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Psychological Stress and Immune Competence
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Elizabeth A. Bachen, Anna L. Marsland, Stephen B. Manuck, Sheldon Cohen
The reasons for these discrepancies are not yet clear but may reflect differences in the hormonal environment surrounding immune cells. Long-term changes in health habits, which influence both immune and neuroendocrine systems, may in part underlie differences that are observed in acute and chronic stress [12,85,86]. Also, it is possible that homeostatic processes, such as receptor down-regulation and desensitization, may be involved. For example, Maisel et al. [87] found that oral administration of the beta-2 agonist terbutaline for 1 week caused a decrease in the number of beta receptors on T suppressor/cytotoxic, NK, and T helper cells, and a substantial drop in isoproterenol-induced cAMP generation in NK and T suppressor/cytotoxic cells in humans. Interestingly, T helper and B lymphocytes showed the least amount of change in either beta-receptor density or cAMP accumulation. If cAMP production is indeed essential in the recruitment of NK cells from the marginating pool of blood vessels to the circulating bloodstream [79], these adaptations may partly explain why peripheral NK cell numbers tend to increase during acute stress conditions and decrease during chronic forms of stress.
Functional characterisation of the GABAA receptors
Published in Adam Doble, Ian L Martin, David Nutt, Calming the Brain: Benzodiazepines and related drugs from laboratory to clinic, 2020
Adam Doble, Ian L Martin, David Nutt
One of the early suggestions was that tolerance developed to the benzodiazepines as a consequence of receptor down-regulation. Most of the early work was carried out using radioligand binding studies and, although a number of different drugs and treatment paradigms were used, it was generally found that no change in the binding capacity occurred (Gallager et al, 1984; Miller et al, 1989). There were some reports of receptor down-regulation but in a number of these very high benzodiazepine doses were used (Rosenberg and Chiu, 1979, 1981).
Anesthesia for Patients with Ventricular Assist Devices
Published in Wayne E. Richenbacher, Mechanical Circulatory Support, 2020
Special attention is given to cardiovascular and pulmonary function. A concern for the anesthesiologist is the recognized defect of adrenergic mechanisms that modulate the heart’s inotropic state. A reduction of beta1 adrenergic receptor density in the failing heart has been demonstrated. This finding is thought to represent receptor down regulation produced by chronic exposure of the heart to I excessive catecholamine levels. Although myocardial norepinephrine stores are decreased in advanced heart failure, circulating norepinephrine levels are elevated. I The majority of patients scheduled for VAD(s) implantation are receiving high doses of inotropes. As these drugs act by stimulation of beta adrenergic receptors, maximal doses of inotropes often produce little effect on blood pressure and cardiac output. Usually more than two inotropes are given at any time and higher doses will be required during the administration of anesthetics.
Takotsubo cardiomyopathy: a rare complication of acute viral gastroenteritis
Published in Journal of Community Hospital Internal Medicine Perspectives, 2020
Ammar Ashfaq, Waqas Ullah, Shristi Khanal, Muhammad Abdullah Zain, Nishanth Thalambedu, Faisal Inayat, Muhammad Umair Atiq
The exact pathophysiology of TCM is yet to be fully understood. However, it is postulated to result from one of the following mechanisms: catecholamine-mediated cardiac toxicity, left ventricular (LV) outflow tract obstruction, multivessel coronary spasm, or microvascular dysfunction [4]. The sustained beta-receptor stimulation secondary to stress-related catecholamines surge is believed to cause beta 1 and beta 2-adrenergic receptor down regulation. This can result in a blunted myocardial adrenergic stimulation, hence, resulting in LV apex stunning or ballooning [9]. Since beta-adrenergic receptors are densely located in the LV apex than in the base, thus the apical myocardium being more susceptible, particularly to epinephrine than the basal segments [10]. Wittstein et al. first reported the significantly raised catecholamines levels during an acute episode of TCM [11]. Hence it is plausible that AVG, as in our case, can cause a release of inflammatory markers and increase catecholamine levels in the blood which could have led to TCM.
Thyroid stimulating hormone (TSH) autoregulation reduces variation in the TSH response to thyroid hormones
Published in Temperature, 2018
Stephen Paul Fitzgerald, Nigel Geoffrey Bean
However, as indicated above, it has been suggested that in prolonged hypothyroidism, TSH autoregulation disappears [3], such that the TSH curve resembles the tsh curve. Possible reasons for this loss of TSH autoregulation include the changing isoforms of TSH in hypothyroidism [25] and receptor down-regulation. In these circumstances of loss of autoregulation in prolonged hypothyroidism, the TSH response to hypothyroidism would be advantageously augmented relative to the euthyroid state, as compared to the TSH response in the absence of there being TSH autoregulation (Figure 5(c)).This mechanism is consistent with the curvature of the population FT4/log TSH relationship [15,16] and the shift in TSH curves in hypothyroidism previously proposed [17].
Current and emerging pharmacotherapy for the treatment of adult attention deficit hyperactivity disorder (ADHD)
Published in Expert Opinion on Pharmacotherapy, 2019
Giulio Perugi, Alessandro Pallucchini, Salvatore Rizzato, Vito Pinzone, Pietro De Rossi
Stimulants and ATX may be destabilizing for ADHD-BD, inducing psychotic symptoms or (hypo)manic switches. On the other hand, the treatment of BD alone may result in residual symptoms of ADHD [132]. However, in patients with an active mood disorder, ADHD should be treated by combining ADHD medications and mood stabilizers until mood stability is reached. Lithium, Valproate, and lamotrigine should be utilized in order to obtain adequate mood stabilization. The use of the combination of second-generation antipsychotics (SGA) and stimulants [134] should be limited only to patients with severe agitation and aggressiveness [135–137]. Indeed, the possibility of a stimulant-antipsychotic syndrome (SAS) warns about the long-term consequences of this combination [138]. Complex dopaminergic models suggest that stimulants increase dopaminergic (DA) tonic levels through presynaptic action (increasing DA in the synaptic gap), leading to decreased burst size and postsynaptic receptor down-regulation. Antipsychotics increase tonic DA levels through postsynaptic action (blocking the postsynaptic DA receptors and subsequently increasing the level of DA in the synaptic gap), leading to decreased burst size and postsynaptic receptor up-regulation [150,151]. Concurrent stimulant and antipsychotic use increase tonic DA levels through both pre and postsynaptic action, consequently decreasing burst size but not postsynaptic up or down-regulation. This synergistic effect could lead to a reduced need for drugs, reducing risks of other side effects [150]. However, we do not know if the association between stimulants and SGAs can lead to a chemical imbalance over the long term. This possibility may be reduced with concomitant stimulant-antipsychotic use at a minimum dosage.