China
Africa
Explore chapters and articles related to this topic
Basic Chemical Hazards to Human Health and Safety — I
Published in Jack Daugherty, Assessment of Chemical Exposures, 2020
Cardiac Sensitization. Cardiac sensitization makes the heart sensitive to biochemical compounds called sympathomimetic amines. Such hormonal compounds, one being adrenaline or epinephrine, make the heart beat faster. When the body anticipates an increase in physical exertion, as when terror causes panic, adrenaline is secreted into the bloodstream. In order to increase the heartbeat rate, the dose of adrenaline must equal or exceed its no-effect level. Cardiac sensitizers lower the no-effect level of adrenaline so that the heart is stimulated by ever lower quantities of adrenaline. They do this by affecting the pacemaking and conduction center of the heart, which determines the rhythm and rate of the heartbeat. Interference with this region leads to arrhythmia with various consequences. Young persons generally have no serious consequences, though fatal arrhythmias are not unknown in healthy young people. Also, either cerebral or myocardial ischemia may result from arrhythmia. Shock may occur. Or, in older people or those who suffer from compromised cardiac systems already, congestive heart failure may occur. Organic solvents are well known as cardiac sensitizers. Fatal cardiac arrhythmias following organic solvent exposure are due to cardiac sensitization to circulating catecholamines.
Antihypertensive Drugs: Controlling Blood Pressure
Published in Richard J. Sundberg, The Chemical Century, 2017
Raymond Ahlquist proposed in 1948 that there were two types of adrenaline receptors, α and β, based on different patterns of response to a series of drugs. Adrenaline increases the force and rate of heart contractions and also causes vasoconstriction and so raises blood pressure. Drugs that counter these effects can lower blood pressure. Sir James Black,a a pharmacologist working at ICI, pursued Ahlquist’s theory by searching for a selective β-antagonist, on the premise that this would reduce the heart’s need for oxygen and alleviate the pain of angina pectoris. Taking a lead from an Eli Lilly compound, dichloroisoprenaline, a compound called pronethalol was synthesized. It proved to be active and decreased heart rate, as well as reducing the occurrence of angina. This compound did not pass toxicological hurdles, but the related compound propranolol did. Not only was angina pectoris successfully treated, but as clinical results accumulated, it was also found to lower blood pressure and reduce the incidence of myocardial infarction.3
Introduction
Published in James P. Kohn, The Ergonomic Casebook, 2020
James Kohn, Celeste Winterberger
The deleterious effects of stress can also be found in the cardiovascular system. Heart attacks are the major cause of death for many Americans. One of the contributing factors in heart attacks is stress. When an individual is subjected to stress, adrenaline, a powerful stimulant, is released by the adrenal glands. Adrenaline causes an increase in respiration and heart rate which can result in muscle tension. For short periods of time, this can cause an individual to be more productive. However, as the heart rate increases, so does the blood pressure. This is the pressure at which blood is pumped through the body. Chronic high blood pressure, if unchecked, can lead to heart attacks.
Exercise intensity regulates the effect of heat stress on substrate oxidation rates during exercise
Published in European Journal of Sport Science, 2020
ED Maunder, Daniel J. Plews, Fabrice Merien, Andrew E. Kilding
Venous blood samples were collected into 6-ml ethylenediaminetetraacetic acid tubes and stored on ice until trial completion. A small sample of whole blood was mixed manually using a vortex and analysed for haematocrit and haemoglobin concentration (AcT 5diff, Beckman Coulter, Miami, USA) to allow correction of plasma volume relative to baseline (Dill & Costill, 1974). Plasma was then isolated from the remaining whole blood by centrifugation at 1500 revs.min−1 in 4°C for 10 min, and stored at −80°C prior to subsequent analyses. Plasma glucose and lactate concentrations were determined through specific enzymatic colorimetric diagnostic assays (CV, 1.0 and 0.4%, respectively) on a Roche Diagnostics automated clinical chemistry analyser (cobas Modular P800, Roche Diagnostics New Zealand Ltd, Auckland, NZ). Plasma adrenaline concentration was determined through an enzyme-linked immunosorbent assay performed in duplicate (CV, 7.1%) according to manufacturer’s instructions (BI-CAT® ELISA, Diagnostika GMBH, Hamburg, GER).
The Neurostructure of Morality and the Hubris of Memory Manipulation
Published in The New Bioethics, 2018
Adrenaline, a stress hormone closely related to its counterpart, cortisol, is released when the adrenal gland receives a signal from the amygdala alerting it to a perceived threat (Glannon 2011, p. 74). As part of the limbic system, the amygdala regulates emotions and, as such, is among the most primitive parts of the brain, playing a critical role in the capacity to survive. Among other effects, adrenaline serves to embed non-conscious emotional memories of threatening events in the amygdala. However, if emotional memory is stored too densely in the amygdala, it can produce a disproportionately heightened fear response to external events. Since emotional memories stored in the amygdala transcend conscious control, they are often difficult to modulate, regulate, or expunge and can therefore detrimentally influence the nature and content of belief, affect, and various states of consciousness. Events erroneously perceived as stressors or threats can trigger chronic fear responses that put the brain, body, and mind on a constant state of alert. This describes both the pathology and the pathophysiology of some manifestations of depression, anxiety, and, most acutely, the emotionally disturbing “flashback” memories of traumatic events that characterize PTSD (Glannon 2011, p. 74).