Showing papers on "Epinephrine published in 1995"

Epinephrine Increases the Severity of Postresuscitation Myocardial Dysfunction

Abstract: Background Epinephrine has been the mainstay for cardiac resuscitation for more than 30 years. Its vasopressor effect by which it increases coronary perfusion pressure is likely to favor initial resuscitation. Its β-adrenergic action, however, may have detrimental effects on postresuscitation myocardial function when administered before resuscitation because it increases myocardial oxygen consumption. In the present study, our focus was on postresuscitation effects of epinephrine when this adrenergic agent was administered during cardiopulmonary resuscitation. Postresuscitation myocardial functions were compared with those of a selective α-adrenergic agent, phenylephrine, when epinephrine was combined with a β1-adrenergic blocking agent, esmolol, and saline placebo. Methods and Results Ventricular fibrillation was induced in 40 Sprague-Dawley rats. Mechanical ventilation and precordial compression was initiated either 4 or 8 minutes after the start of ventricular fibrillation. The adrenergic drug or salin...

No-reflow after cardiac arrest

Abstract: Successful resuscitation of the brain requires unimpaired blood recirculation. The study addresses the question of the severity and reversibility of no-reflow after cardiac arrest. Adult normothermic cats were submitted to 5, 15 and 30 min cardiac arrest by ventricular fibrillation. The extent of no-reflow was assessed in each cardiac arrest group after 5 min closed chest cardiac massage in combination with 0.2 mg/kg epinephrine or after successful resuscitation followed by 30 min recirculation. Reperfusion of the brain was visualized by labelling the circulating blood with FITC-Albumin. Areas of no-reflow, defined as absence of microvascular filling, were identified by fluorescence microscopy at 8 standard coronal levels of forebrain, and expressed as percent of total sectional area. During cardiac massage, noreflow affected 21±5%, 42±38% and 70±27% of forebrain after 5, 15 and 30 min cardiac arrest, respectively. After 30 min spontaneous recirculation following successful resuscitation of the heart, no-reflow significantly declined to 7±11% after 5 min cardiac arrest (p<0.05) but persisted in 30±11% and 65±21% of forebrain after 15 and 30 min cardiac arrest, respectively (n.s.). Our observations demonstrate that resuscitation of the heart by closed chest massage causes severe (and after prolonged cardiac arrest irreversible) no-reflow of the brain. This suggests that no-reflow is an important cause of postresuscitation brain pathology.

Effects of aging on epinephrine secretion and regional release of epinephrine from the human heart.

Abstract: In contrast to the sympathetic nervous system, which is activated by aging in at least some sympathetic nervous outflows, epinephrine release from the adrenal medulla appears to be either normal or low in the elderly. Using isotope dilution methodology, we studied the effect of aging on the secretion of epinephrine in 19 men, aged 20-30 yr, and 15 men, aged 60-75 yr. Measurements were made both at rest and during the application of laboratory stressors, as diminished adrenal medullary responsiveness possibly contributes to the impairment of some cardiovascular and metabolic responses to stress described previously in the elderly. Epinephrine secretion at rest was lower in the older men (mean +/- SEM, 0.86 +/- 0.10 nmol/min) than in the younger men (1.45 +/- 0.17 nmol/min; P < 0.05). Due to 20% lower plasma epinephrine clearance in the older men (P < 0.01), the reduction in the plasma concentration of epinephrine (0.37 +/- 0.03 vs. 0.52 +/- 0.06 nmol/L; P = 0.06) was proportionally less than that in epinep...

Lymphocyte Subset Redistribution in Response to Acute Experimental Stress: Effects of Gender, Ethnicity, Hypertension, and the Sympathetic Nervous System

Abstract: This study examined demographic and adrenergic characteristics associated with enumerative immune responses to acute laboratory stress. Lymphocyte subsets and plasma catecholamines were measured in 110 subjects at rest and following a naturalistic speaking stressor. Lymphocyte β2-adrenergic receptor sensitivity and density were measured at rest. The speaking task caused marked increase in natural killer cells, T-suppressor/cytotoxic cells, total WBC, norepinephrine, and epinephrine and decreases in T-helper cells, B cells, and the T-helper/suppressor ratio. Multiple regression analyses demonstrated that, in general, cellular immune responses were best predicted by a combination of lower basal norepinephrine, higher β2-adrenergic receptor sensitivity, and a greater stress-induced increase in norepinephrine. The findings suggest that traditional epidemiologic characteristics such as gender, ethnicity, and mild hypertension have limited influence on lymphocytosis. Rather, interindividual differences in sympathetic nervous system characteristics play a more prominent underlying role in acute cellular immune system activation.

The Clinical Efficacy of Nebulized Racemic Epinephrine and Albuterol in Acute Bronchiolitis

Abstract: Objective: To investigate whether nebulized racemic epinephrine or albuterol improves respiratory distress in infants with acute bronchiolitis. Design: A randomized, placebo-controlled, double-blind study. Setting: A university hospital providing primary hospital care for all pediatric patients in a defined area. Patients: One hundred consecutive infants younger than 24 months treated in the hospital for acute bronchiolitis. Intervention: The patients received two inhalations at 30-minute intervals: racemic epinephrine followed by physiologic saline (REP group; n=24), albuterol followed by physiologic saline (AP group; n=27), physiologic saline followed by racemic epinephrine (PRE group; n=24), and physiologic saline followed by albuterol (PA group; n=25). All patients received intramuscular epinephrine 60 minutes after the beginning of the study. Main Outcome Measures: Oxygen saturation, respiratory rate, and two clinical scores were used: one based on wheezing and retractions (Respiratory Distress Assessment Instrument) and the other based on changes in wheezing, retractions, and respiratory rate (Respiratory Assessment Change Score). Main Results: During the study, there were no significant differences among the four groups in clinical scores, oxygen saturations, and respiratory rates. Mean Respiratory Distress Assessment Instrument scores improved significantly within the REP, PRE, and AP groups 15 minutes after the first inhalation. In only the REP group, which received racemic epinephrine, the confidence limits did not overlap. A comparison of paired data of each patient revealed that the difference in Respiratory Assessment Change Score was significant between racemic epinephrine and physiologic saline, but not between albuterol and physiologic saline. Intramuscular epinephrine significantly improved Respiratory Distress Assessment Index scores in those groups treated earlier with racemic epinephrine (REP and PRE groups). No significant adverse effects were seen in any group or at any phase of the study. Conclusions: Elimination of hypoxia by supplemental oxygen and moistening of inspired air relieve the symptoms of acute bronchiolitis. Nebulized racemic epinephrine and albuterol are safe and useful in the treatment of acute bronchiolitis. Improvements in symptom scores at 15 minutes favor the use of racemic epinephrine. As the action of epinephrine is short, the effect can be increased by repeated inhalations. (Arch Pediatr Adolesc Med. 1995;149:686-692)

Sustained elevation in circulating catecholamine levels during polymicrobial sepsis.

Abstract: Although studies have indicated that the levels of catecholamines increase during sepsis, it remains unknown whether the elevated levels of epinephrine, norepinephrine, and dopamine observed in early sepsis are sustained during late, hypodynamic stages of sepsis. In this study, rats were subjected to sepsis by cecal ligation and puncture (CLP, i.e., polymicrobial sepsis). Immediately after CLP or sham operation, animals received 3 mL/100 g body weight normal saline subcutaneously. At .5, 2, 10 (i.e., early sepsis), or 20 h (late sepsis) after CLP, blood samples were drawn and the plasma was separated. Plasma levels of epinephrine, norepinephrine, and dopamine were determined using a [3H]-radioenzymatic assay. The results indicate that plasma levels of epinephrine, norepinephrine, and dopamine increased significantly as early as .5 h after CLP. The increase in catecholamine levels persisted throughout the study periods. Thus, circulating levels of catecholamines were elevated in both early and late stages of polymicrobial sepsis. These results suggest that the increased catecholamine levels at .5-10 h after CLP may contribute to the hypermetabolic conditions that occur during early, hyperdynamic sepsis. However, there is a lack of an association between the elevated plasma catecholamine levels and hypometabolic/hypodynamic state in late sepsis.

Role of epinephrine in TNF and IL-6 production from isolated perfused rat liver

Abstract: A bidirectional communication exists between the nervous system and the immune system. Evidence has accumulated suggesting that cytokines-immune peptides influence sympathetic neuronal survival and that cytokines can promote the secretion of catecholamines. Using an isolated perfused rat liver (IPRL) preparation, we have shown that the liver is an important source of circulating cytokines in response to lipopolysaccharide (LPS) and that corticosterone dose dependently influenced LPS-induced production of tumor necrosis factor (TNF) and interleukin-6 (IL-6). In this study, we investigated the direct effect of epinephrine (another stress hormone) on the production of TNF and IL-6 in liver. We demonstrated that epinephrine (1 microM/ml) alone did not induce TNF bioactivity but significantly increased IL-6 bioactivity from IPRL effluent. When the IPRL was infused with LPS, epinephrine significantly decreased TNF bioactivity. Epinephrine in LPS-treated livers also significantly increased IL-6 bioactivity. Both responses were totally inhibited by the beta-blocker propranolol (10 microM/ml). Anisomycin, a protein synthesis inhibitor, infused into the IPRL completely blocked the rise in TNF and IL-6 concentrations in the effluent leaving the IPRL, supporting the hypothesis that the synthesis (or release) of these cytokines was dependent on protein synthesis. We then attempted to determine whether epinephrine exerts similar effects in vitro. Using isolated Kupffer cells and hepatocytes, we found that epinephrine alone had no effect on TNF and IL-6 production in Kupffer cells and hepatocytes but significantly decreased LPS-induced TNF bioactivity and increased LPS-induced IL-6 bioactivity in Kupffer cells. Our data support the hypothesis that epinephrine can promote IL-6 secretion from IPRL.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of chronic NO synthase inhibition in rats on renin-angiotensin system and sympathetic nervous system.

Abstract: This study was designed to assess the role of renin and of the sympathoadrenal system in the maintenance of the hypertension induced by chronic nitric oxide synthase (NOS) inhibition in rats kept on a normal (RS) or a low-sodium (LS) diet. With the administration of NG-nitro-L-arginine methyl ester (L-NAME) in drinking water (0.4 milligrams) for 6 wk, mean intra-arterial blood pressure rose to a similar extent to 201 mmHg in the RS and 184 mmHg in the LS animals. Simultaneously, plasma norepinephrine was increased to 838 and 527 pg/ml and epinephrine to 2,041 and 1,341 pg/ml in RS and LS, respectively. Plasma neuropeptide Y levels did not change. Plasma renin activity rose to 21 ng.ml-1.h-1 in RS but remained at 44 ng.ml-1.h-1 in the LS. Both losartan (10 mg/kg) and phentolamine (0.1 mg/kg) intravenous bolus injections reduced blood pressure considerably in the L-NAME hypertensive animals. Whole brain NOS activity was reduced by 84%. Hypertension induced by chronic NOS inhibition in LS as well as in RS fed rats seems to be sustained by an interaction of several mechanisms, including the activation of the sympathetic nervous system and the renin-angiotensin system.

Anaphylactoid and Anaphylactic Reactions

Abstract: Studies have demonstrated greater hazards associated with anaphylaxis in patients receiving β-blockers. Serious anaphylaxis is more frequent. Evidence suggests this occurs via modulation of adenylate cyclase, which can influence release of anaphylactogenic mediators. Treatment of anaphylaxis in patients exposed to β-blockers is complicated because therapeutic administration of epinephrine (adrenaline) may be ineffective or promote undesired α-adrenergic and vagotonic effects. Risk reduction efforts should be considered for patients receiving β-blockers who are prone to experience anaphylaxis.

Epinephrine prolongs duration of subcutaneous infiltration of local anesthesia in a dose-related manner. Correlation with magnitude of vasoconstriction.

Abstract: Background and Objectives. Epinephrine is frequently combined with local anesthesia to prolong analgesia. Determination of the minimal concentration and the dose of epinephrine that produces prolongation of analgesia is important in the face of epinephrine9s potential for systemic and local toxicity. The authors undertook this study to determine a dose-response curve of epinephrine on duration of analgesia of both 1% lidocaine and 0.25% bupivacaine after local infiltration. In order to determine whether epinephrine-induced vasoconstriction affected duration of analgesia, the authors correlated duration of analgesia with magnitude of local vasoconstriction as measured with laser Doppler flowmetry. Methods. Six volunteers were studied in a randomized double-blind manner. Ten skin wheals of 0.2 mL solution were subcutaneously injected into both forearms of each volunteer. The solutions consisted of 1% lidocaine with epinephrine concentrations of 0, 1:50,000, 1:200,000, 1:800,000, and 1:3,200,000, and 0.25% bupivacaine with the same epinephrine concentrations. Duration of loss of sensation to pinprick at each wheal was recorded. Skin wheals with 0.2 mL of these same solutions were also subcutaneously injected into the abdomen of the same 6 volunteers, and laser Doppler flowmetry readings of skin blood flow were measured for 6 hours after injection. Results. Epinephrine prolonged duration of analgesia for both lidocaine and bupivacaine in a dose-related manner (P Conclusions. Epinephrine prolongs duration of analgesia after local infiltration in a dose-related manner. Addition of epinephrine in concentrations of 1:50,000 or 1:200,000 increases duration of analgesia after local infiltration by approximately 200%. Addition of doses as dilute as 1:3,200,000 still increases duration of analgesia by approximately 100%. Duration of analgesia appears to correlate with magnitude of epinephrine-induced vasoconstriction using laser Doppler flowmetry. Based on study data, the use of epinephrine in concentrations from 1:200,000 to 1:3,200,000 is recommended for prolongation of analgesia after local infiltration.

Circadian rhythm of vital signs, norepinephrine, epinephrine, thyroid hormones, and cortisol in schizophrenia

Abstract: Changes in the circadian rhythmicity in vital signs, catecholamines, thyroid hormones, and cortisol have been observed in psychiatric disorders, most notably in depression. With respect to schizophrenia, the literature is scanty. We report here on the circadian parameter estimates of the vital signs, epinephrine, norepinephrine, triiodothyronine, thyroxine, thyroid stimulating hormone, and cortisol in the blood of 34 healthy subjects, 89 drug-free schizophrenic patients, and 25 neuroleptic-treated schizophrenic patients. The analyses are based on the cosine model to fit the experimental data. The circadian profiles of heart rate, blood pressure, and oral temperature are similar among schizophrenic patients and healthy subjects. Neuroleptic-treated patients have significantly higher MESORs (the daily mean) of serum norepinephrine and epinephrine than healthy subjects. The TSH MESOR is significantly lower in schizophrenic patients; the MESOR of triiodothyronine also shows a tendency to be nonsignificantly lower in schizophrenic patients compared with control subjects. The circadian serum thyroxine and cortisol profiles are similar in the three groups. The data show that the circadian profiles of vital signs in drug-free chronic schizophrenic patients who are not chronically hospitalized are similar to those of healthy subjects and that the increase in serum catecholamines and the apparent lowering in some thyroid indices might induce a down-regulation in the noradrenergic receptor system that could contribute to the pathophysiology of schizophrenia.

The effects of epinephrine on lidocaine spinal anesthesia: a cross-over study.

Abstract: The efficacy of epinephrine for prolonging the duration of lidocaine spinal anesthesia remains controversial. Seven volunteers were randomized in a double-blind manner to receive two 50-mg lidocaine (in dextrose 7.5%) spinal anesthetics with and without epinephrine (0.2 mg). Sensory analgesia was assessed with transcutaneous electrical stimulation (TES) equivalent to surgical incision and compared to standard pinprick dermatomal levels. Motor block was assessed with surface electromyography (EMG) and isometric force dynamometry. Intravenous fluids were administered by a standardized regimen, and time until ability to void was determined. Addition of epinephrine significantly prolonged duration of surgical anesthesia in the lumbar and sacral dermatomes by an average of 16-29 min (P = 0.03), but not in thoracic dermatomes. Although there was a trend toward prolongation of motor block with addition of epinephrine, this did not reach statistical significance. Epinephrine significantly prolonged duration until ability to void from 153 +/- 27 to 234 +/- 50 min (P = 0.0001). Thus, addition of epinephrine to lidocaine may be indicated to prolong duration of anesthesia for lower body operations. However, delayed recovery of ability to void may also prolong time until discharge after ambulatory surgery.

A blind, randomized comparison of the circulatory effects of dopamine and epinephrine infusions in the newborn piglet during normoxia and hypoxia.

Abstract: Objective: To determine the hemodynamic responses to dopamine and epinephrine infusions in newborn piglets during normoxia and hypoxia Design: Prospective, randomized, blind crossover study Subjects: Newborn piglets (n=7) Interventions: Animals were acutely instrumented for measurements of cardiac output, pulmonary and systemic pressures, carotid and coronary artery blood flow, and coronary artery oxygen consumption Dopamine at infusion rates of 2 to 16 μg/kg/min and epinephrine 02 to 16 μg/kg/min were administered during normoxia Six piglets were similarly prepared and were then made hypoxic to an arterial O 2 saturation of 45% to 50% Epinephrine at infusion rates of 02 to 32 μg/kg/min and dopamine at rates of 2 to 32 μg/kg/min were administered in random order during hypoxia Measurements and Main Results: During normoxia, cardiac output increased similarly with both drugs and was significantly increased by ≥02 μg/kg/min of epinephrine and significantly increased by 8 or 16 μg/kg/min of dopamine Mean arterial blood pressure was not affected by dopamine but was significantly increased by epinephrine at a rate of 16 μg/kg/min The relative effects of the drugs on pulmonary and systemic vascular resistance differed, the pulmonary/systemic vascular resistance ratio was reduced at the higher doses of epinephrine (ie, 08 and 16 μg/kg/min) and was unaffected by dopamine Coronary artery oxygen consumption and coronary blood flow increased significantly with both medications at rates >04 and 4 μg/kg/min, respectively Increases of both variables were greater with epinephrine than with dopamine Myocardial extraction ratio was unaffected by dopamine and reduced at 02 and 16 μg/kg/min of epinephrine Hypoxia caused significant increases in cardiac index, systemic blood pressure, pulmonary arterial pressure, carotid artery blood flow, coronary artery blood flow, coronary oxygen consumption, coronary oxygen extraction ratio, and the pulmonary/systemic vascular resistance ratio Mean systemic arterial blood pressure increased significantly with 16 and 32 μg/kg/min of epinephrine, but was not significantly affected by dopamine at any infusion rate Cardiac index was not affected significantly by either of the medications Thus, there was a significant increase in the calculated systemic vascular resistance index with the highest dose of epinephrine, in contrast to the slight, statistically significant, decrease in calculated systemic vascular resistance index with the highest dose of dopamine Epinephrine significantly reduced pulmonary arterial pressures at 02, 04, and 08 μg/kg/min Dopamine had no effect on this variable The pulmonary/systemic vascular resistance ratio was significantly reduced by epinephrine at doses of 02 and 32 μg/kg/min, whereas the highest dose of dopamine caused a significant increase in the pulmonary/systemic vascular resistance ratio Conclusions: Epinephrine infusion during normoxia increases systemic pressure more than pulmonary arterial pressure at doses ≥8 μg/kg/min, and furthermore, produces a more appropriate hemodynamic profile in the presence of hypoxic pulmonary hypertension than dopamine infusion, in the acutely operated anesthetized piglet

Sodium bicarbonate may improve outcome in dogs with brief or prolonged cardiac arrest.

Abstract: Objective Despite the absence of outcome evaluation, the use of sodium bicarbonate in cardiac arrest has declined based on advanced cardiac life-support guidelines. The effects of bicarbonate therapy on outcome in a canine model of ventricular fibrillation cardiac arrest of brief (5-min) and prolonged (15-min) duration were examined. Design Prospective, randomized, controlled trial. Setting Experimental animal laboratory in a university medical center. Subjects Thirty-two adult dogs, weighing 10 to 17 kg. Interventions The animals were prepared with ketamine, nitrous oxide/oxygen, halothane, and pancuronium. Ventricular fibrillation was then electrically induced and maintained in arrest for 5 mins (n = 12) or 15 mins (n = 20). Canine advanced cardiac life-support protocols were instituted, including defibrillation, cardiopulmonary resuscitation (CPR), and the administration of epinephrine (0.1 mg/kg), atropine, and lidocaine. The bicarbonate group received 1 mmol/kg of sodium bicarbonate initially, and base deficit was corrected to -5 mmol/L with additional bicarbonate, whereas acidemia was untreated in the control group. Cardiopulmonary values were recorded at intervals between 5 mins and 24 hrs, and the neurologic deficit score was determined at 24 hrs after CPR. Measurements and Main Results The treatment group received an additional 2 to 3 mmol/kg of bicarbonate in the early postresuscitation phase. Compared with controls, the bicarbonate group demonstrated equivalent (with brief arrest) or improved (with prolonged arrest) return of spontaneous circulation and survival to 24 hrs, with lessened neurologic deficit. The acidosis of arrest was decreased in the prolonged arrest group without hypercarbia. Improved coronary and systemic perfusion pressures were noted in the bicarbonate group with prolonged arrest, and the epinephrine requirement for return of spontaneous circulation was decreased. Conclusions The empirical administration of bicarbonate improves the survival rate and neurologic outcome in a canine model of cardiac arrest.

Plasma catecholamines in patients with Addison's disease

Abstract: Summary BACKGROUND AND OBJECTIVE TWO endocrine tissues are present within the adrenal gland: the steroid producing cortical cells and the catecholamine producing chromaffin cells. Glucocorticolds occur in high concentrations in the adrenal medulla. In vitro, glucocorticolds have been shown to induce the enzyme phenyl-N-methyl-transferase which is necessary for the production of adrenaline in adrenal medullary cells. The purpose of this study was to evaluate the possible significance of a local glucocorticold effect on adrenomedullary function. DESIGN Plasma catecholamine levels were measured in patients with autoimmune Addison's disease where local production of corticosterolds is deficient In the presence of intact chromaffin tissue. MEASUREMENTS Catecholamines were measured by high pressure liquid chromatography and ACTH, renin and adrenal steroids by radioimmunoassay. PATIENTS Nineteen Addisonian patients (9 females, 10 males) were treated according to a standard reglie with oral cortisone acetate (37·5 mg/day) and fludrocortisone (0·1 mg/day). All patients were clinically well. RESULTS Mean plasma adrenallne in patients with Addison's disease was significantly reduced compared to a sex and age matched control group (males (n= 10) 143 ± 36 pmol/1, controls (n= 27) 303 ± 30 pmol/1, P < 0·01; females (n= 9) 77 ± 25pmol/1, controls (n= 27) 293 ± 21 pmol, P < 0·001). The noradrenallne: adrenallne ratio was clearly higher in patients with Addison's disease (males 24 ± 4, controls 9 ± 1, P < 0·01; females 45 ± 6, controls 9 ± 1, P < 0·01 CONCLUSION We conclude that the physiologically high local glucocorticold concentration may be responsible for normal adrenaline production under basal conditions.

Regional epinephrine kinetics in human heart failure: evidence for extra-adrenal, nonneural release

Abstract: A number of neurohumoral processes are activated in heart failure, including an increase in the plasma concentration of epinephrine. Radiotracer methods were applied in 42 patients with severe heart failure and 31 healthy volunteers to ascertain the rate at which epinephrine is released to plasma and to evaluate the contribution of extra-adrenal sources. The increase in arterial plasma epinephrine observed in the heart failure patients was explained principally by a 34% (P < 0.001) reduction in the whole body clearance rate of epinephrine from plasma. Regional venous sampling from the heart, lungs, and hepatomesenteric beds was performed in a subgroup of the study population, revealing a significant increase in the release rate of epinephrine to plasma from these organs in heart failure which accounted for 26% of the whole body plasma epinephrine appearance rate. To establish whether the cardiac epinephrine release was of neuronal origin, a physical (cycling) or mental (difficult mental arithmetic) stressor was applied as a sympathoexcitatory stimulus, given that a proportional release of norepinephrine and epinephrine could be expected if sympathetic nerves were the source. These interventions caused significant increases in the regional spillover of norepinephrine to plasma but not that of epinephrine. These findings suggest that nonadrenal tissues contribute significantly to the whole body epinephrine release rate in heart failure and that this may arise from a site other than sympathetic neurons.

Acute Psychological Stress and Epinephrine Infusion in Normolipidemic and Hyperlipidemic Men: Effects on Plasma Lipid and Apoprotein Concentrations

Abstract: This study examined whether psychological stress and the infusion of epinephrine increase plasma lipid and apoprotein concentrations in normolipidemic and hyperlipidemic men. Subjects were studied during three separate 6-hour laboratory sessions: a control session, during which subjects rested quietly while blood samples and hemodynamic measurements were obtained; a stress session, during which subjects were presented with two challenging mental tasks, followed by quiet rest; and an epinephrine infusion session, during which subjects received a low-dose infusion of epinephrine followed by quiet rest. The stress and epinephrine infusion manipulations produced the expected changes in plasma epinephrine and norepinephrine levels, blood pressure, and heart rate. Free fatty acid concentration increased markedly during epinephrine infusion and less dramatically but consistently during mental stress. Both stress and epinephrine infusion produced acute increases in plasma total, low-density lipoprotein, very low-density lipoprotein, and high-density lipoprotein cholesterol and apoprotein B concentrations, but comparable increases during the control session were not observed. Changes in albumin concentration (an index of plasma volume) were associated with changes in lipid concentrations during psychological stress. Epinephrine increases during psychological stress were correlated with increases in free fatty acid and triglyceride levels both during and after task administration. It was concluded that psychological or pharmacological stress induced in the laboratory produces changes in lipid concentrations, which at least during psychological stress, may be attributed to concomitant changes in plasma volume. The association between task-induced changes in epinephrine and changes in free fatty acid and triglyceride levels, also supports the hypothesis that psychological stress increases lipolysis.

Role of the Vagus Nerve in the Antidysrhythmic Effect of Dexmedetomidine on Halothane/Epinephrine Dysrhythmias in Dogs

Abstract: BackgroundDexmedetomidine, an alpha2 -adrenergic agonist, can prevent the genesis of halothane/epinephrine dysrhythmias through the central nervous system. Because stimulation of alpha2 adrenoceptors in the central nervous system enhances vagal neural activity and vagal stimulation is known to inhib

Racial Differences in Epinephrine and β2-Adrenergic Receptors

Abstract: This study examined the effects of ethnicity and hypertension on beta 2-adrenergic receptors and on plasma catecholamines in a group of 77 unmedicated mildly hypertensive and normotensive men. Black hypertensive subjects had the most sensitive and white hypertensive subjects the least sensitive beta-receptors (as assessed by isoproterenol-stimulated cyclic AMP in lymphocytes [P = .02]). In contrast, postreceptor adenylate cyclase activation (as assessed by forskolin stimulation) was similar among groups. As with beta-receptor sensitivity, black hypertensive subjects had the highest beta-receptor density and white hypertensive subjects the lowest (P = .03). Blacks demonstrated lower plasma epinephrine values compared with whites (P = .03). Across all subjects, plasma epinephrine was negatively correlated with beta-receptor density (r = -.26, P < .05) and sensitivity (r = -.25, P < .05). There were no group differences in binding affinity to the beta-antagonist iodopindolol. The findings support the notion of increased beta-adrenergic receptors in hypertension in blacks.

An echocardiographic study of interactions between pindolol and epinephrine contained in a local anesthetic solution.

Abstract: An increasing number of dental patients are taking beta-adrenergic blockers for the treatment of hypertension or angina pectoris. If epinephrine-containing local anesthetics are administered to such patients, interactions between epinephrine and the beta-blocking agent may induce cardiovascular complications. We assessed in volunteers the effects of intraoral injection with 2% lidocaine containing 1:80,000 epinephrine (L-E) on cardiac function after pretreatment with the beta-blocking agent pindolol. M-Mode echocardiography was used for the assessment. The injection of L-E after administration of pindolol did not alter cardiac preload, whereas it reduced the stroke volume, due to an increase in afterload and a decrease in myocardial contractility. Reductions in stroke volume and heart rate led to a decrease in cardiac output. Because total peripheral vascular resistance increased markedly, blood pressure was elevated despite the reduced cardiac output. These results suggest that cardiac function of dental patients on beta-blocker therapy can be adversely affected by epinephrine-containing local anesthetics. Therefore, when such an anesthetic solution has to be used in patients on beta-blocker therapy, careful systemic monitoring is needed.

Effect of local epinephrine on cutaneous bloodflow in the human neck.

Abstract: The effectiveness of local anesthetics is improved by the addition of a vasoconstrictor which increases duration of action and decreases both ayatemic toxic reactions and local bleeding. Epinephrine, the standard drug for vasoconstriction, has some limitations due to potential dose-related cardiac and local toxic effects. The authors examined the minimal effective epinephrine concentration required for minimal cutaneous vasoconstriction in the human subject so as to limit potential dose-related side effects. In a randomized, double-blinded prospective study, 23 patients undergoing head and neck surgical procedures under general anesthesia were enrolled to quantify the effect of subdermal infiltration of 1% lidocaine with epinephrine at varying concentrationa on local cutaneous bloodflow utilizing laser Doppler flowmetry. A comparison of the onset of vasoconatriction and magnitude of diminished bloodflow was made for several commonly used concentrations of epinephrine, with 1% lidocaine and normal saline serving as controls. There were no significant differences (P>.05) between epinephrine concentrations of 1:400,000, 1:200,000, 1:100,000, and 1:50,000 when examining onset and magnitude of vasoconstriction

Effect of Circulating Epinephrine on Platelet Function and Hematocrit

Abstract: We investigated the effect of raising arterial plasma epinephrine within the lower pathophysiological concentration range on various indicators of blood platelet function and hematocrit. Epinephrine was raised over 60 minutes by a stepwise increasing intravenous infusion in 40 healthy men aged 20 to 40 years. Platelet count increased progressively with increasing arterial epinephrine to a maximal change of 69 +/- 6 x 10(9)/L in EDTA-anticoagulated blood and a maximal change of 42 +/- 6 x 10(9)/L in acid-citrate-dextrose (ACD)-anticoagulated blood, and the weight of circulating platelets increased by 29% (P < .001). Platelet size increased significantly in EDTA and decreased in ACD, and the difference between EDTA and ACD was significant (P < .0001) for both count and size, suggesting that epinephrine not only recruits platelets into the circulation but also induces some microaggregation in vivo or adhesion ex vivo. Aggregation of platelets in vitro induced by epinephrine decreased (P < .003 for delta optical density and P = .038 for maximal optical density) after epinephrine infusion compared with saline but did not change when stimulated with ADP or collagen. These findings suggest a selective downregulation of the epinephrine-activating mechanisms concomitant with a rise in the platelet content of epinephrine by 81% (P < .001) and no change in the platelet sodium-proton membrane exchange. The release of granular content (beta-thromboglobulin and platelet factor 4) to the circulation in response to epinephrine was not significant. Thus, under acute conditions it seems that the platelets may protect themselves against inappropriate overstimulation by epinephrine. The importance of platelet epinephrine uptake is still unknown, but sodium-proton exchange does not seem to be involved in regulating the effects of circulating epinephrine on platelet function. Epinephrine has a pronounced effect on raising hematocrit (maximal change of 1.74 +/- 0.13 x 10(-2), P < .0001).

Renovascular interaction of epinephrine, dopamine, and intraperitoneal sepsis.

Abstract: ObjectiveTo determine the effect of intraperitoneal sepsis on the systemic and renal actions of the continuous infusion of epinephrine or dopamine, and during the concurrent administration of both drugs.DesignProspective, randomized study.SettingLaboratory at a university hospital.SubjectsSeven cons

Effect of neurovestibular stimulation on autonomic regulation.

Abstract: Conditions associated with nausea and vomiting, such as motion sickness or side effects of medications, are commonly associated with a clinical picture consistent with parasympathetic activation and sympathetic withdrawal. It can be postulated, therefore, that vestibular stimulation contributes to sympathetic withdrawal. To test this hypothesis five normal volunteers, 24-33 years old, were studied during caloric vestibular stimulation while monitoring muscle sympathetic nerve activity directly through a needle electrode placed in a peroneal nerve. The ear was irrigated with water at a flow rate of 450 ml/min and 37 degrees C. The water temperature was sequentially lowered by 7 degree C intervals until intolerable side effects developed or a temperature of 16 degrees C was reached. Nystagmus was induced in all subjects, but heart rate, blood pressure, muscle sympathetic nerve activity and plasma norepinephrine levels did not change significantly during or after caloric stimulation, even when the subjects felt dizzy and nauseated. No evidence of sympathetic withdrawal was observed in any subject either by muscle sympathetic nerve activity or plasma norepinephrine measurements. In conclusion, we have found that selective vestibular stimulation is not accompanied by significant changes in the sympathetic nervous system function. In particular, no sympathetic withdrawal was observed. It could be argued that lack of sympathetic stimulation is an inadequate response to the symptoms associated with caloric stimulation.