Disease relevance of terbutaline

• Terbutaline, as currently used to prevent premature labor, is a potent inotropic and chronotropic agent [1].
• The effect of terbutaline on cardiac function in patients with stable chronic obstructive lung disease [2].
• Pulmonary edema accompanying terbutaline treatment is probably not due to cardiac failure [1].
• Ventricular tachycardia after terbutaline [3].
• Angina pectoris associated with use of terbutaline for premature labor [4].

Psychiatry related information on terbutaline

• Our results indicate that terbutaline is a neurotoxicant that elicits biochemical alterations and structural damage in the immature brain during a critical period [5].
• Beta-receptor agonist (terbutalin or isoxsuprin) administration to pregnant women either because of premature labor (therapy group; T; n = 8) or as prophylactic treatment (prophylaxis group; p; n = 8) resulted in a marked drop in serum potassium (p less than 0.001) during the first two hours of infusion in all patients [6].
• To characterize the effect of smoking cessation and nicotine replacement on pulmonary symptomatology, baseline pulmonary function and response to terbutaline, and purified T lymphocyte beta 2-receptor regulation; and the relationship between T lymphocyte beta 2-receptor density and pulmonary function [7].
• A good patient compliance was achieved with this dosage of terbutaline two times daily [8].
• Effect of atropine and terbutaline on motor activity of the continent caecal reservoir for urine [9].

High impact information on terbutaline

• We investigated whether tolerance develops to the protective effect of inhaled terbutaline on airway responsiveness to the bronchoconstrictors methacholine (which acts directly on airway smooth muscle) and AMP (which acts indirectly by stimulating the release of mediators from mast cells) during sustained treatment with terbutaline [10].
• After seven days of treatment with terbutaline, the protective effect of terbutaline against methacholine decreased to 2.2 doubling doses (95 percent confidence interval, 1.3 to 3.0; P = 0.04), and that against AMP decreased even more, to 1.7 doubling doses (95 percent confidence interval, 1.1 to 2.4; P less than 0.001) [10].
• To assess whether an extension tube between the aerosol source and the patient improves drug-inhalation therapy in children with acute bronchoconstriction, we treated 20 children under double-blind conditions with placebo or terbutaline delivered by a conventional aerosol or an aerosol with a tube spacer [11].
• Both terbutaline treatments resulted in a significant increase in forced expiratory volume in one second, as compared with placebo (P less than 0.001), but treatment with the tube-spacer aerosol produced significantly more improvement than did treatment with the conventional aerosol (P less than 0.01) [11].
• In 17 patients with moderate to severe asthma, we compared acute bronchodilator effects of the following drugs or drug combinations using a double-blind crossover design: terbutaline, 5; aminophyline 400; terbutaline, 5, plus aminophyline, 400; terbutaline, 2.5; aminophylline, 200; terbutaline, 2.5, plus aminophyline, 200 mg; and placebo [12].

Chemical compound and disease context of terbutaline

• Treatment of the systemic capillary leak syndrome with terbutaline and theophylline. A case series [13].
• A beta 2-agonist, terbutaline, and a phosphodiesterase inhibitor, aminophylline, were administered in combination in a mouse model of amyloidosis induced by inflammatory stimulation with silver nitrate [14].
• Terbutaline (TERB) and isoproterenol (ISO) increased lung edema clearance in control nonventilated rats (from 0.50 +/- 0. 02 ml/h to 0.81 +/- 0.04 ml/h and 0.99 +/- 0.05 ml/h, respectively) and restored the lung's ability to clear edema in HVT ventilated rats (from 0.25 +/- 0.03 ml/h to 0.64 +/- 0.02 ml/h and 0.88 +/- 0. 09 ml/h, respectively) [15].
• In addition to placebos, the following were administered during hypoglycemia (2 h after insulin injection) in IDDM patients: oral glucose, 10 and 20 g; subcutaneous glucagon, 1.0 mg; oral Ala, 40 g; oral terbutaline, 5.0 mg; and subcutaneous terbutaline, 0.25 mg [16].
• We conclude that subcutaneous terbutaline is at least as effective as epinephrine in the management of reversible bronchospasm and may be considered a drug of choice in stable asthmatics [17].

Biological context of terbutaline

• During terbutaline therapy, heart rate, ejection fraction, and cardiac output increased significantly [1].
• Patients taking formoterol had a longer time to their first severe asthma exacerbation (relative-risk ratio 0.55 [95% CI 0.34-0.89]), took fewer inhalations of study drug, and had larger increases in FEV1 (5%) and morning and evening peak expiratory flow (mean difference in increase 11 L/min and 8 L/min) than those taking terbutaline [18].
• In normal rats, terbutaline administration (32 micrograms.min-1.kg-1 body wt) increased both cardiac output and portal tributary blood flow, thus mimicking hemodynamic changes in cirrhotic rats [19].
• In cirrhotic rats, despite a significant increase in portal tributary blood flow (from 19.9 +/- 1.7 ml/min to 22.7 +/- 1.5 ml/min), terbutaline decreased portal pressure from 17.4 +/- 1.0 mm Hg to 15.0 +/- 0.8 mm Hg [19].
• In vivo intravenous infusions of terbutaline (dose range 25 to 300 ng/kg body weight per min for 15 min) dose dependently increased heart rate and shortened the pre-ejection period and heart rate-corrected electromechanical systole (QS2) time [20].

Anatomical context of terbutaline

• We observed tolerance to the nonbronchodilator actions of the inhaled beta 2-agonist terbutaline in patients with mild asthma, an effect that may be more pronounced in mast cells than in bronchial smooth muscle [10].
• Significantly fewer patients receiving albuterol experienced one or more central nervous system or musculoskeletal side effects than patients receiving terbutaline [21].
• By contrast, a 7-d treatment with terbutaline caused a reduction in the circulating number of lymphocytes in some subsets that was identical to that seen in heart failure patients [22].
• When adipose tissue was pretreated with the beta 1/beta 2-selective adrenoceptor blocker propranolol the glycerol increasing effect of dobutamine or terbutaline was inhibited by 80-85% but the glycerol response to CGP 12177 was not influenced [23].
• Effect of terbutaline, a beta 2-adrenoreceptor agonist, on gastric acid secretion and serum gastrin concentrations in humans [24].

Associations of terbutaline with other chemical compounds

• We investigated, in 36 healthy volunteers, the effects of prednisone and ketotifen on recovery of lymphocyte beta 2-adrenoceptor density (determined by (-)-125iodocyanopindolol binding) and responsiveness (assessed by lymphocyte cyclic AMP [cAMP] responses to 10 microM (-)-isoprenaline) after desensitization by the beta 2-agonist terbutaline [25].
• The airway response and cardiovascular and hypokalaemic effects of fenoterol, salbutamol, and terbutaline given in multiples of standard doses from metered-dose inhalers were studied in ten patients with mild asthma [26].
• In the first study in 8 subjects, 500 and 2000 micrograms terbutaline thrice in 1 day protected against histamine-induced bronchoconstriction, and the increase in PD20 compared with placebo remained high throughout the day and overnight [27].
• Subcutaneous terbutaline (0.25 mg) reduced acid secretion during intravenous infusion of a submaximal dose of pentagastrin by 30%-40% (p less than 0.005), even though terbutaline increased serum gastrin levels (p less than 0.05) [24].
• Terbutaline 0.2 micrograms/kg/min increased heart rate by 15 +/- 2 beats/min, and this response doubled (to 29 +/- 3 beats/min) when the terbutaline infusion followed atropine pretreatment, whereas atenolol pretreatment had no significant effect [28].

Gene context of terbutaline

• The terbutaline-induced down-regulation of IL-6 gene production was mediated by an inhibitory effect of terbutaline on TNF-alpha, which was exerted through the MAPK and cAMP pathways, whereas the up-regulation appeared to be due to a direct action of intracellular cAMP [29].
• Furthermore, the time course effects of terbutaline on cAMP, MAPK (p42/p44), and TNF-alpha release were evaluated in the cells [29].
• The beta 3-, beta L-, and beta 2-adrenoceptor agonists BRL 37344, dobutamine, and terbutaline inhibited ob gene expression in mouse brown adipocytes differentiated in culture with EC50 values of 0.3, 1.0, and 85 nM, respectively [30].
• In contrast, treatment with Prl or terbutaline, but not hCG, inhibited 20 alpha-hydroxysteroid dehydrogenase (20 alpha-HSD) activity by decreasing the apparent maximal velocity of the enzyme with no change in its Km value [31].
• While endogenous IL-18 produced by salbutamol and terbutaline reached a sufficient concentration to induce IL-12 production, these beta 2-AR agonists did not induce the production of IL-12 at all [32].

Analytical, diagnostic and therapeutic context of terbutaline

• In a randomized, double-blind, crossover study, 12 patients with mild asthma each inhaled a single dose of terbutaline (500 micrograms) or placebo before a challenge with a series of doubling doses of inhaled methacholine or AMP, before and after treatment for seven days with 500 micrograms of terbutaline four times daily or placebo [10].
• The bronchodilator effects of aerosolized terbutaline. A controlled, double-blind study [33].
• The effectiveness of the nebulizer regimen for children with chronic asthma is better when cromolyn is used alone or in combination with terbutaline than when the beta-agonist is used alone [34].
• Hand tremor, heart rate, and electrolyte, plasma (pl) insulin, blood (bl) glucose, and pl terbutaline levels were measured in 11 healthy men during infusion and oral administration of terbutaline [35].
• The administration of 0.25 mg terbutaline sulfate by subcutaneous injection prior to A. suum challenge prevented the changes in mucus velocity, pulmonary resistance, and arterial PO2 [36].

References