al. 1995). It closely interacts with the sympathoadrenal-medullary (SAM-)system and the hypothalamic-pituitary-adrenal (HPA-)axis in the body’s stress response to acute and chronic stressors (Groeschel and Braam 2011). Acute stress leads to the activation of the SAM-system, which stimulates the excretion of renin, which is followed by increases in angiotensin II (ANG II) and finally aldosterone. Aldosterone is an important agent for the reabsorption of sodium and water and thereby for the blood pressure regulation and plays a prominent role in the initiation of the stress response and stress-induced depressive behaviour (Hlavacova and Jezova 2008; Hlavacova et al. 2012; Franklin et al. 2015; Terock et al. 2017).