scispace - formally typeset
Search or ask a question

Showing papers on "Epinephrine published in 1981"


Journal ArticleDOI
TL;DR: It is concluded that the combined infusion of epinephrine, glucagon, and cortisol produces a greater than additive hyperglycemic response in normal humans, suggesting that the clinical occurrence of fasting hyperglycemia in a setting of hypersecretion of multiple antiinsulin hormones (stress hyper glycemia) may result, at least in part, from synergistic interactions among these hormones.
Abstract: We infused epinephrine, glucagon, and cortisol in combination into health y overnight-fasted subjects in doses designed to simulate changes in severe stress. Whenall three hormones were infused simultaneously, glucose levels rose above 200 mg/dl in spite of a 100–200% increase in plasma insulin. In contrast, infusion of each hormone individually produced eithera mild (<120 mg/dl) or a transient elevation in the plasma glucoseconcentration. With the combined hormone infusion,the increment in plasmaglucose was 3-fold greater than the sum of the responses to the individual hormones (< 0.001). The marked hyperglycemia in this setting is a resultof ongoing glucose overproduction which is stimulated by epinephrine and glucagon and sustained by cortisol. Furthermore, epinephrine(and possibly cortisol) inhibited glucose disposal despite concomitant hyperinsulinemia. In contrast to their effects on glucoseregulation, the simultaneous infusion of epinephrine, glucagon, and cortisol failed to cause hyperketonemia. W...

270 citations


Journal ArticleDOI
01 Mar 1981-Stroke
TL;DR: The high plasma norepinephrine in the stroke group is consistent with an increase in peripheral sympathetic activity which could produce the cardiac abnormalities of cerebral infarction.
Abstract: Cardiac arrhythmias, myocardial necrosis and ECG abnormalities in stroke may result from abnormally high levels of sympathetic activity. To examine this possibility, plasma norepinephrine, epinephrine and dopamine were measured in 74 patients with cerebral infarction, 18 with transient ischemic attacks and 33 non-stroke controls. Mean norepinephrine, epinephrine and dopamine values (pg/ml) in cerebral infarction (433.2, 81.6, 75.6 were higher (p less than 0.01) than in controls (281.1, 60.1, 40.5, respectively). Transient ischemic attacks produced values intermediate to these two groups (391.3, 80.9, 54.9). The elevated catecholamine concentrations in cerebral infarction could not be explained by differences in age, blood pressure, heart rate, stress, type or severity of stroke. The high plasma norepinephrine in the stroke group is consistent with an increase in peripheral sympathetic activity which could produce the cardiac abnormalities of cerebral infarction.

259 citations


Journal ArticleDOI
TL;DR: It is suggested that physiological levels of catecholamines normally down-regulate beta receptors in man and that blockade of this down-regulation by propranolol allows receptor density to increase.
Abstract: High levels of beta receptor agonist have previously been shown to down-regulate beta receptor density on circulating leukocytes in man; however, the factors controlling receptor density under physiological conditions have not previously been defined. To determine whether beta receptor density is normally down-regulated by circulating, physiological levels of catecholamines we have examined the relationship between receptor density and catecholamine levels. Urinary epinephrine and norepinephrine were significantly reciprocally correlated to lymphocyte receptor density. A similar relationship existed between beta receptor density and supine plasma epinephrine, norepinephrine, upright epinephrine, and norepinephrine levels. Change in sodium intake from 10 to 400 meq/d caused a 52% increase in lymphocyte and a 48% increase in polymorphonuclear beta receptor density. The changes in receptor density were accompanied by an increase in the sensitivity to isoproterenol measured as a fall in the dose of isoproterenol required to raise the heart rate by 25 beats per minute. Beta receptor density on both lymphocyte and polymorphonuclear cells was significantly correlated to the cardiac sensitivity to isoproterenol. Propranolol administration resulted in an increase in the density of beta receptors on lymphocyte and polymorphonuclear cells that correlated with the subject's pretreatment catecholamine levels. These findings, therefore, suggest that physiological levels of catecholamines normally down-regulate beta receptors in man and that blockade of this down-regulation by propranolol allows receptor density to increase.

205 citations


Journal ArticleDOI
TL;DR: It is concluded that CAs and clonidine are inhibitory to the maintained activity of SPNs and that an alpha2-adrenergic receptor may be involved in the action of these compounds.
Abstract: The neuropil surrounding sympathetic preganglionic neurons (SPNs) receives an abundant catecholaminergic innervation originating from the brain stem. The effect of catecholamines (CA) released at this spinal level on the activity of SPNs is still controversial as is the extent to which this particular CA transmission is affected by central antihypertensive drugs, such as clonidine and alpha-methyldopa. The present study was initiated, therefore, to determine the effects of iontophoretic applications of CAs and clonidine on the discharges of identified SPNs and to determine the type of receptor mediating the action of these compounds. Extracellular recordings were made with five- or six-barrel electrodes in 20 pigeons anesthetized with urethane, artificially ventilated, and immobilized. Data were obtained on 83 SPNs localized in the three first thoracic segments and identified on the basis of constancy of antidromic activation latency and collision. All of the cells sampled were inhibited by the application of low iontophoretic currents of clonidine and by a series of CAs, including alpha-methylnorepinephrine, epinephrine, and phenylephrine. For each compound, the amount of charge necessary to decrease the level of cell firing to 50% of control was calculated. Using this value as an index of drug potency, the following rank order could be determined: clonidine greater than alpha-methylnorepinephrine greater than epinephrine greater than norepinephrine greater than phenylephrine. The inhibitory effects of both clonidine and norepinephrine were antagonized by iontophoretic applications of the alpha antagonists, yohimbine, piperoxan, and phentolamine. In contrast, the beta antagonist, sotalol, and the alpha 1 antagonist, prazosin, were found ineffective when similarly applied. It is concluded that CAs and clonidine are inhibitory to the maintained activity of SPNs and that an alpha2-adrenergic receptor may be involved in the action of these compounds.

190 citations


Journal ArticleDOI
TL;DR: The effect of epinephrine on basal and insulin-stimulated glucose uptake in perfused hindlimbs of fed rats was studied in this article, where the authors found that the effect of insulin on glucose uptake was completely reversed by propranolol, but were not significantly altered by phentolamine.
Abstract: The effect of epinephrine on basal and insulin-stimulated glucose uptake in perfused hindlimbs of fed rats was studied. Insulin increased glucose uptake in a dose-dependent manner from a basal value of 1.5+/-0.3 up to a maximum value of 5.3+/-0.9 mumol/min per 100 g with 6 nM (1 m U/ml). Epinephrine at 10 nM and 0.1 muM also increased glucose uptake to 2.6+/-0.1 and 3.1+/-0.1 mumol/min per 100 g, respectively. These same concentrations of epinephrine, however, suppressed the insulin-stimulated glucose uptake to 3.2+/-0.3 mumol/min per 100 g. Both the stimulatory and inhibitory effects of epinephrine on glucose uptake were completely reversed by propranolol, but were not significantly altered by phentolamine. Uptake of 3-O-methylglucose and 2-deoxyglucose into thigh muscles of the perfused hindlimbs was stimulated fivefold by insulin, but was unaffected by epinephrine. Epinephrine also did not inhibit the stimulation of uptake by insulin. Epinephrine decreased the phosphorylation of 2-deoxyglucose, however, and caused the intracellular accumulation of free glucose. These last two effects were more prominent in the presence of insulin. Whereas epinephrine caused large rises in glucose-6-P and fructose-6-P, insulin did not alter the concentration of these metabolites either in the absence or presence of epinephrine.THESE DATA INDICATE THAT: (a) epinephrine has a stimulatory effect on glucose uptake by perfused rat hindlimbs that does not appear to be exerted on skeletal muscle; (b) epinephrine does not affect hexose transport in skeletal muscle; (c) epinephrine inhibits insulin-stimulated glucose uptake in skeletal muscle by inhibiting glucose phosphorylation. It is hypothesized that the inhibition of glucose phosphorylation is due to the stimulation of glycogenolysis, which leads to the accumulation of hexose phosphates, which inhibit hexokinase.

176 citations


01 Jan 1981
TL;DR: The data indicate that (a) the lipolytic effects of epinephrine occur at plasma levels approximately threefold basal values and (b) lipolysis is more sensitive than glycogenolysis to increments in plasma epinphrine.
Abstract: To determine the plasma epinephrine thresholds for its lipolytic effect, 60-min epinephrine infusions at nominal rates of 0.1, 0.5, 1.0, 2.5, and 5.0 micrograms/min were performed in each of four normal young adult men while they also received a simultaneous infusion of [1-13C]palmitic acid to estimate inflow transport of plasma free fatty acids. These 20 infusions resulted in steady-state plasma epinephrine concentrations ranging from 12 to 870 pg/ml. Plasma epinephrine thresholds for changes in blood glucose, lactate, and beta-hydroxybutyrate were in the 150--200-pg/ml range reported by us previously (Clutter, W. E., D. M. Bier, S. D. Shah, and P. E. Cryer. 1980. J. Clin. Invest. 66: 94--101.). Increments in plasma glycerol and free fatty acids and in the inflow and outflow transport of palmitate, however, occurred at lower plasma epinephrine thresholds in the range of 75 to 125 pg/ml. Palmitate clearance was unaffected at any steady-state epinephrine level produced. These data indicate that (a) the lipolytic effects of epinephrine occur at plasma levels approximately threefold basal values and (b) lipolysis is more sensitive than glycogenolysis to increments in plasma epinephrine.

148 citations


Journal ArticleDOI
TL;DR: The data indicate that the hyperdynamic circulation (high cardiac output and renal blood flow) of borderline hypertension is found predominantly in patients younger than age 30 years, whereas older patients are characterized by an elevated total peripheral resistance and normal cardiac output.
Abstract: The relationships between age, systemic and renal hemodynamics, circulating catecholamines (norepinephrine, epinephrine and dopamine) and intravascular volumes were studied in 38 normotensive subjects and in 77 patients with borderline essential hypertension. Borderline hypertensive patients had a higher cardiac index (p less than 0.02) and renal blood flow (p less than 0.05) than normotensive subjects if they were younger than 30 years of age, whereas in older patients no difference was observed. In contrast, total peripheral resistance was normal in young borderline hypertensive patients, but significantly increased (p less than 0.02) in patients older than age 40 years. Cardiac output (r = -0.28, p less than 0.01) and renal blood flow (r = -0.47, p less than 0.001) correlated inversely with age in the entire population and in both subgroups. Cardiac output also correlated closely with renal blood flow in all subjects (r = 0.45, p less than 0.001). Circulating norepinephrine levels increased with age (r = 0.25, p less than 0.05), whereas epinephrine concentration tended to decrease. Plasma and total blood volume correlated directly with cardiac output (r = 0.39, p less than 0.001) and inversely with peripheral resistance (r = -0.34, p less than 0.001). These data indicate that the hyperdynamic circulation (high cardiac output and renal blood flow) of borderline hypertension is found predominantly in patients younger than age 30 years. Older patients are characterized by an elevated total peripheral resistance and normal cardiac output. The age-dependent increase in circulating norepinephrine and decrease in epinephrine levels may participate in the shift of the hemodynamic profile from high-cardiac-output hypertension in the young to a high-arteriolar-resistance hypertension in the older patient.

147 citations


Journal ArticleDOI
TL;DR: Clutter et al. as discussed by the authors showed that the lipolytic effects of epinephrine occur at plasma levels approximately threefold basal values and lipolysis is more sensitive than glycogenolysis to increments in plasma Epinephrine.
Abstract: To determine the plasma epinephrine thresholds for its lipolytic effect, 60-min epinephrine infusions at nominal rates of 0.1, 0.5, 1.0, 2.5, and 5.0 micrograms/min were performed in each of four normal young adult men while they also received a simultaneous infusion of [1-13C]palmitic acid to estimate inflow transport of plasma free fatty acids. These 20 infusions resulted in steady-state plasma epinephrine concentrations ranging from 12 to 870 pg/ml. Plasma epinephrine thresholds for changes in blood glucose, lactate, and beta-hydroxybutyrate were in the 150--200-pg/ml range reported by us previously (Clutter, W. E., D. M. Bier, S. D. Shah, and P. E. Cryer. 1980. J. Clin. Invest. 66: 94--101.). Increments in plasma glycerol and free fatty acids and in the inflow and outflow transport of palmitate, however, occurred at lower plasma epinephrine thresholds in the range of 75 to 125 pg/ml. Palmitate clearance was unaffected at any steady-state epinephrine level produced. These data indicate that (a) the lipolytic effects of epinephrine occur at plasma levels approximately threefold basal values and (b) lipolysis is more sensitive than glycogenolysis to increments in plasma epinephrine.

143 citations


Journal ArticleDOI
TL;DR: The effects of adrenochrome and other metabolites of epinephrine on the ultrastructure and contractile activity of isolated rat hearts perfused under conditions in which the heart rate and coronary flow were controlled are examined to show consistency with the concept that oxidation products of catecholamines such as Adrenochrome are partly responsible for inducing myocardial necrosis and failure following massive catechlamine injections in intact animals.

139 citations


Journal ArticleDOI
TL;DR: It is concluded that the efficacy of epinephrine in aiding resumption of spontaneous circulation from asphyxial arrest is due to alpha adrenergic receptor stimulation and that beta receptor stimulation is not important in determining outcome.
Abstract: To determine the relative importance of the alpha and beta adrenergic effects of epinephrine in resuscitation, 32 dogs were studied in four groups. Group A (alpha blocked) received phenoxybenzamine, 70 mg/kg; group B (beta blocked), propranolol 5 mg/kg; group C (alpha and beta blocked) both drugs; and group D (control), no drug. After this treatment and 5 min of asphyxial arrest, all animals received closed chest cardiac massage (CCCM), artificial ventilation (AR), and epinephrine, 1 mg, iv. Resumption of spontaneous circulation occurred with the following frequency: group A, 0/8; group B, 6/8, group C, 0/8, group D, 7/8. The difference in successful resuscitation of the alpha blocked animals and the not alpha blocked animals is statistically significant (P less than or equal to 0.01). It is concluded that the efficacy of epinephrine in aiding resumption of spontaneous circulation from asphyxial arrest is due to alpha adrenergic receptor stimulation and that beta receptor stimulation is not important in determining outcome.

135 citations


Journal ArticleDOI
TL;DR: Thyrotopin releasing factor acts with the brain to elevate plasma levels of epinephrine and norepinephrine and is associated with the TRF induced increase in plasma catecholamines, effects which are prevented by adrenalectomy.

Journal ArticleDOI
TL;DR: In this paper, the role of the vascular o-adrenergic receptor in these alterations was investigated, using the α-1 selective radioligand, (3H)-WB-4101, [phenoxy-3-H(JV)]-(2,6-dimethoxyphenoxy- ethyl)aminomethyl-l,4-benzodioxane.
Abstract: Vascular smooth muscle sensitivity to catecholamine-induced contraction is increased after catecholamine depletion by chemical sympathectomy and decreased after exogenous catecholα-mine administration. To investigate the role of the vascular o-adrenergic receptor in these alterations, we used the α-1 selective radioligand, (3H)-WB-4101, [phenoxy-3-H(JV)]-(2-(2,6-dimethoxyphenoxy- ethyl)aminomethyl-l,4-benzodioxane, to characterize the vascular postsynaptic a-adrenergic receptor in a membrane-rich particulate fraction of the rat mesenteric artery. Binding (3H)-WB-4101 was rapid, readily reversible, stereospecific, and saturable. Scatchard analysis described a single class of binding sites with a dissociation constant (Kd) of 0.76 ± 0.15 nM, and maximal binding capacity (B max ± 13 fmol/mg protein. Alpha-adrenergic agonists competed for the ()3H)-WB-4101 binding site in the α-edrenergic potency order of (-)-epinephrine (Kd = 3.0 /IM) > (-)-norepinephrine (Kd 8.8(-)-isoproterenol (Kd = 57 FIM), and the α-adrenergic antagonist phentolamine (Kd 7.6 nM) was 1000 times more potent than the /?-adrenergic antagonist, (±)-propranolol (Kd = 7400 nM). The number and affinity of α-adrenergic binding sites were studied in hyper- and hypo-adrenergic states. In mesenteric arteries from rats treated with exogenous epinephrine for 4 days, Bmal was decreased to 53 ± 10 fmol/ mg protein (n = 4, P < 0.01), whereas Kd for (3H)-WB-4101 was unchanged. Conversely, in mesenteric arteries from rats depleted of catecholamines with reserpine, Bmo, was unchanged (96 ± 15 fmol/mg protein), whereas Kd for (3H)-WB-4101 was decreased to 0.34 ± 0.07 nM (n = 6, P < 0.01), and Kd for (-)-epinephrine was decreased to 0.40 ± 0.19 μ (n = 6, P < 0.01). The effect of reserpine treatment was time dependent, being evident within 1 hour, and reaching a maximum after 3-7 days. The effects of catecholamine depletion with 6-hydroxydopamine were similar to those of reserpine. Thus, experimentally induced hyper- and hypo-adrenergic states can result in regulation of the vascular α-adrenergic receptor through changes in either receptor number or affinity. Circ Res 48: 104-111, 1981

Journal ArticleDOI
01 Aug 1981-Diabetes
TL;DR: During insulin-induced hypoglycemia, patients with autonomic neuropathy had impaired activation of the adrenal medulla, probably due to sympathetic neuropathy, and serum glucose recovery was unaffected and lipolytic responses and blood pressure increments were exaggerated, suggesting increased sensitivity of hepatic glycogenolysis, adipose tissue lipolysis and the cardiovascular system toward the action of catecholamines in diabetics with autonomIC neuropathy.
Abstract: Hormonal, metabolic, and cardiovascular responses to insulin-induced hypoglycemia were investigated in 10 juvenile-onset diabetics who showed signs of autonomic neuropathy, in 8 control patients of similar age and duration of diabetes without neuropathy, and in 6 healthy subjects. In an attempt to normalize intermediary metabolism, the diabetics were treated with soluble insulin only (given subcutaneously and intravenously) for 48 h preceding the study. Plasma epinephrine concentrations were significantly lower in patients with autonomic neuropathy before the experiment as well as 15 min after serum glucose nadir compared with diabetics without neuropathy (P In conclusion, during insulin-induced hypoglycemia, patients with autonomic neuropathy had impaired activation of the adrenal medulla, probably due to sympathetic neuropathy. Furthermore, they had no increase in glucagon concentrations. Compared with noneuro-pathic diabetics, serum glucose recovery was unaffected and lipolytic responses and blood pressure increments were exaggerated, suggesting increased sensitivity of hepatic glycogenolysis, adipose tissue lipolysis, and the cardiovascular system toward the action of catecholamines in diabetics with autonomic neuropathy.

Journal ArticleDOI
TL;DR: In this paper, the α-adrenergic specificity of ACTH secretion was demonstrated by the following order of potency of catecholaminergic agents: epinephrine (20 nM) > norepinephrine (30 nM), isoproterenol = doparnine (10μM).
Abstract: Specificity of the a-adrenergic control of ACTH secretion was studied in rat anterior pituitary cells in primary culture. The α-adrenergic specificity of ACTH secretion is demonstrated by the following order of potency of catecholaminergic agents: epinephrine (20 nM) > norepinephrine (30 nM) » isoproterenol = doparnine (10μM). While epinephrine and norepinephrine lead to a 7- to 10-fold stimulation of ACTH secretion, clonidine and phenylephrine act as partial agonists and cause a 3- to 4-fold increase of ACTH release. Paraaminoclonidine and methoxamine have no significant effect up to 10 μM. α-Adrenergic antagonists inhibit epinephrine-induced ACTH release in the following order of potency: prazosin > WB-4101 » yohimbine, with Ka values of 0.06, 0.4, and 70 nM, respectively, thus indicating that the α-adrenergic receptor controlling ACTH secretion is of the α1 type. Dihydroergocornine and dihydroergocryptine, two ergot derivatives, show a-adrenergic antagonistic activity at low Kd values of 0.8 and 1.5 nM...

Journal ArticleDOI
TL;DR: The data are consistent with the hypothesis that endorphins act at a presently unknown brain site(s) to increase the central sympathetic outflow to adrenal medulla and peripheral sympathetic nerve endings, thus stimulating peripheral catecholamine release and increasing plasma concentrations of epinephrine, norepinephrine, and dopamine.
Abstract: Intracisternal administration of synthetic human beta-endorphin (0.058-7.25 nmol) in chronically cannulated, conscious, freely moving, adult male rats increased plasma concentrations of epinephrine, norepinephrine, and dopamine in a dose-related manner. Epinephrine secretion was the most sensitive to the stimulatory effect of intracerebral beta-endorphin; plasma epinephrine increased transiently in response to 0.058 nmol. Of the three catecholamines, plasma epinephrine showed the greatest and most rapid response to the largest dose (7.25 nmol) studied. Plasma norepinephrine increased significantly in response to 1.45 nmol, peaking later than plasma epinephrine. Plasma dopamine increased only in response to the highest dose examined. These beta-endorphin effects on plasma catecholamines were inhibited by intraarterial naloxone (1.1 mumol/kg), supporting mediation at opioid receptors. Pretreatment with the ganglionic blocking agent chlorisondamine inhibited the responses of all three catecholamines to intracisternal beta-endorphin. Bilateral adrenal denervation completely prevented the plasma epinephrine response to beta-endorphin and blunted the plasma norepinephrine and dopamine responses. Prior intracisternal administration of hemicholinium-3 blocked the plasma responses of all three catecholamines to intracisternal beta-endorphin, providing evidence for the involvement of central cholinergic neurons in the mechanism mediating beta-endorphin-induced increases in plasma catecholamines. The data are consistent with the hypothesis that endorphins act at a presently unknown brain site(s) to increase the central sympathetic outflow to adrenal medulla and peripheral sympathetic nerve endings, thus stimulating peripheral catecholamine release and increasing plasma concentrations of epinephrine, norepinephrine, and dopamine.

Journal ArticleDOI
TL;DR: Repeated immobilization stress has been found to decrease significantly the number of beta-adrenoceptors in hypothalamus and brain stem while increasing thenumber of alpha 2-ad Renoceptor agonists.

Journal ArticleDOI
TL;DR: It is suggested that epinephrine and possibly norepinephrine are involved in neural control of feed intake, but not water consumption in chickens.

Journal Article
TL;DR: Data are presented that Li, too, markedly reduces activity of beta-adrenergic adenylate cyclase in humans, and the effect is specific, since the plasma cyclic AMP response to glucagon is not inhibited.

Journal ArticleDOI
TL;DR: The combination of sympathomimetics and aminophylline appear more effective, and no more toxic, than epinephrine alone for the initial treatment of acute episodes of asthma.
Abstract: Eighty-nine patients who presented to the hospital for treatment of acute episodes of asthma were randomly assigned to initial therapy with subcutaneously administered epinephrine or 1 of 2 combination regimens consisting of intravenously administered aminophylline and either subcutaneously administered of epinephrine or inhaled isoproterenol. During the first hour of treatment, as a group, the patients treated with the 2-drug regimens showed greater objective improvement than did patients who received epinephrine alone. This was particularly true for patients with either severe airway obstruction or a subtherapeutic theophylline concentration at the time of presentation. There were no differences in the heart rate and blood pressure responses to the 3 regimens, and symptoms consistent with drug side effects were not reported more frequently by patients treated with 2 drugs. Thus, the combination of sympathomimetics and aminophylline appear more effective, and no more toxic, than epinephrine alone for the initial treatment of acute episodes of asthma.

Journal ArticleDOI
TL;DR: The practicability of the electrochemical detector in combination with liquid chromatography for the routine quantitative determination of norepinephrine and epinephrine in plasma is described.

Journal ArticleDOI
TL;DR: The rat provides a good model for the study of local anesthetic-induced myonecrosis, and lidocaine with epinephrine destroyed most of the muscle in which it was injected.
Abstract: Myotoxic effects of 2% lidocaine with 1:100,000 epinephrine were evaluated in rats and humans. Sprague-Dawley rats were give injections in the left gastrocnemius muscle of 0.5 ml of the lidocaine preparation or a control vehicle; they were killed in groups of four at 0, 8, 24, and 48 hours. Blood samples were taken for serum enzyme determinations, and muscle specimens were removed and processed for histologic evaluation. In eight patients undergoing radical neck dissection, 1.8 ml of lidocaine with epinephrine or its control was injected into the sternocleidomastoid muscle approximately 18 hours before surgery. Patients' muscle specimens obtained at surgery were handled similarly to those of the rat. Serum creatine kinase, aspartate aminotransferase, and alanine aminotransferase activities were markedly elevated in the rat at 8 hours in the experimental group, but not in the control group. Histologically, control injections elicited no damage in the rat other than a mild inflammatory reaction along the presumptive needle track. Lidocaine with epinephrine, however, destroyed most of the muscle in which it was injected. Myonecrosis was qualitatively similar in humans. The rat provides a good model for the study of local anesthetic-induced myonecrosis.

Journal ArticleDOI
TL;DR: There was a small reduction in the speed of decay of nerve block, but this only reached statistical significance with regard to total recovery, which took 40 to 50 minutes longer with the epinephrine-containing solutions.
Abstract: The effect of adding 0.1, 0.2, or 0.3 ml of 1:1000 epinephrine to 1.5 ml of 5% lidocaine in 7.5% dextrose for spinal anesthesia was assessed in 40 patients in a double-blind study. The addition of epinephrine produced little or no clinically useful prolongation of block. There was a small reduction in the speed of decay of nerve block, but this only reached statistical significance with regard to total recovery, which took 40 to 50 minutes longer with the epinephrine-containing solutions. No difference could be seen between the three doses of epinephrine.

Journal ArticleDOI
TL;DR: The results suggest the presence of a-and β-2 adrenoreceptors in the feline pulmonary vascular bed and that both types of adrenergic receptors are innervated by the sympathetic nervous system.
Abstract: We investigated the effects of catecholamines and sympathetic nerve stimulation in the feline pulmonary vascular bed under conditions of controlled pulmonary blood flow. Norepinephrine and nerve stimulation caused dose- and stimulus frequency-dependent increases in pulmonary vascular resistance. However, when pulmonary vascular tone was enhanced and alpha receptors blocked, norepinephrine and nerve stimulation caused dose- and frequency-dependent decreases in pulmonary vascular resistance. The decreases in pulmonary vascular resistance were blocked with propranolol and were of greater magnitude than were constrictor responses observed under basal conditions. Vasodilator responses to nerve stimulation were not modified by atropine. Epinephrine and isoproterenol had marked vasodilator activity in the pulmonary vascular bed when pulmonary vascular tone was elevated. When alpha receptors were blocked, isoproterenol and epinephrine had similar vasodilator activity, and when beta receptors were blocked, epinephrine and norepinephrine had marked vasoconstrictor activity. Selective beta-1 receptors antagonists had little effect on vasodilator responses to isoproterenol, whereas responses to this substance were blocked by propranolol. These results suggest that presence of alpha-and beta-2 adrenoreceptors in the feline pulmonary vascular bed and that both types of adrenergic receptors are innervated by the sympathetic nervous system.

Journal ArticleDOI
TL;DR: It seems likely that in addition to secretion by adrenal medulla a considerable portion of the beta-endorphin-induced increase in norepinephrine is derived from sympathetic nerve endings, and blockade of these endorphin effects by the prior systemic administration of naloxone supports mediation of the effects at opioid receptors.

Journal ArticleDOI
TL;DR: 2-chloro-3-trifluoromethyl-α-benzylamine administration elevated plasma corticosterone and this effect was highly correlated to the decrease in hypothalamic epinephrine concentration in both sham operated and adrenal demedullated rats, arguing for tonic epinergic inhibition of pituitary-adrenal function.

Journal ArticleDOI
TL;DR: It is suggested that borderline hypertension may be maintained by inappropriately increased cardiovascular response to norepinephrine and angiotensin II in the presence of normal sympathetic and renin activity and a normal body sodium-volume state.
Abstract: The role of various pressor factors and cardiovascular responsiveness to norepinephrine or angiotensin II in the pathogenesis of borderline hypertension was evaluated. Exchangeable body sodium, blood volume, plasma renin activity, norepinephrine or dopamine levels, and norepinephrine or epinephrine excretion rates were similar between 24 patients with borderline hypertension (mean age 34 +/- 4 (SEM) years and 22 normal subjects matched for age; the patients had a slight increase in supine plasma epinephrine. Pressor doses of norepinephrine or angiotensin II were significantly lower (p less than 0.01 and 0.001, respectively) in the borderline hypertensive group. These findings suggest that borderline hypertension may be maintained by inappropriately increased cardiovascular response to norepinephrine and angiotensin II in the presence of normal sympathetic and renin activity and a normal body sodium-volume state.

Journal ArticleDOI
TL;DR: A diminished responsiveness of the sympathetic—adrenal medullary system may underlie the reduced capacity of aged animals to adapt to stressful stimulation.

Journal ArticleDOI
TL;DR: In this article, the effects of the slow channel inhibitor verapamil on the antiarrhythmic and cardiovascular effects of halothane anesthesia in the dog were studied.
Abstract: The antiarrhythmic and cardiovascular effects of the slow channel inhibitor, verapamil, were studied during 1.1 MAC halothane anesthesia in the dog. The control epinephrine arrhythmogenic dose to induce ventricular arrhythmias was 2.58 +/- 0.77 microgram . kg-1 . min-1 (mean +/- SEM). Three consecutive doses of 0.2 mg/kg verapamil each elevated the dose of epinephrine required to produce a ventricular arrhythmia to 5.17 +/- 1.27, 8.07 +/- 1.85, and 12.03 +/- 2.76 microgram . kg-1 . min-1, respectively, all of which were significantly elevated above the control value of the preceding values. A second group of dogs, unperturbed by epinephrine, received the same sequence of verapamil doses at similar time intervals for evaluation of effects on cardiovascular function and atrioventricular conduction. Heart rate remained unchanged. Mean arterial pressure decreased maximally by 37 per cent of control, left ventricular dP/dt by 24 per cent, and systemic vascular resistance by 51 per cent. These effects were transient with recovery times up to one hour. Central venous pressure increased by 44 per cent and left ventricular end diastolic pressure by 27 per cent, while PR interval was prolonged by 40 per cent. Thus, verapamil raised the dose of epinephrine required to elicit a ventricular arrhythmia during halothane anesthesia promptly and cumulatively. At the same time verapamil produced transient peripheral vasodilation, direct depression of myocardial contractility, and prolongation of atrioventricular conduction time that was not cumulative at the intervals studied.

Journal ArticleDOI
TL;DR: Post‐relaxation training values for monoamine oxidase, epinephrine, norepinephrine and the anxiety levels were found to be significantly lower than the pre‐treatment values for the index group and no significant changes were seen in the control group values.
Abstract: Levels of platelet monoamine oxidase activity, state anxiety and trait anxiety were quantified twice in 20 drug-free subjects with generalized anxiety and an equal number of healthy drug-free controls at 4-week intervals. Fiften subjects in each group also had plasma epinephrine and norepinephrine measured. The index group received relaxation training during the interval between the two evaluation sessions. Post-relaxation training values for monoamine oxidase, epinephrine, norepinephrine and the anxiety levels were found to be significantly lower than the pre-treatment values for the index group. No significant changes were seen in the control group values. For the index group, catecholamine levels and monoamine oxidase activity were seen to correlate significantly before and after relaxation training.

Journal ArticleDOI
TL;DR: It is suggested that immobilization stress causes desensitization of alpha- and beta 1-receptors but not beta 2-receptionors by immobilization, similar to that after isoproterenol treatment, possibly due to increased turnover of phospholipids.
Abstract: Immobilization stress (2.5 h daily) or repeated injection of isoproterenol (1 mg/kg, 3 times daily) for 1 wk caused a subsensitivity to the chronotropic and pressor effect of epinephrine in pithed rats. Propranolol (1 mg/kg) inhibited, to a greater extent in control than in immobilized rats, the chronotropic effect of epinephrine. The residual heart rates did not differ significantly among control, immobilized, and isoproterenol-treated rats. Practolol (1 mg/kg) but not butoxamine (5 mg/kg) mimicked the effect of propranolol. The subsensitivity in the blood pressure responses was not abolished by injection of either of the beta-adrenoceptor blockers. Butoxamine or propranolol shifted the epinephrine dose-blood pressure response curves to the left. The degree of shift was similar in control and immobilized or isoproterenol-treated rats. Daily injection of quinacrine (16 mg/kg), an antimalarial agent that inhibits phospholipase A2, blocked the subsensitivity to the chronotropic effect of epinephrine, but not that to the pressor effect of epinephrine. These observations suggest that immobilization stress causes desensitization of alpha- and beta 1-receptors but not beta 2-receptors. The mechanism of desensitization of beta 1-receptors by immobilization appears to be similar to that after isoproterenol treatment, possibly due to increased turnover of phospholipids.