Epinephrine

About: Epinephrine is a research topic. Over the lifetime, 9772 publications have been published within this topic receiving 285916 citations.

Overview of the effects of beta-adrenergic receptor agonists on animal growth including mechanisms of action

Abstract: The beta-adrenergic receptors (beta-AR) are present on the surface of almost every type of mammalian cell. These receptors are stimulated physiologically by the neurotransmitter, norepinephrine and the adrenal medullary hormone, epinephrine. There are three subtypes of beta-AR, namely, beta1-AR, beta2-AR, and beta3-AR; the pharmacological and physiological responses of an individual cell result from the particular mixture of the three beta-AR subtypes present on that cell. Species-specific structure (amino acid sequence) also causes modification of the function of a given beta-AR subtype. Knowledge of the beta-AR subtypes present in various cell types, coupled with knowledge of receptor structure (sequence), will allow an understanding of the complexity of physiological function regulated by beta-AR. Oral administration of some beta-AR agonists increases muscle and decreases fat accretion in cattle, pigs, poultry, and sheep. The large number of physiological functions controlled by beta-AR suggests that the mechanism(s) for the observed changes in carcass composition may be extremely complex. Any proposed mechanism must begin with the possibility of direct effects of the agonist on skeletal muscle and adipocyte beta-AR. However, many other mechanisms, such as modification of blood flow, release of hormones, or central nervous system control of feed intake may contribute to the overall effects observed with a given beta-AR agonist in a given species. Furthermore, the pharmacodynamic properties of a particular agonist are complex and expected to vary among species as well as within the same species at different ages or when fed different diets.

The effect of epinephrine on immunoreactive insulin levels in man.

Abstract: While training in 1989 with Richard Have1 in San Francisco, I became interested in his studies of the role of the sympathetic nervous system in the regulation of free fatty acid (FFA) mobilization from adipose tissue.’ Therefore, when I arrived at the laboratory of Robert H. Williams as a postdoctoral endocrine fellow in 1963, I chose to study the effects of catecholamines on carbohydrate and lipid metabolism. To evaluate these effects, Alan Graber and I gave prolonged infusion of epinephrine to a male subject. We found that FAA levels rose and then returned to basal values despite continued administration of the amine. Since hyperglycemia and tachycardia persisted, we concluded that reesterification of FFA in adipose tissue or inhibition of lipolysis by insulin might be involved. To determine which mechanism was most likely, we asked Takashi Kuzuya (now at Jichi Medical School, Japan), another postdoctoral fellow, to assay the plasma samples from our catecholamine infusions for insulin using the newly developed radioimmunoassay. To our surprise, insulin levels did not change during the epinephrine infusions but rose dramatically upon their termination. Since the concept of the autonomic nervous system regulating the peripheral endocrine system was not considered likely at that time, we performed a number of control studies to stimulate the p-cell with glucose and other insulin secretagogues; all were inhibited by epinephrine. This finding had important implications for metabolic regulation and suggested that many older studies in which insulin secretion had been assumed to parallel glucose levels would need to be reexamined. Before submission of the work, I had the opportunity to present it at the meeting of the American Society of Clinical Investigation. Afterward, I received a letter and reprint’ from Arthur Colwell pointing out that he had suggested such a possibility 30 years earlier when he observed inhibition of glucose oxidation during an epinephrine infusion. So much for the originality of my scientific finding! Nevertheless, the concept was new to most scientists and opened up enough new questions that I spent the next 20 years studying its implications. What developed is the idea that the peripheral nervous system regulates many hormones, not just those of the endocrine pancreas. Eventually, a critical role for the neural control of islet function in the development of stress hyperglycemia was delineated.3 Later, I began studies of the possibility that the central nervous system, in turn, is regulated by peptide hormones secreted by peripheral endocrine cells. The central neural connections to the pancreas were eventually shown to originate in the ventral hypothalamus, an area of the brain important to glucose regulation and body energy balance. Because of this finding, Steve Woods and I developed the concept of feedback from the /?-cell to the hypothalamus via insulin for the regulation of food intake and energy expenditure.4*5 This idea of a peripheral metabolic signal for the brain has been given a big boost recently with the discovery of the ob gene and its circulating adipose tissue hormonal gene product, leptin.6 Interestingly, leptin and insulin both appear to regulate the same neural circuit, the synthesis and release of neuronal NPY in the arcuate nucleus?,* The newness of the original finding with epinephrine, and later norepinephrine, and its applicability to many other endocrine glands, plus the large number of diabetes-related investigators, led to ‘frequent citations, and in 1984 this article was recognized as a citation “classic” in Current

Epinephrine absorption in adults : intramuscular versus subcutaneous injection

Abstract: We report a prospective, randomized, blinded, placebo-controlled, 6-way crossover study of intramuscular versus subcutaneous injection of epinephrine in young men. Peak plasma epinephrine concentrations were significantly higher (P < .01) after epinephrine was injected intramuscularly into the thigh than after epinephrine was injected intramuscularly or subcutaneously into the upper arm. We recommend intramuscular injection of epinephrine into the thigh as the preferred route and site of injection of this life-saving medication in the initial treatment of anaphylaxis. (J Allergy Clin Immunol 2001;108:871-3.)

Mechanisms by which epinephrine augments cerebral and myocardial perfusion during cardiopulmonary resuscitation in dogs.

Abstract: The goals of this study were to quantify the effects of epinephrine on myocardial and cerebral blood flow during conventional cardiopulmonary resuscitation (CPR) and CPR with simultaneous chest compression-ventilation and to test the hypothesis that epinephrine would improve myocardial and cerebral blood flow by preventing collapse of intrathoracic arteries and by vasoconstricting other vascular beds, thereby increasing perfusion pressures. Cerebral and myocardial blood flow were measured by the radiolabeled microsphere technique, which we have previously validated during CPR. We studied the effect of epinephrine on established arterial collapse during CPR with simultaneous chest compression-ventilation with the abdomen bound or unbound. Epinephrine reversed arterial collapse, thereby eliminating the systolic gradient between aortic and carotid pressures and increasing cerebral perfusion pressure and cerebral blood flow while decreasing blood flow to other cephalic tissues. Epinephrine produced higher cerebral and myocardial perfusion pressures during CPR with simultaneous chest compression-ventilation when the abdomen was unbound rather than bound because abdominal binding increased intracranial and venous pressures. In other experiments we compared the effect of epinephrine on blood flow during 1 hr of either conventional CPR or with simultaneous chest compression-ventilation with the abdomen unbound. Epinephrine infusion during conventional CPR produced an average cerebral blood flow of 15 ml/min . 100 g (41 +/- 15% of control) and an average myocardial blood flow of 18 ml/min . 100 g (15 +/- 8% of control). In our previous studies, cerebral and myocardial blood flow were less than 3 +/- 1% of control during conventional CPR without epinephrine. Although flows during CPR with simultaneous chest compression-ventilation without epinephrine were initially higher than those during conventional CPR, arterial collapse developed after 20 min, limiting cerebral and myocardial blood flow. The use of epinephrine throughout 50 min of CPR with simultaneous chest compression-ventilation maintained cerebral blood flow at 22 +/- 2 ml/min . 100 g (73 +/- 25% control) and left ventricular blood flow at 38 +/- 9 ml/min . 100 g (28 +/- 8% control). The improved blood flows with epinephrine correlated with improved electroencephalographic activity and restoration of spontaneous circulation.(ABSTRACT TRUNCATED AT 400 WORDS)