Showing papers on "Epinephrine published in 1994"

Mechanisms responsible for sympathetic activation by cigarette smoking in humans.

Abstract: BACKGROUNDThe pressor and tachycardic effects of cigarette smoking are associated with an increase in plasma catecholamines, suggesting the dependence of these effects on adrenergic stimulation. Whether the stimulation occurs at a central or a peripheral level and whether reflex mechanisms are involved is unknown.METHODS AND RESULTSIn nine normotensive healthy subjects (age, 33.0 +/- 3.5 years, mean +/- SEM), we measured blood pressure (Finapres device), heart rate (ECG), calf blood flow and vascular resistance (venous occlusion plethysmography), plasma norepinephrine and epinephrine (high-performance liquid chromatography assay), and postganglionic muscle sympathetic nerve activity (microneurography from the peroneal nerve) while subjects were smoking a filter cigarette (nicotine content, 1.1 mg) or were in control condition. Cigarette smoking (which raised plasma nicotine measured by high-performance liquid chromatography from 1.0 +/- 0.9 to 44.2 +/- 7.1 ng/mL) markedly and significantly increased mean ...

Ventromedial hypothalamic lesions in rats suppress counterregulatory responses to hypoglycemia.

Abstract: The central nervous system has been implicated in the activation of counterregulatory hormone release during hypoglycemia. However, the precise loci involved are not established. To determine the role of the ventromedial hypoglycemia, we performed hypoglycemic clamp studies in conscious Sprague-Dawley rats with bilateral VMH lesions produced by local ibotenic acid injection 2 wk earlier. Rats with lesions in the lateral hypothalamic area, frontal lobe, sham operated (stereotaxic needle placement into hypothalamus without injection), and naive animals served as control groups. The clamp study had two phases. For the first hour plasma glucose was fixed by a variable glucose infusion at euglycemia (approximately 5.9 mM). Thereafter, for an additional 90 min, glucose was either allowed to fall to (a) mild hypoglycemia (approximately 3.0 mM) or (b) more severe hypoglycemia (approximately 2.5 mM). Glucagon and catecholamine responses of lateral hypothalamic area-, frontal lobe-lesioned, sham operated, and naive animals were virtually identical at each hypoglycemic plateau. In contrast, glucagon, epinephrine, and norepinephrine responses in the VMH-lesioned rats were markedly inhibited; hormones were diminished by 50-60% during mild and by 75-80% during severe hypoglycemia as compared with the other groups. We conclude that the VMH plays a crucial role in triggering the release of glucagon and catecholamines during hypoglycemia.

Norepinephrine-induced human platelet activation in vivo is only partly counteracted by aspirin.

Abstract: BACKGROUND Epinephrine and mental stress may, via platelet stimulation, enhance the risk of thrombus formation. Norepinephrine is more likely than epinephrine to activate platelets in vivo because of higher levels in plasma but is less well studied in this respect. The antiplatelet drug of choice for patients with coronary artery disease, aspirin, may be less effective during sympathoadrenal activation. We therefore investigated platelet responses in vivo to exogenous norepinephrine with and without aspirin pretreatment. METHODS AND RESULTS Platelet aggregability in vivo was assessed in 11 healthy male subjects, by filtragometry ex vivo (which reflects platelet aggregability in vivo) and by measurements of plasma beta-thromboglobulin (beta-TG, which reflects platelet secretion). Norepinephrine infusions elevated venous plasma norepinephrine from 1.5 to 4 and 15 nmol/L, respectively, and enhanced platelet aggregability (filtragometry) concentration dependently (P < .001). Platelet secretion (beta-TG levels) increased during high-dose infusion (P < .01). Aspirin pretreatment (500 mg orally 12 hours earlier) reduced the excretion of 11-dehydrothromboxane B2 by 62 +/- 5% (P < .001) and attenuated platelet aggregability at rest (P < .05) but not the effect of norepinephrine infusion on platelet aggregability. Conversely, resting plasma beta-TG levels and the urinary excretion of high-molecular-weight beta-TG were not altered by aspirin pretreatment, whereas the norepinephrine-induced increase in plasma beta-TG was abolished. CONCLUSIONS Norepinephrine, at plasma levels easily attained during exercise, enhances platelet aggregability and platelet secretion in vivo in healthy humans. Aspirin may be less effective as an antithrombotic drug during sympathoadrenal activation in humans.

High-dose epinephrine results in greater early mortality after resuscitation from prolonged cardiac arrest in pigs: a prospective, randomized study.

Abstract: To determine whether high-dose epinephrine (0.2 mg/kg) during cardiopulmonary resuscitation (CPR) results in improved outcome, compared with standard-dose epinephrine (0.02 mg/kg). A prospective, randomized, blinded study. Research laboratory of a university medical center. Thirty domestic swine were randomized to receive standard- or high-dose epinephrine during CPR after 15 mins of fibrillatory cardiac arrest. Three minutes of CPR were provided, followed by advanced cardiac life support per American Heart Association guidelines. Animals that were successfully resuscitated were supported for 2 hrs in an intensice care unit (ICU) setting, and then observed for 24 hrs. Electrocardiogram, aortic blood pressure, right atrial blood pressure, and end-tidal CO2 were monitored continuously until the intensice care period ended. Survival and neurologic outcome were determined. Return of spontaneous circulation was attained in 14 of 15 animals in each group. Four of 14 high-dose epinephrine pigs died during the ICU period after return of spontaneous circulation vs. zero of the 14 standard-dose pigs (p < .05). Six standard-dose pigs survived 24 hrs vs. four high-dose pigs. Twenty-four-hour survival rate and neurologic outcome were not significantly different. Within 10 mins of defibrillation, severe hypertension (diastolic pressure >120 mm Hg) occurred in 12 of 14 high-dose pigs vs. two of 14 standard-dose pigs (p 250 beats/min) occurred in seven of 14 high-dose pigs vs. zero of 14 standard-dose pigs (p < .01). All four high-dose epinephrine pigs that died during the ICU period experienced both severe hypertension and tachycardia immediately postresuscitation. High-dose epinephrine did not improve 24-hr survival rate or neurologic outcome. Immediately after return of spontaneous circulation, most animals in the high-dose epinephrine group exhibited a hyperadrenergic state that included severe hypertension and tachycardia. High-dose epinephrine resulted in a greater early mortality rate. (Crit Care Med 1994; 22:282–290)

Rapid and Selective Cyclic Voltammetric Measurements of Epinephrine and Norepinephrine as a Method To Measure Secretion from Single Bovine Adrenal Medullary Cells

Abstract: : Background-subtracted cyclic voltammetry at a scan rate of 800 V/s with carbon fiber microelectrodes has been used to detect and differentiate between epinephrine and norepinephrine. At very positive potentials (>l V vs. SSCE) in pH 7.4 aqueous buffer, a second oxidation wave is observed for epinephrine, a secondary amine. In contrast, the second oxidation wave is not observed for norepinephrine, a primary amine. The amplitude of the second wave for epinephrine is enhanced when the waveform employed does not allow reduction of the electrogenerated o-quinone back to epinephrine. This indicates that the oxidation process at the second wave must be preceded by adsorption of the o- quinone at the electrode surface. The temporal response of the method was investigated by iontophoretic ejection of catecholamine onto an electrode. The response time was found to be limited by the repetition rate of the cyclic voltammograms (16.7 ms in this work). This electrochemical technique was used to resolve catecholamine release from individual vesicles of cultured bovine adrenal medullary cells. Most of the adrenal medullary cells released either epinephrine or norepinephrine but 17% of the cells released mixtures of these two compounds. In these cells, each secretory vesicle appeared to contain either epinephrine or norepinephrine.

Norepinephrine and epinephrine levels in affected versus unaffected limbs in sympathetically maintained pain.

Abstract: Objective: To test the hypothesis that there is relative sympathetic hyperactivity in the affected limb in patients with sympathetically maintained pain syndromes by measuring serum norepinephrine and epinephrine in the affected versus the unaffected sides. Design: Venous pool samples were drawn just proximal to the affected area and from an identical site on the unaffected side. Serum norepinephrine and epinephrine were measured by high-pressure liquid chromatography with electrochemical detection. Subjects: Sixteen women and seven men with a mean age of 44.4 years diagnosed as having sympathetically maintained pain on the basis of a positive response to paravertebral block and a criteria-based diagnostic scheme. Results: The serum norepinephrine level was significantly lower in the affected limbs than the unaffected limbs (p = 0.024). The serum epinephrine level was not significantly different. Conclusions: These results are not consistent with the hypothesis of segmental sympathetic hyperactivity in the affected limb in sympathetically maintained pain and support a hypothesis of peripheral receptor upregulation with pathologic response to circulating catecholamines. Other possible explanations are discussed.

Epinephrine increases ATP production in hearts by preferentially increasing glucose metabolism.

Abstract: Although epinephrine is widely used clinically, its effect on myocardial energy substrate preference in the intact heart has yet to be clearly defined. We determined the effects of epinephrine on g...

Urinary and plasma catecholamines and urinary catecholamine metabolites in pheochromocytoma: diagnostic value in 19 cases.

Abstract: We review our data on the measurement of catecholamines and their metabolites in 19 patients with pheochromocytoma. All the assays were specific high-performance liquid chromatographic procedures with electrochemical detection. The assay of fractionated metanephrines was 100% sensitive. Normal values for both urinary norepinephrine and epinephrine were found in two asymptomatic patients with pheochromocytoma. Normal values for 3-methoxy-4-hydroxymandelic acid (VMA) were found in two patients with pure epinephrine-secreting tumors and in one patient with multiple endocrine neoplasia type II. Plasma catecholamines were usually less increased than their urinary counterparts. We recommend the specific measurement of norepinephrine and epinephrine as the initial test for patients with suggestive symptoms, and specific measurement of normetanephrine and metanephrine for patients in whom an adrenal mass is incidentally found. We argue against the use of total metanephrines, total catecholamines, and VMA because of their lack of diagnostic sensitivity.

Evidence that the effect of bicycle exercise on blood mononuclear cell proliferative responses and subsets is mediated by epinephrine.

Abstract: The present study was designed to test the hypothesis that the exercise-induced changes in blood mononuclear cell (BMNC) subsets, BMNC proliferative responses and lymphokine activated killer (LAK) cell activity are mediated by increased epinephrine concentrations. Healthy male volunteers 1) exercised on a bicycle ergometer (75% of VO2max, 1 h) and 2) on another day were given epinephrine as an intravenous infusion to obtain plasma epinephrine concentrations comparable with those seen during exercise. Blood samples were collected in the basal state, during the last minutes of exercise or epinephrine infusion and 2 h later. During both perturbations the %CD3+ and %CD4+ T cells declined and the %CD16+ NK cells increased. Two h afterwards the CD14+ monocytes increased, while no changes were observed in %CD8+ T cells or %CD20+ B cells. The phytohemagglutinin (PHA) response declined during both epinephrine infusion and exercise experiments. The changes in interleukin-2 (IL-2) effect on proliferation and cytotoxic activity (LAK cell activity) were more pronounced in exercise experiments than during epinephrine. Exercise and epinephrine caused increase in concentrations of lymphocytes and neutrophils, but the changes were more pronounced in exercise experiments. The results indicate that, in response to physical exercise, the rise in plasma epinephrine may contribute to the changes in cellular immunity.

Humans Anesthetized with Sevoflurane or Isoflurane Have Similar Arrhythmic Response to Epinephrine

Abstract: BackgroundAnesthetics can alter the dose of exogenously administered epinephrine that causes cardiac arrhythmias. The purpose of this study was to test the hypothesis that in humans anesthetized with sevoflurane, the arrhythmic response to epinephrine is not different from the response in humans ane

Effects of different techniques of endotracheal epinephrine administration in pediatric porcine hypoxic-hypercarbic cardiopulmonary arrest.

Abstract: ObjectiveTo compare three endotracheal epinephrine instillation techniques in a pediatric porcine hypoxic-hypercarbic cardiopulmonary arrest model.DesignProspective, randomized, laboratory comparison of three instillation techniques.SettingLarge animal research facility at a children's hospital.Subj

Differential secretion of catecholamines in response to peptidergic and cholinergic transmitters in rat adrenals.

Abstract: 1. Rat adrenal medulla is stimulated by cholinergic and peptidergic transmitters released from splanchnic nerves. The peptidergic transmitter has been identified as vasoactive intestinal polypeptide (VIP) and its contribution in comparison to that of acetylcholine (ACh) is more prominent at low neuronal activity. The purpose of this study is to determine if ACh and VIP cause differential secretion of adrenaline and noradrenaline and whether the differential secretion also occurs when splanchnic nerves are stimulated at different frequencies. 2. Perfusion of the left adrenal gland with Krebs solution for several hours did not change adrenaline and noradrenaline contents (15.2 micrograms and 3.5 micrograms, respectively) and their ratio (4.4) from those of the unperfused right adrenal medulla (15.2 micrograms, 3.3 micrograms and 4.8, respectively). 3. Perfusion with ACh (10 microM for 4 min) resulted in the secretion of 109 ng of catecholamines and the ratio of adrenaline to noradrenaline was 3.8. Although the secretion increased with increased concentrations of ACh (30 and 100 microM), the ratios remained between 3 and 4. 4. Perfusion with VIP (10 microM for 4 min) resulted in the secretion of 27 ng of catecholamines and the ratio of adrenaline to noradrenaline was 9.7. A higher concentration of VIP (20 microM for 4 min) resulted in the secretion of greater amounts of catecholamines (102 ng) without significantly altering the ratio of adrenaline to noradrenaline (10.9). 5. Perfusion with as low as 0.01 microM pituitary adenylate cyclase-activating polypeptide (PACAP) increased the secretion of catecholamines to 31 ng and the secretion increased in a dose-dependent manner up to 0.3 microM.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemostatic effects of stress hormone infusion

Abstract: Background Surgery causes changes in hemostasis, leading to a hypercoagulable state. This postoperative increase in hemostatic function is attenuated in patients receiving regional anesthesia compared with those receiving general anesthesia. Regional anesthesia also decreases the neuroendocrine response to surgery compared with general anesthesia, and this effect is hypothesized to be responsible for the differences in hemostatis. To test the hypothesis that neuroendocrine hormones cause changes in hemostasis, we infused stress hormones into normal volunteers and measured hemostatic function. Methods After drug screening, 12 normal volunteers were studied. On two admissions, volunteers randomly received either stress hormone (epinephrine, cortisol, or glucagon) or placebo infusion for 24 h. During infusion, patients remained at bed rest and received controlled meals. Blood was obtained from indwelling venous catheters before infusion and 2, 8, and 24 h after the start of infusion. Blood was analyzed for neuroendocrine hormone concentrations, glucose, complete blood count, coagulation proteins, platelet reactivity, and activity of the fibrinolytic system. Results In the stress hormone group, concentrations of epinephrine, norepinephrine, cortisol, glucagon, and insulin were increased during the infusion period compared with those in the placebo group. Glucose concentrations and white blood cell counts were increased in the stress hormone group compared with those in the placebo group. Circulating fibrinogen concentrations increased 30% and ex vivo collagen-induced platelet reactivity increased 123% (aggregation) and 103% (dense granule release) in the stress hormone infusion group, whereas there was no change in the placebo group. Fibrinolytic proteins were similar in both groups, demonstrating a decrease in plasminogen activator inhibitor-1 activity at 8 and 24 h (196% in the hormone group vs. 199% in the placebo group). Conclusions Infusion of stress hormones to concentrations found during surgery is safely tolerated and causes metabolic changes observed with surgery. Stress hormone infusion increases ex vivo platelet reactivity and fibrinogen concentrations that resemble changes seen postoperatively but does not recreate the postoperative decrease in fibrinolytic activity. Differences in neuroendocrine response between types of anesthesia may explain some postoperative changes in platelet function and acute phase reactivity, but additional uncharacterized factors are responsible for the differences in fibrinolysis.

High-Dose Epinephrine in Adult Cardiac Arrest

Abstract: Background. Recent studies suggest that doses of epinephrine of 0.1 mg per kilogram of body weight or higher may improve myocardial and cerebral blood flow as well as survival in cardiac arrest. Such studies have called into question the traditional dose of epinephrine (0.007 to 0.014 mg per kilogram) recommended for advanced cardiac life support. Methods. We randomly assigned 650 patients who had had cardiac arrest either in or outside the hospital to receive up to five doses of high-dose (7 mg) or standard-dose (1 mg) epinephrine at five-minute intervals according to standard protocols for advanced cardiac life support. Patients who collapsed outside the hospital received no advanced-life-support measures other than defibrillation before reaching the hospital. Results. There was no significant difference between the high-dose group (n = 317) and the standard-dose group (n = 333) in the proportions of patients who survived for one hour (18 percent vs. 23 percent, respectively) or who survived un...

Pathophysiology of obesity-related hypertension: role of insulin and the sympathetic nervous system

Abstract: Reviewed herein are data supporting the hypothesis that insulin and the sympathoadrenal system are involved in the pathogenesis of hypertension in the obese. Data from the Normative Aging Study, a population-based cohort followed in Boston, confirm other epidemiologic reports of a direct relationship between upper-body obesity, hyperinsulinemia, and hypertension. Because insulin is known to stimulate the sympathetic nervous system (SNS), the possibility that insulin-mediated sympathetic stimulation contributed to hypertension in the obese was investigated by the analysis of 24-h urinary norepinephrine (NE) excretion in this group. Urinary NE was directly correlated with body mass index and waist/hip ratio, supporting increased SNS activity in the obese. Epinephrine excretion, an index of adrenal medullary activity, was inversely related to obesity, and both high insulin and low epinephrine levels were independently correlated with lower levels of high-density lipoprotein cholesterol and higher levels of triglycerides. These results are consistent with the hypothesis that insulin-mediated sympathetic stimulation results in hypertension from concomitant sympathetic stimulation of the heart, vessels, and kidney. Reciprocal changes in adrenal medullary function contribute to the associated dyslipidemia. Therapeutic strategies aimed at diminishing insulin resistance and lowering insulin levels, and antagonizing the effects of sympathetic stimulation on the heart, the vessels, and the kidneys, would appear to have a solid physiological rationale in the obese.

Spectral-analysis of hemodynamics during infusions of epinephrine and norepinephrine in men

Abstract: Spectral analysis of fluctuations in heart rate (HR) and arterial blood pressure (BP) during a 6-h infusion of epinephrine (15 ng.kg-1.min-1) or norepinephrine (30 ng.kg-1.min-1) in 10 normotensive...

Low cord blood levels of catecholamine from a newborn of a pheochromocytoma patient.

Abstract: Association of pheochromocytoma and pregnancy is rare and usually related to high maternal and fetal mortality rates. Maternal effects of the tumor have been studied extensively and the clinical outcome has markedly improved during the last decade. However, the role of excess catecholamines on fetal development has been discussed very little. We report here a case of pheochromocytoma during pregnancy. In which catecholamine levels from the cord blood were low despite simultaneous elevated maternal values (1.93 and 29.46 nmol/l norepinephrine, respectively), possibly owing to the high activity of the catecholamine degradative enzymes monoamine oxidase and COMT at the placental level. We suggest that in pregnancies complicated by pheochromocytoma, fetal well-being may be related mainly to good control of maternal blood pressure instead of the amount of catecholamines in the fetal circulation, because the placenta performs a protective role through an effective process of hormone inactivation.

Involvement of capsaicin-sensitive nerves in regulation of insulin secretion and glucose tolerance in conscious mice

Abstract: The impact of sensory nerves in glucose-stimulated insulin secretion and glucose tolerance was investigated in conscious mice treated neonatally with either capsaicin (Cap) or vehicle (Veh). At 10-12 wk after Cap, both the early (1 min) insulin secretory response to intravenous glucose (2.8 mmol/kg) (by 67%) and glucose elimination were potentiated (P < 0.05). In contrast, basal insulin, glucagon, and glucose were not affected by Cap. Plasma norepinephrine and epinephrine levels did not differ between Cap- and Veh-treated animals, whereas the increase in plasma insulin levels normally induced by alpha-adrenoceptor blockade by phentolamine was absent after Cap treatment. In isolated islets, the insulin secretory response to glucose (20 mmol/l), carbachol (0.1 mmol/l), or phentolamine (0.5 mmol/l) was not affected after Cap. It is concluded that sensory denervation by Cap results in increased glucose tolerance, which is in part because of a potentiated early insulin response to glucose. This potentiation does not seem secondary to altered plasma catecholamine levels or to altered islet secretory capacity. The results suggest rather that Cap-sensitive nerves, by a local effector function and/or as the afferent loop of a neural reflex, exert inhibitory influences on insulin secretion.

Phentolamine reversal of epinephrine-induced digital vasospasm. How to save an ischemic finger.

Abstract: A 17-year-old girl accidently injected her thumb with an adult autoinjector epinephrine syringe, resulting in rapid digital ischemia. Local infiltration of 0.5% phentolamine mesylate injected at the puncture site immediately resolved the ischemia and resulted in no long-term sequelae. Similar cases of epinephrine-induced digital ischemia are reviewed herein, revealing phentolamine to be the drug of choice for reversal of this type of ischemia. Alternative attempts to restore blood flow included warm water immersion, amyl nitrite inhalations, metacarpal nerve block, and application of topical nitroglycerin paste; each was found to be ineffective. We conclude that digital ischemia secondary to accidental injection of epinephrine can be quickly and safely reversed with the use of 0.5% phentolamine locally infiltrated in the region of accidental injection.

Effects of estrogen on free fatty acid metabolism in humans.

Abstract: To determine whether estrogen directly affects effective adipose lipolysis, palmitate rate of appearances ([14C]palmitate) was measured in 15 postmenopausal women. Each volunteer was studied after > or = 2 mo of estrogen treatment and again after > or = 2 mo of estrogen deficiency. Plasma hormone concentrations were controlled and identical on the 2 study days with use of the pancreatic clamp technique, and the lipolytic response to epinephrine and epinephrine + phentolamine was assessed. Results showed that overall palmitate flux was greater (10-20%, P < 0.05) during the estrogen-deficient than during the estrogen-replete study. Adrenergic stimulation of lipolysis was not specifically influenced by estrogen treatment, and control of plasma hormone concentrations did not eliminate the difference in palmitate flux between the estrogen-deficient and estrogen-replete study days. We conclude that estrogen deficiency is associated with increased plasma free fatty acid availability and that estrogen likely has direct, albeit small, effects on adipose tissue lipolysis.

Pharmacokinetics of Cardiovascular Drugs in Children Inotropes and Vasopressors

Abstract: Infants and children with congenital or acquired heart disease and children with systemic disease often require pharmacological support of their failing circulation. Catecholamines may serve as inotropic (enhance myocardial contractility) or vasopressor (elevate systemic vascular resistance) agents. Noncatecholamine inotropic agents, such as the cardiac glycosides or the bipyridines, may be used in place of, or in addition to, catecholamines. Developmental changes in neonates, infants and children will affect the response to inotropic or pressor therapy. Maturation of the gastrointestinal tract, liver and kidneys alters absorption, metabolism and elimination of drugs, although there are few clear examples of this among the vasoactive drugs considered in this review. Changes in body composition affect the volume of distribution (Vd) and clearance (CL) of drugs. Developmentally based pharmacodynamic differences also affect the responses to both therapeutic and toxic effects of inotropes. These pharmacodynamic differences are based in part upon developmental changes in myocardial structure, cardiac innervation and adrenergic receptor function. For example, the immature myocardium has fewer contractile elements and therefore a decreased ability to increase contractility; it also responds poorly to standard techniques of manipulating preload. Available data suggest that dopamine and dobutamine pharmacokinetics are similar to those in adults. Wide interindividual variability has been noted. A consistent relationship between CL and age has not been demonstrated, although one investigator demonstrated an almost 2-fold increase in the CL of dopamine in children under the age of 2 years. The CL of dopamine appears to be reduced in children with renal and hepatic failure. Fewer data are available regarding the pharmacokinetics of epinephrine (adrenaline), norepinephrine (noradrenaline) and isoprenaline (isoproterenol). Digoxin pharmacokinetics have been extensively evaluated in infants and children. The Vd for digoxin is increased in infants and children. Children beyond the neonatal period display increased CL of digoxin, approaching adult values during puberty. Although it was previously thought that children both needed and tolerated higher serum concentrations of digoxin than adults, more recent studies indicate that adequate clinical response can be achieved with serum concentrations similar to those aimed for in adults, with decreased toxicity. Evaluation of studies of digoxin pharmacokinetics is complicated by the presence of an endogenous substance with digoxin-like activity on radioimmunoassay. Limited studies of amrinone pharmacokinetics in infants and children indicate a dramatically larger Vd, and a decreased elimination half-life in older infants and children, compared with values observed in adults.

Rank-related differences in cardiovascular function among wild baboons: role of sensitivity to glucocorticoids

Abstract: In a population of wild baboons living in East Africa, we have observed endocrine differences among individuals as a function of dominance rank. Among these differences, we previously observed indirect evidence for dominant males being more. responsive to sympathetic catecholamines than were subordinate males. The present report tests this explicitly. Male baboons of known rank were anesthetized, and sympathetic and parasympathetic activity was pharmacologically inhibited. In experiment I, males were challenged with epinephrine; over a wide dose range, dominant males had the largest and fastest rises in systolic pressure, the greatest peak systolic pressure, and the most rapid recovery from the epinephrine challenge. Similar rank-related differences in heart rate response to epinephrine also occurred. Experiment II showed that this phenomenon probably reflects rank-related differences at both the heart and vasculature. As evidence, the same rank differences in systolic blood pressure responsiveness occurred when males were challenged with the alpha receptor agonist phenylephrine (which predominantly constricts systemic veins and arterioles), while the same rank differences in heart rate responses occurred following stimulation with the beta receptor agonist isoproterenol (which selectively works at the heart). These data were obtained from animals stressed by anesthetization, known to cause considerable glucocorticoid secretion in this population. Such steroids are well known for their capacity to augment catecholamine action. In experiment III, we blocked endogenous glucocorticoid secretion with the steroidogenesis inhibitor metyrapone, and repeated the epinephrine challenge. Under these conditions, the rank differences in epinephrine responsiveness were eliminated. Thus, dominant males are not so much preferentially sensitive to catecholamine action, as much as to the potentiating effects of glucocorticoids upon such action. In agreement, we have observed previously that dominant males are also more sensitive to glucocorticoid negative feedback regulation. © Wiley-Liss, Inc.

The role of liver glucosensors in the integrated sympathetic response induced by deep hypoglycemia in dogs.

Abstract: The significance of the portohepatic glucosensors for counterregulation in deep hypoglycemia (i.e., glycemia 0.10). When compared with protocols I and III, the catecholamine response above basal was significantly greater during protocol II with liver and systemic deep hypoglycemia (7.30 +/- 1.51 and 2.89 +/- 0.5 nM for epinephrine and norepinephrine, respectively, P < 0.005). These values reflect net increases in the catecholamine responses of 100% and 85% for epinephrine and norepinephrine when compared with protocol I.(ABSTRACT TRUNCATED AT 250 WORDS)

Epinephrine, norepinephrine, and cortisol concentrations in cannulated seawater‐acclimated rainbow trout (Oncorhynchus mykiss) following black‐box confinement and epinephrine injection

Abstract: The present study investigates the effect of cannulation and chronic‘black-box’ confinement, as well as epinephrine administration (4–0 μg kg−1), on the degree and time-course of alterations in trout (Oncorhynchus mykiss) catecholamine and cortisol concentrations. Plasma cortisol concentrations in seawater trout acclimated to 3–6° C reached 104 ng ml−1 1 day after cannulation/confinement and remained elevated above resting levels (8 ng ml−1) until 6 days post-confinement. Although plasma epinephrine and norepinephrine generally declined over the period of confinement (day 1 approx. 12 nM; day 7 approx. 6 nM), norepinephrine titres were usually higher and more variable. Epinephrine injection caused elevations in plasma epinephrine levels but not in norepinephrine levels; epinephrine titres reaching 107 ± 26 nM (range 65–238 nM) at 2 min post-injection and returning to pre-injection levels by 30 min post-injection. Plasma cortisol increased by 20 ng ml−1 following epinephrine administration. Based on the time-course for post-confinement alterations in plasma cortisol, it appears that up to a week may be required before cannulated fish are completely acclimated to ‘black-box’ confinement. The findings suggest that meaningful results from experiments utilizing epinephrine injection and ‘black-box confinement are contingent upon: (1) knowledge of circulating epinephrine levels shortly after injection (i.e. within 2 min post-injection); and (2) an experimental design that takes into account the elevated cortisol titres that are inherent with cannulation/confinement and epinephrine injection.

Interleukin-1 regulates corticosterone secretion from the rat adrenal gland through a catecholamine-dependent and prostaglandin E2-independent mechanism.

Abstract: Studies from this and other laboratories have shown that interleukin-1 alpha (IL-1 alpha) stimulates corticosterone and prostaglandin (PG) release from primary cultures of rat adrenal cells. A previous report from our laboratory (1) indicated involvement of the alpha-adrenergic system in IL-1 alpha-stimulated corticosterone secretion from primary cultures of rat adrenal cells. The present experiments were conducted to determine the role of catecholamines and eicosanoids in IL-1-stimulated corticosterone release from primary rat adrenal cells. Primary adrenal cells were incubated for 24 h at 37 C with IL-1 alpha (10 nM), medium, or the appropriate agonist. After incubation, the supernatant was removed and assayed for epinephrine, prostaglandin E2 (PGE2), and corticosterone concentrations. At this time, untreated adrenal cells were fixed for immunohistochemical staining with a specific antirat tyrosine hydroxylase antibody. The results indicate that the primary adrenal cells contained 3.1 +/- 0.45% tyrosine...

Epinephrine-induced in vivo muscle glycogen depletion enhances insulin sensitivity of glucose transport.

Abstract: Muscle glycogen depletion by means of exercise is associated with increased insulin-stimulated glucose transport activity. To determine whether reduction in muscle glycogen content independent of m...