Showing papers on "Epinephrine published in 1996"
TL;DR: Epinephrine, either endogenously produced or administered as a component of sepsis treatment, may have a net antiinflammatory effect on the cytokine network early in the course of systemic infection.
Abstract: Short-term preexposure of mononuclear cells to epinephrine inhibits LPS-induced production of TNF, whereas preexposure for 24 h results in increased TNF production. To assess the effects of epinephrine infusions of varying duration on in vivo responses to LPS, the following experiments were performed: (a) Blood obtained from eight subjects at 4-24 h after the start of a 24-h infusion of epinephrine (30 ng/kg per min) produced less TNF after ex vivo stimulation with LPS compared with blood drawn before the start of the infusion, and (b) 17 healthy men who were receiving a continuous infusion of epinephrine (30 ng/kg per min) started either 3 h (EPI-3; n = 5) or 24 h (EPI-24; n = 6) were studied after intravenous injection of LPS (2 ng/kg, lot EC-5). EPI-3 inhibited LPS-induced in vivo TNF appearance and also increased IL-10 release (both P < 0.005 versus LPS), whereas EPI-24 only attenuated TNF secretion (P = 0.05). In separate in vitro experiments in whole blood, epinephrine increased LPS-induced IL-10 release by a combined effect on alpha and beta adrenergic receptors. Further, in LPS-stimulated blood, the increase on IL-10 levels caused by epinephrine only marginally contributed to concurrent inhibition of TNF production. Epinephrine, either endogenously produced or administered as a component of sepsis treatment, may have a net antiinflammatory effect on the cytokine network early in the course of systemic infection.
523 citations
TL;DR: It is suggested that IL-6 secretion is stimulated during exercise, possibly by catecholamines, whereas exogenous glucocorticoids attenuate this effect without affecting the catechlamine levels.
Abstract: In experimental animals, stress and catecholamines stimulate endogenous interleukin-6 (IL-6) secretion, whereas glucocorticoids inhibit it. To examine whether physical stress alters the secretion of IL-6 in humans, and to what extent this is correlated with catecholamines and modified by glucocorticoids, we performed high-intensity treadmill exercise test runs on 15 male volunteers, in a double-blind crossover design, after pretreatment with placebo, hydrocortisone, or dexamethasone. Plasma epinephrine and norepinephrine concentrations peaked 15 min after the start of exercise, whereas plasma IL-6 concentrations peaked twice, 15 min and 45 min after the onset of the test run. There was no difference in either the epinephrine or norepinephrine peaks among the three treatments, but the net area under the curve for IL-6 was smaller after hydrocortisone or dexamethasone than after placebo and smaller after dexamethasone than after hydrocortisone. A positive correlation was observed between peak plasma epinephrine or norepinephrine and IL-6 levels at 15 min. These findings suggest that IL-6 secretion is stimulated during exercise, possibly by catecholamines, whereas exogenous glucocorticoids attenuate this effect without affecting the catecholamine levels.
238 citations
TL;DR: Norepinephrine acts as a neurotransmitter at certain sites in the central nervous system and in the sympathetic nervous system at postganglionic neuroeffector junctions and can also act as a circulating hormone.
Abstract: The endogenous catecholamines — norepinephrine and epinephrine — are involved in the regulation of virtually every organ system. Norepinephrine acts as a neurotransmitter at certain sites in the central nervous system and in the sympathetic nervous system at postganglionic neuroeffector junctions. Epinephrine is primarily a circulating hormone produced by the adrenal medulla and other chromaffin tissue. Because norepinephrine comes from chromaffin tissue and overflows from sympathetic-nerve synapses, plasma concentrations of norepinephrine exceed those of epinephrine. Hence, norepinephrine can also act as a circulating hormone. Norepinephrine and epinephrine act through adrenergic receptors (also termed adrenoceptors). In this review, I will summarize . . .
185 citations
TL;DR: LpA may become the technique of choice for surgical removal of adrenal lesions and may also become the preferred method for removing pheochromocytoma.
Abstract: This study compares the outcome of laparoscopic adrenalectomy (LpA) in 23 patients using CO2 insufflation with the outcome of this procedure in another 8 patients with pheochromocytoma (7 unilateral, 1 bilateral) using helium for pneumoperitoneum. The adrenal lesions in the first group included nonfunctional adenoma (n = 3), aldosterone adenoma (n = 11), Cushing's adenoma (n = 6), and Cushing's disease (n = 3). The latter patients were compared with a third group of 8 patients with pheochromocytoma undergoing conventional transabdominal adrenalectomy (CTA). With both procedures, intraoperative changes in plasma catecholamine levels were studied during pheochromocytoma removal and the changes correlated with intraoperative cardiovascular derangements. LpA was successfully performed in 95% of patients with adrenal lesions and in 100% of patients with pheochromocytoma. There was no significant difference in laparoscopic adrenalectomy for pheochromocytoma compared to that for other adrenal lesions in terms of operative time, blood loss, hospital stay, analgesic requirements, and return to normal activity. The outcome was less favorable in pheochromocytoma patients undergoing CTA. The largest increase of catecholamine levels in pheochromocytoma patients occurred during tumor manipulation with both LpA (17.4-fold for epinephrine and 8.6-fold for norepinephrine) and CTA (34.2-fold for epinephrine and 13.7-fold for norepinephrine), but cardiovascular instability was associated only with CTA. LpA may become the technique of choice for surgical removal of adrenal lesions and may also become the preferred method for removing pheochromocytoma.
176 citations
TL;DR: It is concluded that in healthy overnight fasted men antecedent physiologic increases of plasma cortisol can significantly blunt epinephrine, norepinephrine, glucagon, and MSNA responses to subsequent hypoglycemia and this data suggest that increased plasma cortisol is the mechanism responsible for antecedents hypoglycingmia associated autonomic failure.
Abstract: The aim of this study was to determine the role of increased plasma cortisol levels in the pathogenesis of hypoglycemia-associated autonomic failure. Experiments were carried out on 16 lean, healthy, overnight fasted male subjects. One group (n = 8) underwent two separate, 2-d randomized experiments separated by at least 2 mo. On day 1 insulin was infused at a rate of 1.5 mU/kg per min and 2 h clamped hypoglycemia (53 +/- 2 mg/dl) or euglycemia (93 +/- 3 mg/dl) was obtained during morning and afternoon. The next morning subjects underwent a 2-h hyperinsulinemic (1.5 mU/kg per min) hypoglycemic (53 +/- 2 mg/dl) clamp study. In the other group (n = 8), day 1 consisted of morning and afternoon 2-h clamped hyperinsulinemic euglycemia with cortisol infused to stimulate levels of plasma cortisol occurring during clamped hypoglycemia (53 mg/dl). The next morning (day 2) subjects underwent a 2-h hyperinsulinemic hypoglycemic clamp identical to the first group. Despite equivalent day 2 plasma glucose and insulin levels, steady state epinephrine, norepinephrine, pancreatic polypeptide, glucagon, ACTH and muscle sympathetic nerve activity (MSNA) values were significantly (R < 0.01) blunted after day 1 cortisol infusion compared to antecedent euglycemia. Compared to day 1 cortisol, antecedent hypoglycemia produced similar blunted day 2 responses of epinephrine, norepinephrine, pancreatic polypeptide and MSNA compared to day 1 cortisol. Antecedent hypoglycemia, however, produced a more pronounced blunting of plasma glucagon, ACTH, and hepatic glucose production compared to day 1 cortisol. We conclude that in healthy overnight fasted men (a) antecedent physiologic increases of plasma cortisol can significantly blunt epinephrine, norepinephrine, glucagon, and MSNA responses to subsequent hypoglycemia and (b) these data suggest that increased plasma cortisol is the mechanism responsible for antecedent hypoglycemia causing hypoglycemia associated autonomic failure.
170 citations
TL;DR: High-dose epinephrine administration during cardiopulmonary resuscitation in a swine pediatric asphyxial cardiac arrest model improves outcome but did not improve 2-hr survival rate, 24-hr Survival rate, or neurologic outcome.
Abstract: ObjectiveTo determine whether high-dose epinephrine administration during cardiopulmonary resuscitation (CPR) in a swine pediatric asphyxial cardiac arrest model improves outcome (i.e., resuscitation rate, survival rate, and neurologic function) compared with standard-dose epinephrine.DesignA random
161 citations
TL;DR: Findings support the concept that ICA cells constitute an ICA signaling system capable of participating in cardiac regulation that appears to be independent of sympathetic innervation.
Abstract: We have identified a previously undescribed intrinsic cardiac adrenergic (ICA) cell type in rodent and human heart. Northern and Western blot analyses demonstrated that ICA cell isolates contain mRNA and protein of enzymes involved in catecholamine biosynthesis. Radioenzymatic catecholamine assays also revealed that the catecholamine profile of adult rat ICA cell isolates differed from that of sympathetic neurons. Unlike sympathetic neuronal cells, isolated ICA cells have abundant clear vesicles on electron microscopy. Endogenous norepinephrine and epinephrine constitutively released by ICA cells in vitro affect the spontaneous beating rate of neonatal rat cardiac myocytes in culture. Finally, ICA cells could be identified in human fetal hearts at a developmental stage before sympathetic innervation of the heart has been documented to occur. These findings support the concept that these cells constitute an ICA signaling system capable of participating in cardiac regulation that appears to be independent of sympathetic innervation.
152 citations
TL;DR: The finding that injections of amphetamine and epinephrine have comparable effects on memory is consistent with the view that amphetamine may modulate memory storage, at least in part, by inducing the release of epine cortisol from the adrenal medulla.
Abstract: This study examined glucocorticoid-adrenergic interactions in modulating acquisition and memory storage for inhibitory avoidance training. Systemically (s.c.) administered amphetamine (1 mg/kg), but not epinephrine (0.1 mg/kg) or the peripherally acting amphetamine derivative 4-OH amphetamine (2 mg/kg), given to rats shortly before training facilitated acquisition performance in a continuous multiple-trial inhibitory avoidance (CMIA) task. Adrenocortical suppression with the 11beta-hydroxylase inhibitor metyrapone (50 mg/kg; s.c.), given to rats 90 min before training, did not block the effect of amphetamine and did not affect acquisition performance of otherwise untreated animals. Retention of CMIA and one-trial inhibitory avoidance was enhanced by either pre- or posttraining injections of amphetamine as well as 4-OH amphetamine and epinephrine. The finding that injections of amphetamine and epinephrine have comparable effects on memory is consistent with the view that amphetamine may modulate memory storage, at least in part, by inducing the release of epinephrine from the adrenal medulla. Metyrapone pretreatment blocked the memory-enhancing effects of amphetamine, 4-OH amphetamine, and epinephrine but did not affect retention performance of otherwise untreated animals. Posttraining injections of different doses of epinephrine (ranging from 0.0001 to 1.0 mg/kg) produced a dose-dependent memory enhancement for inhibitory avoidance training and metyrapone blocked the memory-enhancing effects of all these doses. These findings provide further evidence that the sympathoadrenal and adrenocortical systems are intimately coupled during processes of memory storage.
129 citations
TL;DR: To evaluate whether arterial blood pressure within the first minutes and hours after return of spontaneous circulation influences neurological recovery in human cardiac arrest survivors, 136 retrospectively evaluated patients after sudden cardiac death were evaluated.
Abstract: Background and Purpose In animal cardiac arrest studies, outcome has been improved by inducing arterial hypertension early after return of spontaneous circulation. The aim of our study was to evaluate whether arterial blood pressure within the first minutes and hours after return of spontaneous circulation influences neurological recovery in human cardiac arrest survivors. Methods Of 136 retrospectively evaluated patients after sudden cardiac death, two groups were defined: group 1, mean arterial blood pressure (MABP) within 5 minutes after return of spontaneous circulation above 100 mm Hg; group 2, MABP of 100 mm Hg or less. Thereafter MABP was measured every 5 minutes until 2 hours after return of spontaneous circulation. The groups were compared in regard to age, sex, in/out of hospital, witnessed/not witnessed, first electrocardiographic rhythm, time from cardiac arrest to beginning of life support and to return of spontaneous circulation, cumulative epinephrine dose administered, and best neurologica...
120 citations
TL;DR: Overall cardiovascular function was not irreversibly or critically impaired after the administration of vasopressin in this pig model of cardiac arrest and there was a reversible depressant effect on myocardial function when compared with epinephrine.
Abstract: OBJECTIVE The administration of vasopressin during cardiopulmonary resuscitation (CPR) provides significantly more vital organ blood flow when compared with epinephrine during cardiac arrest in pigs. The effects of this potent vasoconstrictor on postresuscitation cardiovascular function remain unknown. The purpose of this study was to compare the effects of vasopressin and epinephrine on cardiovascular function in the postresuscitation phase after CPR. DESIGN Prospective, randomized, experimental study. SETTING University research laboratory. SUBJECTS Domestic pigs, 12 to 14 wks of age. INTERVENTIONS Sixteen pigs were randomly allocated to receive either 0.045 mg/kg of epinephrine or 0.4 U/kg of vasopressin after 4 mins of cardiac arrest. MEASUREMENTS AND MAIN RESULTS Hemodynamics, left ventricular contractility, and myocardial blood flow were measured for an interval of 240 mins after successful CPR. Differences between animals treated with epinephrine vs. vasopressin were most pronounced 15 mins after restoration of spontaneous circulation. At this time, mean aortic pressure was 64 +/- 6 (SEM) mm Hg in the epinephrine group and 84 +/- 6 mm Hg (p < .05) in the vasopressin group. Systemic vascular resistance was 1285 +/- 72 dyne.sec/cm5 in the epinephrine group and 2314 +/- 130 dyne.sec/cm5 (p < .001) in the vasopressin group. Cardiac index was 140 +/- 9 mL/min/kg in animals treated with epinephrine and 99 +/- 9 mL/min/kg (p < .01) in animals treated with vasopressin. Myocardial contractility (dp/ dtmax/P) was 52.8 +/- 3.4/sec with epinephrine as compared with 36.3 +/- 2.9 sec-1 (p < .01) with vasopressin. Left ventricular epicardial blood flow was 241 +/- 35 mL/min/100 g with epinephrine and 142 +/- 22 mL/min/100 g (p < .05) with vasopressin. Four hours after CPR, no significant differences were observed between groups. CONCLUSIONS In the early postresuscitation phase, vasopressin provided higher systemic blood pressures and there was a reversible depressant effect on myocardial function when compared with epinephrine. Overall cardiovascular function was not irreversibly or critically impaired after the administration of vasopressin in this pig model of cardiac arrest.
102 citations
TL;DR: The additional injection of absolute alcohol after endoscopic epinephrine injection confers no advantage and no difference was observed between the two with respect to either rebleeding or need for emergency operation.
TL;DR: This work recommends using an epinephrine concentration of 1:200,000 or 1:400,000 to provide optimal initial hemostasis while minimizing potential side effects.
Abstract: The addition of epinephrine to local anesthetics decreases bleeding, reduces systemic toxicity, and increases duration of action. However, epinephrine has significant side effects. Four concentrations of epinephrine were compared to determine the minimum concentration required for maximal vasoconstriction. Eighty-one subjects undergoing surgical procedures with general anesthesia were injected with 1% lidocaine containing varying concentrations of epinephrine. Blood flow measurements were then made at 1-minute intervals for 10 minutes using a laser Doppler flowmeter. There were no differences in blood flow reduction between epinephrine concentrations of 1:100,000, 1:200,000, and 1:400,000. However, epinephrine 1:800,000 provided significantly less vasoconstriction. We recommend using an epinephrine concentration of 1:200,000 or 1:400,000 to provide optimal initial hemostasis while minimizing potential side effects.
TL;DR: Lower-body adipose tissue FFA release increased in response to epinephrine in men but not women, whereas upper-body palmitate release increasedIn both groups, consistent with some in vitro findings and suggest that catecholamine action may play a role in determining gender-based differences in body fat distribution.
Abstract: Upper-body and lower-body adipocytes respond differently to physiological catecholamines in vitro. It is not known whether this is true in vivo or whether gender differences exist in the regional adipose tissue responses to epinephrine. These studies were therefore conducted to examine free fatty acid (FFA) release ([3H]palmitate) from lower-body (leg), splanchnic, and upper-body adipose tissue in normal-weight adult men (n = 8) and women (n = 7). In response to intravenous epinephrine (10 ng.kg-1.min-1), palmitate release increased (P < 0.01) in both men (168 +/- 10 to 221 +/- 15 mumol/min) and women (177 +/- 12 to 234 +/- 18 mumol/min). Basal leg palmitate release was similar in women and men (16.8 +/- 2.9 and 12.4 +/- 1.3 mumol/min, P = not significant) but doubled (P < 0.01) in response to epinephrine in men and was virtually unchanged in women. Splanchnic palmitate release increased (P < 0.05) in men (n = 6) but not in women (n = 6), whereas nonsplanchnic upper-body palmitate release increased more in women than in men. Upper-body (splanchnic and nonsplanchnic) palmitate release increased (P < 0.05) in both men and women in response to epinephrine. In summary, lower-body adipose tissue FFA release increased in response to epinephrine in men but not women, whereas upper-body palmitate release increased in both groups. These findings are consistent with some in vitro findings and suggest that catecholamine action may play a role in determining gender-based differences in body fat distribution.
01 Jan 1996
TL;DR: Investigating the effects of elevated EPI concentration on peripheral glucose disposal and insulin secretion by using the stable labeled intravenous glucose tolerance test in conjunction with the minimal models of labeled glucose disappearance and C-peptide secretion concluded that EPI selectively impairs peripheral glucose metabolism.
Abstract: Epinephrine (EPI) plays a pivotal role in regulating glucose metabolism both in splanchnic and peripheral tissues. Nevertheless, previous studies did not clarify the mechanisms by which EPI affect both glucose disposal processes in peripheral tissues and β-cell secretion. The aim of this study was to investigate, in six normal volunteers, the effects of elevated EPI concentration on peripheral glucose disposal and insulin secretion by using the stable labeled (either [6,6-2H2] or [2-2H1]glucose) intravenous glucose tolerance test (IVGTT) in conjunction with the minimal models of labeled glucose disappearance and C-peptide secretion. Elevated plasma EPI concentration significantly decreased glucose effectiveness (SG*) by 29% (0.0059 ± 0.0013 vs. 0.0083 ± 0.0011 min−1, P < 0.05), and even more, 61%, insulin sensitivity (SI*); (22 ± 6 · 10(4) vs. 54 ± 20 · 10(4) min−1.pmol.l−1; P < 0.01). These findings are not due to an isotopic effect induced by an enhanced glycogen breakdown, because the [2-2H1]glucose tracer, which is not incorporated into glycogen, gave results similar to those of [6,6-2H2]glucose tracer. No differences were observed in first phase cell sensitivity, phi 1, in the EPI study (199 ± 91 vs. 245 ± 144 10(9), NS), but there was a significant increase in the second-phase cell sensitivity to glucose phi 2, (15.2 ± 1.7 vs. 17.7 ± 4.4 10(9).min−1, P < 0.05). In conclusion, EPI selectively impairs peripheral glucose metabolism because of its unique ability to simultaneously and independently decrease glucose effectiveness and insulin sensitivity. Furthermore, EPI enhances phi 2, the ratio between the C-peptide amount secreted during the second phase and the area under the curve of the glucose signal, indicating that the observed increase of C-peptide concentration is due not only to the augmented glucose signal but also to a specific EPI-mediated enhancement of β-cell responsivity to glucose.
TL;DR: Cortisol plays a pivotal role in the metabolic response to stress hormone infusion by sustaining gluconeogenesis through a stimulatory effect on hepatic gluconeogenic precursor supply and by maintaining hepatic glycogen availability.
Abstract: The role of cortisol in directing the metabolic response to a combined infusion of glucagon, epinephrine, norepinephrine, and cortisol (stress hormones) was investigated. Chronically catheterized, conscious fasted dogs were studied before hormone infusion and after a 70-hour stress hormone infusion containing glucagon, epinephrine, norepinephrine, and cortisol (n = 11) or containing all these hormones except cortisol (n = 5). Combined stress hormone infusion increased arterial plasma glucagon, cortisol, epinephrine, and norepinephrine approximately sixfold. Whole-body glucose production (Ra), glycogenolysis, and gluconeogenesis were assessed using tracer and arteriovenous-difference techniques. The absence of an increase in cortisol during stress hormone infusion attenuated the increase in arterial plasma glucose concentration and Ra (delta 81 +/- 16 v 24 +/- 3 mg/dL and 1.7 +/- 0.3 v 0.8 +/- 0.4 mg/ kg/min, respectively). However, it did not alter the increase in net hepatic glucose output (delta 0.7 +/- 0.3 v 0.8 +/- 0.4 mg/kg/min). When the increase in cortisol was absent, the increase in net hepatic gluconeogenic precursor uptake was attenuated (delta 0.7 +/- 0.3 v 0.1 +/- 0.3 mg glucose/kg/min) due to a decrease in gluconeogenic precursor levels. The efficiency of gluconeogenesis increased to a greater extent (delta 0.19 +/- 0.07 v 0.31 +/- 0.11) when cortisol was not infused. The absence of an increase in cortisol also led to marked glycogen depletion in the liver (10 +/- 4 v 55 +/- 10 mg/g liver). Cortisol thus plays a pivotal role in the metabolic response to stress hormone infusion by sustaining gluconeogenesis through a stimulatory effect on hepatic gluconeogenic precursor supply and by maintaining hepatic glycogen availability.
TL;DR: It is likely that cortisol is the active adrenal hormone involved, supporting the theory that cortisol plays a crucial role in the clearance of lung liquid at birth.
Abstract: Our aim was to determine the role of the fetal adrenal glands in the gestational age-related increase in the ability of epinephrine to induce the reabsorption of lung liquid. Fetal lung liquid volumes and secretion rates were measured in five chronically catheterized control and six bilaterally adrenalectomized (ADX) fetal sheep at approximately 5-day intervals from 120 to 144 days of gestation (term approximately 146 days). The ability of epinephrine to induce the reabsorption of fetal lung liquid was then determined on day 144. Fetal adrenalectomy prevented the preparturient increase in fetal plasma cortisol and 3,5,3'-triiodothyronine (T3) concentration and significantly reduced the gestational age-related increase in fetal lung liquid volumes and secretion rates. Close to term (144 days), epinephrine infusions caused a significantly greater rate of lung liquid reabsorption in control (32.2 +/- 4.8 ml/h) compared with ADX (3.7 +/- 0.7 ml/h) fetuses. We conclude that the presence of the fetal adrenal glands is necessary for the age-related increase in 1) the lung liquid secretion rate and 2) the ability of the fetal lung to reabsorb liquid late in gestation. It is likely that cortisol is the active adrenal hormone involved, supporting the theory that cortisol plays a crucial role in the clearance of lung liquid at birth.
TL;DR: Epinephrine and norepinephrine stimulated macrophages to suppress the growth of Mycobacterium avium and mediates its effect by stimulating the expression of macrophage activation genes.
TL;DR: Hemodynamic responses to intravascular injection of test doses vary with dose of epinephrine and depth and type of general anesthetic used, Thus, the 15 micro gram epinphrine contained in the standard test dose may not be sufficient during all anesthetic conditions.
Abstract: Background Epidural anesthesia is sometimes initiated during general anesthesia, yet few data exist concerning efficacy of epinephrine-containing test doses. Methods Thirty-six patients were randomized to receive either 0.5 MAC isoflurane, 1 MAC isoflurane, or 0.5 MAC each (1 MAC total) of isoflurane and nitrous oxide. Each subject received intravenous saline followed by three test doses containing 45 mg lidocaine with 7.5, 15, and 30 micro gram epinephrine in a randomized, double-blind fashion. Heart rate and systolic, diastolic, and mean blood pressures were measured for 5 min after injection. Positive hemodynamic criteria identifying intravascular injection were determined from peak increases in hemodynamics during administration of saline. Dose-effect relationships between epinephrine and peak increases in hemodynamics were assessed with linear regression. Minimum required doses of epinephrine to produce peak positive hemodynamic increases on average were determined from linear regression. Results Positive hemodynamic criteria were identified as increases in heart rate greater or equal to 8 beats/min, systolic blood pressure greater or equal to 13 mmHg, diastolic blood pressure greater or equal to 7 mmHg, and mean blood pressure greater or equal to 9 mmHg. Significant dose-effect relationships were observed for epinephrine and peak increases in hemodynamics (correlation coefficients ranged from 0.61–0.91). Minimum required doses of epinephrine ranged from 6 to 19 micro gram depending on hemodynamic measurement and anesthetic group. Conclusions Hemodynamic responses to intravascular injection of test doses vary with dose of epinephrine and depth and type of general anesthetic used. Thus, the 15 micro gram epinephrine contained in the standard test dose may not be sufficient during all anesthetic conditions.
TL;DR: In this article, the severity and reversibility of no-reflow after cardiac arrest was investigated in adult normothermic cats with 5, 15 and 30 min cardiac arrest by ventricular fibrillation.
TL;DR: The responsiveness of platelets only to epinephrine was markedly impaired in 23/140 (16%) healthy Japanese and 3H methyl-yohimbine binding studies indicated that this defect was due to the decreased number of alpha 2 adrenergic receptor.
TL;DR: Neither the plasma renin-angiotensin activity, aldosterone concentration nor cardiovascular parameters were significantly influenced by repeated cold water immersions, and apparently, the repeated cold stimuli were not sufficient to induce significant adaptational changes in sympathetic activity and hormone production.
Abstract: The purpose of this study was to determine whether or not repeated short-term cold water immersions can induce a change in the activity of the sympathetic nervous system and, consequently, in cardiovascular functions in healthy young athletes. Changes in some plasma hormone concentrations were also followed. A single cold water immersion (head-out, at 14°C, for 1 h) increased sympathetic nervous system activity, as evidenced by a four-fold increase (P < 0.05) in plasma noradrenaline concentration. Plasma adrenaline and dopamine concentrations were not increased significantly. Plasma renin-angiotensin activity was reduced by half (P < 0.05) during immersion but plasma aldosterone concentration was unchanged. Stimulation of the sympathetic nervous system during immersion did not induce significant changes in heart rate, but induced peripheral vasoconstriction (as judged from a decrease in skin temperature) and a small increase (by 10%) in systolic and diastolic blood pressures. No clear change in reactivity of the sympathetic nervous system was observed due to repeated cold water immersions (three times a week, for 6 weeks). Neither the plasma renin-angiotensin activity, aldosterone concentration nor cardiovascular parameters were significantly influenced by repeated cold water immersions. A lowered diastolic pressure and an increase in peripheral vasoconstriction were observed after cold acclimation, however. Evidently, the repeated cold stimuli were not sufficient to induce significant adaptational changes in sympathetic activity and hormone production.
TL;DR: In conclusion, neural and humoral mechanisms exert redundant control with regard to responses of catecholamines and pituitary hormones (growth hormone and adrenocorticotropic hormone) in contrast, neural input from motor centers and feedback from working muscle are important for glucose production and lipolysis during exercise in humans.
Abstract: Hormonal and metabolic responses to electrically induced dynamic exercise were investigated in eight healthy young men with afferent neural influence from the legs blocked by epidural anesthesia (25 ml of 2% lidocaine) at L3-L4. This caused cutaneous sensory anesthesia below T8-T9 and complete paralysis of the legs. Cycling increased oxygen uptake to 1.90 +/- 0.13 (SE) l/min, and fatigue developed after 22.7 +/- 2.7 min. Compared with voluntary exercise at the same oxygen uptake and heart rate, concentrations of blood and muscle lactate (musculus vastus lateralis) as well as plasma potassium increased more while muscle glycogen decreased more during electrically induced exercise. Hepatic glucose production always rose during exercise. However, during involuntary exercise with sensory blockade, it did not match the rise in peripheral glucose uptake and plasma glucose decreased (P < 0.05). Plasma glycerol increased less in electrically induced vs. voluntary exercise, and free fatty acids and beta-hydroxybutyrate decreased only during electrically induced exercise. Epinephrine, growth hormone, adrenocorticotropic hormone, and cortisol levels were higher during involuntary vs. voluntary exercise (P < 0.05). In conclusion, neural and humoral mechanisms exert redundant control with regard to responses of catecholamines and pituitary hormones (growth hormone and adrenocorticotropic hormone). In contrast, neural input from motor centers and feedback from working muscle are important for glucose production and lipolysis during exercise in humans. Humoral feedback is apparently not sufficient to trigger normal mobilization of extramuscular fuel stores.
TL;DR: Data suggest that the major electrocardiographic effect of epinephrine infusion is mediated by increased calcium current, and at dosages > 80 ng/kg/min, plasma epinphrine concentrations are comparable to those observed with severe stress, and hypokalemia is common.
Abstract: Although increases in serum epinephrine are known to cause hypokalemia, the epinephrine dosages and concentrations at which this effect occurs, and the electrocardiographic consequences, have not been evaluated. Because epinephrine infusion is now being used to provoke arrhythmias in some patients, we have determined the physiologic effects of a range of dosages of epinephrine. The effects of pretreatment with propranolol and diltiazem on these indexes of epinephrine effect were also evaluated. Epinephrine dose ranging started at 10 ng/kg/min, with doubling of the dose every 10 minutes until a predetermined end point was reached. At the end of each dosage level, serum electrolytes, catecholamines, and an electrocardiogram were recorded. Whereas even the lowest dosage of epinephrine significantly increased heart rate, serum glucose levels increased and serum potassium decreased only when dosages of 160 to 320 ng/kg/min were administered. Plasma concentrations of epinephrine at these dosages were mean +/- SD 1,328 +/- 902 pg/ml, comparable to those observed in these subjects during maximal exercise (1,003 +/- 527 pg/ml). The major electrocardiographic effect of epinephrine infusion was a dose-related increase in QTc, but pretreatment with propranolol blunted this effect and tended to shorten QTc. At an epinephrine dose of 40 ng/kg/min, QTc prolongation persisted and was inhibited by diltiazem. These data suggest that the major electrocardiographic effect of epinephrine infusion is mediated by increased calcium current. At dosages > 80 ng/kg/min, plasma epinephrine concentrations are comparable to those observed with severe stress, and hypokalemia is common. The use of epinephrine as an electrophysiologic provoker at dosages > 80 ng/kg/min results in both a direct effect, as well as an indirect effect due to hypokalemia.
TL;DR: The role of the hippocampal cholinergic neurons during immobilization stress in rats using a microdialysis technique was investigated and the response of acetylcholine and the other responses to immobilization Stress were not parallel.
TL;DR: This review presents an emerging view that the selective control of EPI and NE cells is accounted for, first, by the existence of separate neural circuits between brain centers and the chromaffin cells, and second, through neuromodulation that selectively influences EPIand NE cells.
Abstract: The innervation of the adrenal medulla regulates the release of catecholamines from the two, epinephrine (EPI) and norepinephrine (NE), populations of chromaffin cells. Adjustments in the neural output to the adrenal medulla are made by centers in the brain that integrate the sensory input arising from a variety of challenges and the resulting changes in secretion assist in the restoration of homeostasis. Interestingly, the adrenal medullary secretory responses do not simply reflect increments a fixed ratio of EPI to NE as might be expected if release was proportional to the number EPI and NE cells. Instead, the ratio of EPI to NE changes depending on the magnitude and type of stimulus that initiates neural activation of the medulla. The variability in the EPI:NE release ratio implies that the EPI and NE cells can be differentially stimulated. Although the underlying mechanisms are not fully characterized, this review presents an emerging view that the selective control of EPI and NE cells is accounted for, first, by the existence of separate neural circuits between brain centers and the chromaffin cells, and second, through neuromodulation that selectively influences EPI and NE cells. The presence of mechanisms that allow for separate control of the EPI and NE cells may significantly augment the range of cardiovascular and metabolic responses mediated through activation of the adrenal medulla.
TL;DR: The results suggest that alpha 2-adrenoceptor mechanisms which mediate analgesia may have evolved early in vertebrate evolution and that descending epinephrine-containing fibers in the amphibian nervous system may be the source of endogenous catecholamines regulating nociceptive sensitivity inThe amphibian spinal cord.
TL;DR: The very low cAMP levels generated by dopamine, dobutamine, and dopexamine (even in high concentrations) support other evidence that these agents have little direct effect on the beta 2-adrenoceptor, andEpinephrine and isoproterenol are the most efficacious and potent direct-acting beta 2 -adrenergic receptor agonists using this lymphocyte cAMP model.
TL;DR: The data indicate that the cryoprotectant output response during freezing of R. sylvatica is mediated by cAMP-dependent mechanisms within the liver under the control of plasma hyperglycemic hormones.
TL;DR: This adrenal gland sympathetic hyperactivity registered in somatic patients is similar to that observed in mammals which fail to cope with stress and contrary to the profile registered in depressed subjects who show NA but not AD rise.
Abstract: Background: Previous clinical research has shown that severely ill (somatic) as well as many psychosomatic patients show raised noradrenaline (NA), adrenaline (AD), cortisol, free serotonin (f5HT) and platelet aggregability. Conversely, they show reduced NA/AD plasma ratio and platelet serotonin (p5HT). They also show adrenal hyperresponsiveness to an oral glucose load. These findings are opposed to those observed in depressed patients who show adrenal gland sympathetic hyporesponsiveness and neural sympathetic hyperactivity. Objective: To investigate adrenal gland and neural sympathetic systems as well as the other parameters in nondrepressed severely ill patients through the orthostasis exercise stress test which in normals triggers NA but no AD rise. Methods: We investigated 35 severely ill patients and their age- and sex-paired controls. Systolic, diastolic pulse pressure (PP), heart rate and neuroendocrine parameters were measured supine (0 min), at orthostasis (1 min) and exercise (5 min). A second test was performed 2 weeks later, after atropine injection. Multivariate analysis of variance, paired t test and Pearson product-moment test were employed. Results: The normal PP orthostasis fall was not observed in patients. At this period, an abnormal AD peak substituted the normal NA peak. The normal p5HT-f5HT orthostasis-exercise peaks were absent in patients. Cortisol and platelet aggregability were raised in patients. Conclusions: Severely ill (somatic) patients responded to the orthostasis-exercise stress test with adrenal and corticosuprarenal but not neural sympathetic activity. They did not show the normal parasympathetic activity at orthostasis. This adrenal gland sympathetic hyperactivity registered in somatic patients is similar to that observed in mammals which fail to cope with stress and contrary to the profile registered in depressed subjects who show NA but not AD rise.
TL;DR: Good functional neurological recovery was independently and positively associated with arterial blood pressure during the first 2 hours after human cardiac arrest but not with hypertensive reperfusion within the first minutes after return of spontaneous circulation.