Alfred Bennun, PhD (Editor)
Full Professor-Emeritus-Rutgers University Consultant, CONICET, AR, USA
Rutgers University, NJ, USA

Series: Endocrinology Research and Clinical Developments
BISAC: SCI007000

The book examines the noradrenaline-emotional psyches (brain-blood barrier) somatic-adrenaline axis. It conceptually updates research advances, diagnostic techniques and therapeutic methods.

The authors enhance their discussions with clear illustrations and explicative texts written for researchers, professionals, educators and students alike, which favor its selection as an essential overview of recent medical and scientific advances, allowing the reader to have the satisfaction of finding first-rate accounts of important work.

Comparative studies between immediately obtained adrenal vein samples (AVS) and 15 minutes thereafter show that the stress reactions induced by catheter manipulation had an effect on serum cortisol and aldosterone values. A transient increase in cortisol release from both adrenal glands occurs in the majority of the patients who undergo AVS. This stress reaction can influence the assessment of both the selectivity of the catheterization during the sequential AVS technique and the lateralization of aldosteronoma bearing gland.

The separation of noradrenaline (NA) at brain and adrenaline at blood functions as a homeostatic lame axis by the blood-brain barrier blocking adrenaline feedback in hypothalamic-pituitary-adrenal (HTPA). This leads to postulate an evolution adaptation for the brain dominance over body, which allows a psychoanalytic treatment to function to signal turn-off and return to circadian homeostasis. Decreased glucose could stress the HTPA axis and leads to decreasing metabolites and releasing Mg2+ for integration of the brain-tissue network. Mg2+ changes adenylyl cyclase (AC) from a Ca2+-AC complex to an Mg2+-AC form with responsiveness to NA for short-term memory. The cAMP generated has been postulated for consolidation of long-term memory.

Trigeminocardiac reflex evoked negative effects on hemodynamics which exaggerated by use of beta-blockers and suggesting either a central control or efferent pathways of TCR partly related to adrenergic responses.

Stress-induced cardiomyopathies such as Tako-Tsubo Syndrome primarily affect post-menopausal women, more susceptible than the rest of the population, which have experienced sudden emotional shock. The symptoms mimic a myocardial infarction without a significant occlusion of the coronary arteries. Instead, they display a left ventricular (LV) dysfunction called the “Apical-Ballooning Syndrome”. Some of these patients show high circulating levels of adrenaline, and symptoms respond to treatment with beta- adrenergic blockers.

Heart adrenoceptors are targets of elevated adrenaline during stress, mainly subtype β1, but also: β2, α1, and β3. The first stage of stress decrease the number of adrenoceptor binding sites but with prolonged stress the number of receptors often returns to initial values. Stress can also affect antagonistic muscarinic receptors. The regulation of G protein-coupled receptors comprises desensitization, internalization or down-regulation of receptors. The changes in total receptor number, degradation and gene expression taking together impact heart fine-tuning and functional signaling.

Stress hormones cause structural transitions in erythrocyte membranes and increase microviscosity in the regions of lipid-lipid and protein-lipid interactions. And the perfusion of the isolated rat heart with the Krebs–Henseleit solution containing erythrocytes preincubated with stress hormones sharply decreases the coronary flow rate and rapidly stops it.

The study of adrenaline physiological effects, remain clinically important, a general appreciation of adrenaline for emergency treatment and as an adjunct to local anaesthesia is mandatory for any doctor in clinical practice, because one day he may well use it to save someone’s life. (Imprint: Nova Biomedical )