Arrhythmogenicity of Epinephrine-Induced Hyperadrenergic Activity: Applied Evidence at the Level of the Organ and the Organism
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1
Suez Canal University, Biotechnology Research Center, Egypt
Epinephrine (adrenaline) is an endogenous stress hormone secreted by the adrenal gland, and it is a naturally occurring sympathetic neurotransmitter, which plays an important role in the sympathetic control of cardiac activity. Epinephrine can be a hidden menace in cases of hyperadrenergic activity at times of extreme stress or emotion when the sympathetic nervous system is over-active. On the other hand, epinephrine is clinically used as an exogenous sympathomimetic and β-agonist to treat cardiac arrest and cardiac dysrhythmias resulting in diminished or absent cardiac output. Recent advances in cardiac research have produced surprising and disconcerting results for the pharmaceutical industry and cardiologists. In particular, considerable problems were recently highlighted when extensive clinical trials revealed potentially lethal side effects of some drugs widely in use. Epinephrine, one of these drugs, is considered the most commonly available inotrope and in many cases the most appropriate drug to maintain blood pressure. However, tachycardia, ventricular arrhythmias, hypertension, hyperglycemia, and even oxidative stress are recorded as side effects of this drug. Therefore, I have undertaken work to define and analyze the latest and most important information on the arrhythmogenicity of hyperadrenergic activity induced by epinephrine, at the level of the organ and the organism, using in vitro and in vivo experimental models. In both isolated hearts and intact animals, cardiac arrhythmias produced by epinephrine included; extrasystoles, tachyarrhythmias and bradyarrhythmias as well as abnormalities of both P-wave and ST segment. In intact animals, epinephrine induced a significant negative chronotropism accompanied by a non-significant negative dromotropism. A gradual and progressive positive inotropism and a non-significant increase in repolarization voltage were also obtained. Vasomotor dysfunction was recorded as an elevated venous blood pressure as well. Recently, I have introduced evidence for the anti-arrhythmic effect of natural wild honey against cardiotoxicity due to catecholamines, in particular epinephrine. More recently, I have proven that natural wild honey managed to reverse the side effects of epinephrine. Meanwhile, it preserved its powerful inotropic effect. So, with the advent of new technologies and great advances in cardiovascular research, more properly conducted clinical trials are needed to objectively substantiate the efficacy of natural wild honey as an important complementary biotherapy, besides epinephrine, as an inotrope, for the treatment of congestive heart failure. Especially, wild honey decreased the venous blood pressure which can reduce the pre-load of the heart and consequently may diminish the congestion in the venous system, the reason this condition is termed congestive heart failure. The outcomes of my latest scientific trials in order to suppress or attenuate the arrhythmogenicity of hyperadrenergic activity induced by epinephrine could result not only in the prevention of the deleterious effects of epinephrine, as an endogenous stress hormone and a chemical mediator, but also in novel anti-arrhythmia therapies against the adverse effects of epinephrine, thereby facilitating its safe use as an effective inotrope.
Keywords:
Arrhythmogenicity,
Calcium waves,
cardiac arrhythmias,
Epinephrine,
Hyperadrenergic activity,
Intracellular calcium dysregulation,
Oxidative Stress,
Vasomotor dysfunction
Conference:
2nd NEUROMED Workshop, Fez, Morocco, 10 Jun - 12 Jun, 2010.
Presentation Type:
Oral Presentation
Topic:
Oral Session 2: Adaptation to environmental stress
Citation:
Rakha
MK
(2010). Arrhythmogenicity of Epinephrine-Induced Hyperadrenergic Activity: Applied Evidence at the Level of the Organ and the Organism.
Front. Neurosci.
Conference Abstract:
2nd NEUROMED Workshop.
doi: 10.3389/conf.fnins.2010.12.00032
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Received:
04 Jun 2010;
Published Online:
04 Jun 2010.
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Correspondence:
Miran K Rakha, Suez Canal University, Biotechnology Research Center, Ismailia, Egypt, miran.rakha@bue.edu.eg