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At least 19 recordsLinked to original sources
PubMed1994

Changes in oxygen consumption relative to oxygen delivery in endotoxemic dogs given adrenergic agents.

Adrenergic agents (AAs) have been used in critically ill patients to increase oxygen delivery (DO2). Associated parallel increases in oxygen consumption (VO2) have been noted and are thought to represent improved tissue oxygen utilization at supraphysiologic levels of DO2. We hypothesize that the increase in VO2 associated with the use of AAs in septic animals is secondary to direct, obligate, metabolic effects of the agents themselves. In this study, mongrel dogs were anesthetised, paralyzed, and had minimum temperature maintained on a warming blanket. Pulmonary and systemic hemodynamics were monitored. DO2 was calculated, while VO2 was measured directly with a metabolic cart. All dogs were given an Escherichia coli challenge and a colloid fluid resuscitation. Two hours after the onset of endotoxemia, baseline values were obtained, followed by four progressively larger doses of saline, dobutamine, or dopamine. At each dose there was a 40-min stabilization period and a 20-min measurement of hemodynamics and VO2. Data were analyzed using analysis of variance with a Scheffe's S test. P values of < 0.05 were considered significant. The control group slowly decreased VO2 during the 6-hr experiment to 73% of baseline. Dobutamine increased VO2 to 119% of baseline (31% above control) and dopamine to 111% of baseline (28% over control). We conclude that adrenergic agents cause a significant increase in whole body VO2 at moderate doses in septic dogs. It is likely, therefore, that the "pathologic" relationship between VO2 and DO2 described in critically ill patients is partially due to the direct metabolic effects of AAs.

Acid-Base Equilibrium↗
PubMed1987

Effects of an anticholinergic bronchodilator on arterial blood gases of hypoxemic patients with chronic obstructive pulmonary disease. Comparison with a beta-adrenergic agent.

Adrenergic bronchodilators have the potential drawback that they may increase hypoxemia in spite of relieving air-flow obstruction in patients with asthma. Anticholinergic bronchodilators are of interest as alternatives to beta-adrenergic agents, particularly in patients with chronic bronchitis and emphysema, yet little is known of the effects of either class of agent on gas exchange in patients with this diagnosis. We compared their effects on gas exchange in 12 patients with chronic bronchitis and emphysema who also had arterial hypoxemia in a double-blind crossover study. We found that nebulized atropine methonitrate, a quaternary ammonium anticholinergic bronchodilator, resulted in only minor and statistically insignificant effects on gas exchange at all times for as long as 60 min after its inhalation. In contrast, the beta-adrenergic bronchodilator metaproterenol hydrochloride resulted in a statistically significant decrease in the PaO2, the greatest mean decrease being 5.0 +/- 2.5 mm Hg (mean +/- 1 SD). The effects of metaproterenol on arterial blood gases in this population of patients were more prolonged than those previously reported in asthmatic subjects with lesser degrees of hypoxemia. An anticholinergic bronchodilator might be preferable in patients with hypoxemia caused by chronic bronchitis and emphysema in that it does not carry the risk of worsening systemic hypoxemia.

Aged↗
PubMed1985

Conformationally defined adrenergic agents. 1. Design and synthesis of novel alpha 2 selective adrenergic agents: electrostatic repulsion based conformational prototypes.

A previous report of the adrenergic selectivity of 2- and 6-fluoronorepinephrine prompted us to formulate a hypothesis that accounted for this selectivity on the basis of a conformational preference induced by electrostatic repulsion between the aromatic fluorine atom and the side-chain hydroxyl group. A series of nitrogen-substituted catechol (aminomethyl)benzocyclobutenes, indanes, tetralins, and benzocycloheptenes were prepared, and when their radioligand binding affinities were determined, it was found that the overall pattern of binding affinity results supported the electrostatic repulsion hypothesis. The radioligand binding assay also revealed several highly alpha 2 selective adrenergic agents among these compounds, with the binding selectivity maximizing for compounds having nitrogen substituted with a group no larger than methyl and having a five-membered carbocyclic ring (i.e., 16, 17, and 19).

Adrenergic alpha-Agonists↗
PubMed1982

Amylase release from parotid glands of hypothyroid rats. I. Altered responsiveness to adrenergic agents.

Effects of adrenergic agents on alpha- and beta-adrenergic receptors of parotid glands from hypothyroid rats were compared with those of euthyroid rats. The sensitivity for amylase release from parotid slices to adrenergic agents did not change even in hypothyroid status because ED50 values for amylase release in both groups were approx. the same: 7 x 10(-8) M for isoproterenol, 4-6 x 10(-6) M for phenylephrine and 10(-5) M for methoxamine. However, the responsiveness of the tissue to those agents which was determined as the maximal amylase release was significantly higher in hypothyroid status than in the euthyroid status. The maximal increases in amylase release in euthyroid and hypothyroid rats were approx. 7.4% and 10.0% of the total in isoproterenol, 3.9% and 7.4% of the total in phenylephrine and 1.3% and 2.7% of the total in methoxamine, respectively. The effect of dibutyryl cyclic AMP mimicked that of isoproterenol, and the responsiveness of the tissue in this case was much higher in the hypothyroid rats than in the euthyroid rats. Furthermore, 10 mM tolbutamide, which completely inhibited the activity of cyclic AMP-dependent protein kinase, blocked isoproterenol-induced amylase release by 66.5% in euthyroid rats, against only 36.3% in hypothyroid rats. These results strongly suggest that the regulation mediated through beta-adrenergic receptors plays a major role in amylase release from rat parotid glands even under hypothyroid status, and the step following cyclic AMP synthesis might, at least in some way, be involved in this regulation.

Adrenergic alpha-Agonists↗
PubMed1978

Treatment of severe attacks of asthma in children with nebulized B2 adrenergic agents.

Selective B2 adrenergic agents given by nebulizer is described as a hospital or office treatment for severe attacks of asthma. Salbutamol and Bronkosol are shown to be effective and safe drugs. The method is a simple alternative to IPPB and is easier to use in small children. The use of long-acting, selective B2 adrenergic drugs by nebulizer is recommended in preference to non-selective and short-acting adrenergic agents like epinephrine and isoproterenol.

Administration, Intranasal↗
PubMed1990

Reactivation of HSV-1 in primates by transcorneal iontophoresis of adrenergic agents.

Transcorneal iontophoresis of adrenergic agents has been shown to reactivate latent herpes simplex virus type 1 (HSV-1) and to produce viral shedding in the tear film in rabbits and mice, but not, to date, in nonhuman primates. In this study, we demonstrated induced reactivation of latent HSV-1, viral shedding, and production of ocular lesions in nine squirrel monkeys (Saimiri sciureus) by iontophoresis of 6-hydroxydopamine (6-HD) with topical instillation of epinephrine or with iontophoresis of timolol. Monkey corneas were scarified and inoculated with McKrae strain HSV-1 on three separate occasions. All monkeys received daily intramuscular prednisolone for 39 or 46 days prior to ionotophoresis. Once latency was established, a single ionotphoresis of 6-HD was performed on both eyes in five of the monkeys, followed by 1% epinephrine given topically four times daily for 5 days. Iontophoresis of timolol was performed on both eyes in the other four monkeys once per day on 3 consecutive days. Eight of the ten eyes receiving 6-HD and epinephrine shed HSV-1; seven eyes developed deep punctate, dendritic, or geographic corneal lesions. Seven of the eight eyes receiving timolol shed HSV-1; six of the eyes developed lesions suggestive of HSV-1 specific corneal lesions. The methods used in this report were slightly different from those used to reactivate HSV-1 in rabbits, in that repeated inoculations with HSV-1 and repeated intramuscular injections with prednisolone were required; however, these results demonstrate that iontophoresis of adrenergic agents can produce shedding and recurrent epithelial lesions in the nonhuman primate.

Animals↗
PubMed1976

Treatment of asthma with theophylline and beta adrenergic agents.

The understanding of the properties of adrenergic receptors and modification of ring and the N-alkyl side chain constituents have resulted in adrenergic agents with a high degree of specificity for the lung and few cardiac and central nervous system stimulating problems. These agents are useful by aerosol and oral routes, alone and in addition to theophylline for asthma. Theophylline, which acts to increase cyclic AMP by inhibition of phosphodiesterase and beta 2 adrenergic agents which increase cyclic AMP by stimulating adenylate cyclase, are the mainstays of asthma therapy. Therapy is usually begun with theophylline. Persistent symptoms with adequate theophylline levels (10-20 mug/ml) indicates the need for a beta 2 adrenergic agent by aerosol or orally as a supplement. Occasional patients will not tolerate theophylline in any preparation and can be treated with beta 2 adrenergic agents with success. The future holds great promise for improved and safer beta 2 adrenergic agents which will offer the physician a more effective means of treating asthma.

Adrenergic beta-Agonists↗
PubMed1985

Direct interaction of guinea pig eosinophils and adrenergic agents.

The effects of alpha- and beta-adrenergic stimulation on guinea pig eosinophil functions were studied. Both enhanced glucose uptake of eosinophils at a concentration of 5 X 10(-5) M after a 24-hour incubation. Decreased eosinophil chemotaxis and dose-dependent inhibition of arylsulfatase release from eosinophils induced by opsonized Candida albicans were observed when eosinophils were incubated with beta-adrenergic agents, but not with alpha-adrenergic agents. On the other hand, alpha stimulation inhibited phagocytosis of opsonized C. albicans by eosinophils and NBT reduction at concentrations of 8 X 10(-5) and 5 X 10(-5) M, respectively, but beta stimulation at the same concentrations did not. This suggests that the regulatory effect of adrenergic agents on phagocytosis in eosinophils is different from that in macrophages and polymorphonuclear leukocytes.

Adrenergic alpha-Agonists↗
PubMed1975

Adrenergic agents. 3. Synthesis and adrenergic activity of some catecholamine analogs bearing a substituted sulfonyl or sulfonylalkyl group in the meta position.

The m-phenolic group of catecholamine beta-adrenergic agonists may be replaced by various functionalities capable of undergoing H bonding. Considerable latitude in the nature of the OH simulating group is permissible with retention of activity; however, the most extensively studied analogs are ones in which a mobile proton is attached to an O or N atom. In a search for new selective bronchodilators a series of catecholamine analogs bearing a substituted sulfonyl or sulfonylalkyl group in the meta position (i.e., groups in which the mobile H is attached to a C atom) was examined. These compounds were studied for beta-adrenergic agonist activity in vitro by measuring their ability to relax tracheal smooth muscle and to increase the rate of spontaneously beating right atria of guinea pigs. Adrenergic activity was influenced by the nature of the alkylene bridge between the sulfonyl and aromatic groups, branching of the ethanolamine side chain, stereochemistry, and substitution of the sulfonyl and amino groups. Beta-adrenergic blockage was noted for some compounds having the sulfonyl attached directly to the ring. Greatest beta-adrenergic agonist potency and tissue selectivity was observed with a m-MeSO2CH2 substituent. One of these compounds, alpha-[[(1,1-dimethylethyl)amino]methyl]-4-hydroxy-3-[(methylsulfonyl)methyl]benzenemethanol hydrochloride (sulfonterol hydrochloride, USAN), was studied more extensively in animals and is presently being examined for bronchodilator activity in man.

Adrenergic beta-Agonists↗
PubMed1989

Luminal adrenergic agents modulate intestinal transport.

Intestinal transport is controlled by luminal solutes, neural pathways, and paracrine or humoral agents. The current study investigated the effect of luminally administered adrenergic agents on the intestinal transport of water and electrolytes. Dogs with 25-cm jejunal Thiry-Vella loops were studied. The loops were luminally perfused with an isotonic solution containing [14C]PEG, and the fluxes of H2O, Na+, and Cl- were calculated. Each experiment consisted of three 1-hr periods: basal, luminal agent infusion, and recovery. Luminal adrenergic agents did not alter heart rate. Norepinephrine (alpha 1 greater than alpha 2 and beta adrenergic agonist) and phenylephrine (alpha 1 adrenergic agonist) caused significant absorption of water and sodium. Clonidine (alpha 2 adrenergic agonist) and isoproterenol (beta adrenergic agonist) caused significant secretion of water, sodium, and chloride. Luminally administered adrenergic agents can influence small intestinal water and electrolyte transport. Alpha 1 agonists have a proabsorptive effect, while alpha 2 and beta agonists have a secretory effect. Luminally administered proabsorptive adrenergic agents may prove useful in pathologic secretory states such as diabetic diarrhea, small bowel transplantation, or diarrhea-associated endocrinopathies.

Animals↗
PubMed1999

Desynchronization of carbachol-induced theta-like activities by alpha-adrenergic agents in guinea pig hippocampal slices.

The effect of alpha-adrenergic agents on theta-like activity (TLA) in guinea-pig hippocampal slices was studied. TLA was induced by a cholinergic agent, carbachol. TLA had a frequency of 4.66+/-0.08 Hz (mean+/-S.E.M.) and an amplitude of 96.3+/-8.3 microV in the dentate gyrus (DG). The alpha-adrenergic agents epinephrine and clonidine increased the frequency and decreased the amplitude of TLA in a concentration-dependent manner. The agents also increased antidromic and orthodromic population spike (PS) amplitudes of the granule cells, but did not have any effect on population EPSP. Another alpha-adrenergic agent, guanabentz, had the same effect as clonidine. The adenylate cyclase inhibitor SQ22536 suppressed the increase in PS amplitude by clonidine. The results suggest that these alpha2-adrenergic agents facilitate the activity of granule cells through the activation of the alpha2-adrenoreceptor and cAMP pathway, and the facilitation causes the desynchronization of TLA.

Adenine↗
PubMed1999

Effects of imidazoline and non-imidazoline alpha-adrenergic agents on canine platelet aggregation.

Aggregatory and antiaggregatory effects of imidazol(in)e and non-imidazol(in)e alpha-adrenergic agents on canine platelets were examined turbidimetrically in citrated platelet-rich plasma or washed platelet solution. Each alpha-adrenoceptor agonist alone did not induce aggregation, but adrenaline and noradrenaline potentiated dose-dependently aggregation stimulated by ADP, collagen or thrombin. Small potentiation of ADP- or collagen-stimulated aggregation was also observed in response to oxymetazoline. The alpha2-adrenoceptor antagonists and/or imidazol(in)e alpha-adrenergic agents inhibit dose-dependently adrenaline-potentiated aggregation, whereas alpha1-adrenoceptor antagonists, a beta-adrenoceptor antagonist and non-imidazol(in)e alpha-adrenergic agents were no or less effective in inhibiting adrenaline-potentiated aggregation. The alpha2-adrenoceptor agonists did not reduce inhibitory effect of alpha2-adrenoceptor antagonists for adrenaline-potentiated aggregation. The alpha2-adrenoceptor antagonists and/or imidazol(in)es were no or less effective in inhibiting aggregation induced by ADP or thrombin alone. These results demonstrated that alpha2-adrenoceptor-blocking agents and/or imidazol(in)e alpha-adrenergic agents inhibit effectively the adrenaline-potentiated platelet aggregation.

Adenosine Diphosphate↗
PubMed1982

Effect of beta-adrenergic agents on immunoglobulin G levels of asthmatic subjects.

Asthmatic subjects using oral beta-adrenergic agents had significantly lower mean serum IgG levels than asthmatics not taking beta-adrenergic agents (984 vs. 1,195 mg/dl, p less than 0.025). Corticosteroid use had the same effect (920 vs. 1,195 mg/dl, p less than 0.005). Concomitant usage of both agents was associated with further depression of IgG levels. These were no differences between the serum levels of IgA, IgM, IgD, IgE and the complement components C3 and C4 associated with the use of either or both agents. These findings suggest that beta-adrenergic agents, used in pharmacologic doses, may have an effect on the immune system.

Adolescent↗
PubMed1997

[Effects of topical application of adrenergic agents on refraction and accommodation].

In an attempt to clarify the functional role of adrenergic receptors on accommodation, effects of various adrenergic agents on the state of accommodation were studied. Fifty-two emmetropic normal subjects (age: 19-28 y) participated in this study. We examined the effect of the alpha agonist phenylephrine hydrochloride (5%), the alpha 1 antagonist adrenergic bunazosin hydrochloride (0.1%), the beta antagonist timolol maleate (0.5%), the beta 2 antagonist betaxolal hydrochloride (0.5%), and the beta agonist isoproterenol hydrochloride (3%). Using an infrared optometer, the refraction, far point and near point of accommodation, resting point of accommodation (empty-field accommodation and dark focus of accommodation), and accommodative adaptation were measured before and after topical application of various adrenergic agents. Application of bunazosin slightly but significantly decreased the near point of accommodation. Isoproterenol evoked a hyperopic shift on the far point of accommodation. None of the agents had any effect on the resting point of accommodation. Accommodative adaptation was increased by timolol and betaxolol, and decreased by isoproterenol. We surmised that beta adrenergic agents exerted an indirect influence on the parasympathetic nervous system. The activation of beta receptors produced a hyperopic shift on the far point of accommodation and decreased accommodative adaptation, which suggests that activation of adrenergic receptors may reduce parasympathetic activity, hence affecting the state of accommodation.

Accommodation, Ocular↗
PubMed1990

Addition of phosphodiesterase inhibitors to adrenergic agents in acutely ill patients.

The addition of enoximone, a phosphodiesterase inhibitor, to adrenergic agents has been found useful in increasing cardiac output in severe heart failure. In one study of 13 patients in cardiogenic shock already receiving adrenergic support, enoximone was administered as a bolus of 0.5 mg/kg over 20 minutes. Pulmonary artery occlusion pressure decreased significantly from 21.7 +/- 5.8 mm Hg to 19.8 +/- 6.0 mm Hg (P less than 0.01) and cardiac index increased markedly. A second study investigated the effects of the addition of small boluses of enoximone to adrenergic agents in low flow states associated with heart failure (n = 8) or postoperative states after cardiac surgery (n = 10). Each of the 18 patients was treated with dobutamine; 12 patients were also treated with dopamine and 4 with noradrenaline. Enoximone was administered as small but increasing intravenous boluses. No significant change in mean arterial pressure was observed, but on 0.5 mg/kg of enoximone pulmonary artery occlusion pressure decreased significantly from 24.6 +/- 8.7 mm Hg to 19.4 +/- 9.9 mm Hg (heart failure) and from 18.2 +/- 3.3 mm Hg to 15.3 +/- 3.8 mm Hg (cardiac surgery) after the initial dose of 0.125 mg/kg. Cardiac index increased markedly after enoximone, 0.25 mg/kg. These changes were significant after the initial dose of 0.125 mg/kg. Thus, the addition of even small doses of enoximone to adrenergic agents can markedly increase cardiac index without significant effect on arterial pressure in medical or surgical cardiac patients.

Adult↗