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Human physiology, hazards and health risks
Published in Stephen Battersby, Clay's Handbook of Environmental Health, 2023
Revati Phalkey, Naima Bradley, Alec Dobney, Virginia Murray, John O’Hagan, Mutahir Ahmad, Darren Addison, Tracy Gooding, Timothy W Gant, Emma L Marczylo, Caryn L Cox
There are many chemicals that act as neurotransmitters. The more common neurotransmitters and those of particular interest in toxicology are: Acetylcholine;Norepinephrine or noradrenaline;Epinephrine or adrenaline;Dopamine;Serotonin;Histamine;Gamma amino butyric acid (GABA);Glycine;Glutamate aspartate. Dopamine, norepinephrine and epinephrine are a group of neurotransmitters called ‘catecholamines’. Norepinephrine used to be known as ‘noradrenaline’ and epinephrine as ‘adrenaline’. Each of these neurotransmitters is produced in a step-by-step fashion by different enzymes.
Introduction
Published in A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha, Clark’s Procedures in Diagnostic Imaging: A System-Based Approach, 2020
A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha
PET patients scheduled for FDG scans are asked to refrain from any strenuous exercise such as long walks, gym sessions swimming or carrying heavy weights 24 hours prior to the appointment as well as on the day of the appointment. This will reduce excessive muscle distribution of the FDG. PET patients are encouraged to drink at least 1 litre of water prior to their appointment to improve distribution of the FDG and encourage quick excretion. PET patients are also asked to continue to take medication as normal. There are medicines that can modify blood glucose levels and will subsequently affect the sensitivity of diagnostic PET by inhibiting FDG uptake. It is important to document if such medicines are being taken as this can be considered during image reporting. Medicines to note include: Oral diabetic medicines, e.g. the oral glucophage, metformin.Insulin.Anticonvulsants, mood stabilising drugs and sedatives, e.g. valporate, carbamazepine, phenytoin and phenobarbital.Steroid hormones used for arthritis due to their anti-inflammatory properties, e.g. corticosteroids.Dopamine and adrenaline derivatives used to treat emphysema, bronchitis, bronchial asthma and stimulate the heart rate, known as catecholamines.
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
The urine catecholamine profile and blood platelet–bound catecholamine are tests that provide a differential determination of the individual adrenal catecholamines, epinephrine, norepinephrine, dopamine, metanephrine, normetanephrine, MHPG, VMS, and serotonin. These may or may not be elevated in the chemically sensitive individual,866 with data revealed in Table 2.31.
Evaluation of the carcinogenicity of carbon tetrachloride
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Samuel M. Cohen, Christopher Bevan, Bhaskar Gollapudi, James E. Klaunig
Benign pheochromocytomas were reported in mice exposed to CCl4 in the two-year inhalation study (Nagano et al. 2007a). These tumors were also found to be increased in mice when dosed by oral gavage in the NCI study in which CCl4 was used as a positive control for liver tumors ((1976a) (Weisburger 1977). Benign pheochromocytomas are tumors that originate in chromaffin cells of the adrenal gland medulla and secrete excessive amounts of catecholamines, usually epinephrine or norepinephrine (DeLellis et al. 2004). In the Nagano et al. (2007a) experiment, an elevated incidence of pheochromocytomas of the adrenal gland occurred at the two highest exposure levels (25 and 125 ppm) in male mice and at the highest exposure level (125 ppm) in female mice (Table 2); no pheochromocytomas occurred in mice at the lower doses or controls (Table 2). These tumors were seen only in the exposed mice but not rats (Table 1).
PRE-WORKOUT SUPPLEMENT INDUCED CARDIAC ISCHAEMIA IN A YOUNG FEMALE
Published in Journal of Sports Sciences, 2020
Theophylline, specifically at high doses can inhibit phosphodiesterase causing increased cyclic adenosine monophosphate activity which triggers increased adrenergic activation and catecholamine release. Toxic levels of theophylline can cause epinephrine and norepinephrine levels to be 4- to 8-times and 4- to 10-times higher than normal, respectively. Such high levels of catecholamine concentrations have a variety of adverse effects such as cardiac arrhythmias (Journey & Bentley, 2018). Another ingredient that likely contributed to the catecholamine surge is alpha Yohimbine. Yohimbine is a well-known cardiac and central nervous system stimulant of the alpha-2 blocking type (Venhuis et al., 2014). Isopropylnorsynephrine is known for sympathomimetic properties however by itself it is not very potent but its cardiac risks can be potentiated by co-administration of other sympathomimetic drugs and caffeine as seen in this case (Venhuis et al., 2014). Caffeine also contributes to the catecholamine surge by antagonising adenosine receptors, this adenosine receptor antagonism promotes neurotransmitter release of catecholamines and its subsequent sympathetic effects (Robertson et al., 1978).
The Neurostructure of Morality and the Hubris of Memory Manipulation
Published in The New Bioethics, 2018
In addition to external properties of bodily perception, properties of internal systems can affect the content and quality of mental states (Glannon, 2011, pp. 11–40 esp p. 16). Adrenaline (epinephrine) and noradrenaline (norepinephrine) – catecholamines secreted by the adrenal medulla – have several critical functions in the body. High levels of these hormones can adversely affect the brain. The release of adrenaline into the bloodstream activates noradrenic mechanisms in the amygdala, which promote formation, consolidation, and reconsolidation of unconscious memories of fearful and emotionally charged events. Distinct from the effects on working memory, the release of hormones to form and strengthen memory of a threatening event is adaptive insofar as it enables an individual to avoid similar threats in the future. However, hypersecretion of adrenaline and noradrenaline in response to a traumatic event can consolidate unconscious memory of the event so potently that it results severe psychological conditions, such as PTSD.4 Moreover, these hormones also contribute to the formation and consolidation of episodic memory in the hippocampus and its reconsolidation in the cerebral cortex. Episodic memory involves first-person recall and consists of links between past and present desires, beliefs, intentions, and emotions. Such psychological continuity is the basis of prospective memory, and thus the foundation of narrative identity: the unified set of characteristics and experiences that comprise the one’s distinctive autobiography (Glannon 2011, pp. 12–18).