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Further, large interventional studies are required to determine the clinical benefit-risk ratio of oral propranolol to prevent vision-threatening ROP in very preterm infants.
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20-ml blood specimens were collected from 40 healthy volunteers who had not taken any drug in the week before collection. 2.0-ml alliquots were incubated at 37 C with different concentrations of the drugs for 30 minutes. In all cases, a control group was incubated with saline (0.9%). Two labelling methods were used: 1) EDTA method, in which 60 l of SnCl2 (10.2 g/ml), 2.0 ml of saline, 0.2 ml EDTA 2.2%, and 7.4 MBq of Na99mTcO4 were added, and the mix was incubated for 5 minutes. 2) The hypochlorite method, in which specimens were initially incubated with SnCl2 (10.2 g/ml) for 5 minutes. Then, 40 l of 1% hypochlorite and all the reagents described in the previous method were added. With both methods, erythrocytes were separated by centrifugation and the labelling yield was estimated.
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Beta-blockers significantly decrease the risk of mortality in patients after myocardial infarction (MI). Furthermore, beta-blockers reduce the risk of reinfarction and mortality in both the immediate and long term after an MI. Guidelines recommend that post-MI patients should be started on beta-blocker therapy and continued indefinitely, unless absolutely contraindicated or not tolerated. Despite compelling evidence, many patients are not prescribed beta-blockers after a myocardial event. In addition, some patients are treated with agents whose long-term use has not been shown to be effective. This article discusses practical implementation of beta-blockers, provides the rationale for choosing specific beta-blockers, and presents protocols for initiating or switching to evidence-based therapies in the acute and chronic post-MI period.
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An on-line coupled reversed-phase liquid chromatographic-gas chromatographic (LC-GC) method with minimal manual sample preparation is developed for the analysis of metoprolol, oxprenolol, propranolol, timolol, and codeine (as an internal standard) in human serum and urine. The method is based on a loop-type interface and concurrent eluent evaporation technique. On-line liquid-liquid extraction (LLE) is used to extract the analytes from aqueous eluent to organic solvent before injection onto the GC, and the two phases are separated with a sandwich-type phase separator. The LC is used for cleanup, and the GC is used for the final separation and detection of the analytes. Total analysis time is less than 45 min, which is much less than those of traditional analysis methods. Recoveries in LC cleanup and on-line LLE are excellent. A marked increase in the recoveries with on-line LLE is obtained by heating the aqueous eluent and the extraction coil. Linearity and repeatability of the method are good for both serum and urine, and the limits of quantitation for the analytes are 18-44 ng/mL.
We have evaluated the effect of 3,4-secoisopimar-4(18),7,15-triene-3-oic acid (compound 1), isolated from the aerial parts of Salvia cinnabarina, on the contractile response elicited by electrical field stimulation (EFS) in the rat isolated urinary bladder. Compound 1 (10 ( - 7) - 10 ( - 4) M) produced a concentration-dependent inhibition of the EFS contractile response without modifying the contractions produced by exogenous acetylcholine (10 ( - 6) M). A number of antagonists/inhibitors including a combination of atropine (10 ( - 6) M), phentolamine (10 ( - 6) M), propranolol (10 ( - 6) M) and hexamethonium (10 ( - 4) M), the NK (1) receptor antagonist SR140333 (10 ( - 7) M) plus the NK (2) receptor antagonist SR48968 (10 ( - 6) M), naloxone (10 ( - 6) M), verapamil (10 ( - 7) M), capsazepine (10 ( - 5) M) and the CB (1) receptor antagonist SR141716A (10 ( - 6) M) did not modify the inhibitory effect of compound 1. However, the nitric oxide (NO) synthase inhibitor L-NAME (3 x 10 ( - 4) M), significantly reduced the inhibitory effect of compound 1. It is concluded that compound 1 inhibits rat bladder contractility with a mechanism involving, at least in part, NO production.
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The cervical sympathetic trunks innervate the carotid bodies, carotid baroreceptors, thyroid gland and the upper airway mucosa, structures which can influence breathing and upper airway resistance. However, their role in the control of ventilation and upper airway patency is poorly understood. A constant airflow was applied to the upper airway through a high-cervical tracheostomy in anaesthetized rats breathing spontaneously through a low-cervical tracheostomy. The peripheral ends of the cut cervical sympathetic trunks were stimulated electrically and airflow resistance and ventilation were measured. The effects of cervical sympathetic trunk section on ventilation were also measured in conscious rats. In conscious rats, cutting the sympathetic trunks caused a decrease in ventilation during normoxia but only slightly affected ventilatory responses to hypoxia and hypercapnia. In anaesthetized rats, sympathetic trunk stimulation caused an inhibition of breathing which was sometimes followed by excitation. These responses were unaffected by alpha- or beta-adrenoceptor blockade but were abolished by cutting the carotid sinus nerves. Sympathetic stimulation also caused a fall in upper airway resistance which was reduced by bypassing the nose, unaffected by propranolol or carotid sinus nerve section and abolished by phentolamine. It was concluded that the cervical sympathetic nerves exert important influences on ventilation and upper airway resistance.
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We measured free intralymphocyte magnesium (Mgi) in 10 hypertensive subjects (HS) before and after treatment with atenolol (A) and in 16 normotensive control subjects (NC). We also carried out in vitro studies on human lymphocytes to test the effect of catecholamines and beta-antagonists on Mgi. Mgi in HS was not statistically different before and after the treatment with A (M +/- SD, basal: 227 +/- 31 + mumol/l; A: 236 +/- 47 mumol/l; NS). Mgi in NC proved not statistically different as compared to HS without treatment (M +/- SD, NC: 232 +/- 35 mumol/l; HS before treatment: 227 +/- 31 mumol/l; NS). The Mgi of the lymphocytes treated in vitro with noradrenaline (NA) significantly decreased in comparison with the control (M +/- SD, basal: 244 +/- 26 mumol/l; NA: 198 +/- 25 mumol/l; p = 0.0001), whereas it did not change after incubation with NA and propranolol (P) (M +/- SD, basal: 238 +/- 32 mumol/l; NA + P: 239 +/- 30 mumol/l; NS). On the other hand Mgi decreased significantly after incubation with NA and A (M +/- SD, basal: 255 +/- 21 mumol/l; NA + A: 202 +/- 34 mumol/l). Our in vivo data show that the Mgi of HS remains unvaried after treatment with A, and that there is not statistical difference between Mgi of NC and of HS before treatment. The in vitro study demonstrated that catecholamines cause a significant reduction in Mgi. This effect is only inhibited by a non-selective beta-blocker such as P. These results seem to explain the ineffectiveness of treatment with atenolol on our patients' Mgi.
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Overall, 265 parts (94.6%) were integral and 213 (76.1%) were considered as adequate for administration. The mean (± standard deviation) weight of quarters judged as suitable and non-suitable for administration was 49.56 ± 5.27 mg and 46.24 ± 7.53 mg, respectively. Splitting caused a mean weight loss in each tablet of 2.97 ± 2.91 mg (median 2.06 mg). The percentage of quarters with weight lower than theoretical was 55.88%, and the remaining weighted more than expected. The mean propranolol content in quarters was 9.52 ± 0.96 mg (median 9.42 mg, range 7.36-12.23 mg) and 42% of quarters were out of the ± 10% acceptance range.
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We report a patient with von Willebrand' s disease who had had recurrent and life-threatening bleeding from the gastrointestinal tract. Despite extensive investigation, no apparent cause of haemorrhage was identified. He was successfully treated with combined administration of octreotide LAR (long-acting release) and propranolol. This is the first report on the successful use of octreotide LAR in a patient with von Willebrand' s disease.
[(18)F] FPTC was synthesized by Cu(I)-catalyzed alkyne-azide cycloaddition. First, (18)F-PEGylated alkyne was prepared by (18)F-fluorination of the corresponding tosylate. Next (18)F-PEGylated alkyne was reacted with an azidoalcohol derivative of 4-hydroxycarbazol in the presence of the phosphoramidite Monophos as a ligand and Cu(I) as a catalyst. After purification with radio-HPLC, the binding properties of [(18)F FPTC were tested in β-AR-expressing C6-glioma cells in vitro and in Wistar rats in vivo using microPET.
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Azygos blood flow is an index of blood flow through gastroesophageal collateral vessels and varices in portal hypertension. Conventional measurement of azygos blood flow involves catheterization of the azygos vein. We studied the feasibility of assessing azygos blood flow with color Doppler endosonography and of monitoring the effects of vasoactive agents on azygos blood flow.
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Eight male volunteers participated in two studies. In the first study subjects received oral dosages of 2.5, 7.5, 15, and 40 mg nadolol or propranolol (both beta1- and beta2-adrenergic receptor antagonists) at random, after which isoproterenol (beta1-, beta2-, and beta3-adrenergic receptor agonist) was infused in an individually determined dosage (range, 19 to 35 ng/kg x min) that increased energy expenditure by 25% without pretreatment. In the second study, 50, 100, and 200 ng/kg x min isoproterenol or saline solution were infused after pretreatment with 80 mg nadolol. In both studies energy expenditure and respiratory exchange ratio were measured by indirect calorimetry and, at the end of each infusion period, blood samples were taken and tremor score (only first study), heart rate, and blood pressure were measured.
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The reactivity of physiological systems and behavior to psychological stress is reduced with increasing familiarity with a repeated stressor. This reduced reactivity, termed habituation, is a crucial adaptation limiting negative health consequences of stress and can be disrupted in psychopathology. We hypothesized that the ability to habituate physiologically and behaviorally to previously experienced stressors depends on β-adrenergic receptor activation (β-AR) in the basolateral amygdala (BLA), a specific neural substrate important for the consolidation of multiple types of memories. We observed that administration of the β-AR antagonist propranolol into the BLA after each of four daily exposures to restraint stress prevented the normal development of neuroendocrine and behavioral habituation measured during the fifth restraint in adult male rats. In contrast, the β-AR agonist clenbuterol administered into the BLA after each restraint on days 1-4 enhanced neuroendocrine habituation at the lowest dose but attenuated behavioral habituation at high doses. We then explored intracellular signaling mechanisms in the BLA that might be a target of β-AR activation during stress. β-AR activation post restraint is necessary for the alteration in basal phosphorylated ERK (pERK) levels, as daily post-stress β-AR blockade on days 1-4 prevented repeated stress from leading to decreased pERK in the BLA on day 5. Finally, we examined the effect of blocking ERK phosphorylation in the BLA after each restraint on days 1-4 with the MEK (MAPK/ERK kinase) inhibitor U0126, and found that this was sufficient to both mimic neuroendocrine habituation in stress-naive animals and to enhance it in repeatedly stressed animals during restraint on day 5. Together, the results suggest that an individual's ability to habituate to repeated stress is regulated by activation of BLA β-AR, which may have these effects by transducing subsequent reductions in pERK. Individual variations in β-AR activation and intracellular signaling in the BLA may contribute significantly to adaptation to psychological stress and consequent resilience to stress-related psychopathology.
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To study the effects of beta 2-adrenergic receptor-selective agonist clenbuterol on nitrogen metabolism and glucose-6-phosphate dehydrogenase activity of rat hepatocyte and its pharmacological mechanism.
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Brain tryptophan concentrations are increased by various stressful treatments, an effect that can be prevented by beta-adrenoceptor antagonists. This study aimed to determine the beta-adrenergic subtype responsible for the tryptophan response. Male CD-1 mice received intraperitoneal injections of nonselective and subtype-selective beta-adrenergic antagonists 20 min before subtype-selective beta-agonists. Selected brain regions were dissected for analysis of tryptophan content by high-performance liquid chromatography with electrochemical detection. The beta(2)-selective agonist clenbuterol (0.3 mg/kg) induced increases in brain tryptophan that reached a peak ( approximately 60%) 1 h following injection and small but statistically significant increases ( approximately 20%) in 5-hydroxyindoleacetic acid: serotonin ratios 2 h following injection. The beta(1)-selective agonist dobutamine (10 mg/kg) produced less robust increases ( approximately 40%) in brain tryptophan, whereas the beta(3)-selective agonists BRL 37344 (0.2 mg/kg (+/-)-(R*,R*)-[4-[2-[[2-(3-chlorophenyl)-2-hydroxyethyl]amino)propyl] phenoxy]acetic acid sodium)) and CL 316243 [0.1 mg/kg disodium 5-[(2R)-2-([(2R)-2-(3-chlorophenyl)-2-hydroxyethyl]amino)propyl]-1,3-benzodioxole-2,2-dicarboxylate)] resulted in larger increases (80 to 100%). Pretreatment with the beta(2)-selective antagonist ICI 118551 (0.5 mg/kg (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxyl]-3-[(1-methylethyl)amino]-2-butanol) attenuated the increases in tryptophan induced by both clenbuterol (0.1 mg/kg) and dobutamine (10 mg/kg). Pretreatment with the beta(1/2)-selective antagonist propranolol (2.5 mg/kg), the beta(3)-selective antagonist SR 59230A [1.5, 2.5, 5, or 20 mg/kg (3-(2-ethylphenoxy)-1[1S)-1,2,3,4-tertahydronaphth-1-yl-amino]-(2S)-2-propanol oxalate)], or ICI 118551 (0.5 mg/kg) did not prevent the BRL 37344-induced increase in brain tryptophan, whereas the beta(1/2/3)-antagonist bupranolol (10 mg/kg) attenuated it. CL 316243 had no effect on brain tryptophan in beta(3)-receptor knockout mice, whereas clenbuterol increased brain tryptophan, indicating that beta-adrenergic modulation of brain tryptophan occurs in the absence of beta(3)-receptors. We conclude that activation of either beta(2)- or beta(3)-adrenergic receptors, but not beta(1)-adrenergic receptors, increases mouse brain tryptophan content.
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I see many children with infantile hemangiomas and have read about new therapeutic options such as propranolol. Is this medication effective and safe for treating hemangiomas in children?
Infantile haemangiomas (also known as strawberry birthmarks) are soft, raised swellings of the skin which are usually uncomplicated and tend to regress spontaneously over time. Some haemangiomas occur in high-risk areas or can develop complications; therefore, intervention may be necessary. Various interventions have been proposed, but it is unclear whether any of these interventions are effective.
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A daily fluctuation of AzBF and PBF was observed, peaking at 24:00 h in nine patients. In three other patients, peak AzBF and PBF were observed both at 16:00 and 24:00 h. Two patients were constant throughout the day. When the daily variation was compared, ANOVA showed a significant difference (P < 0.001). Propranolol administration at 19:00 h reduced AzBF (-40.7 +/- 17.9% vs. baseline, P < 0.001) and PBF (-26.5 +/- 10.7% vs. baseline, P < 0.01) at 24:00 h.
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Interactions between widely used anthranoid laxatives and other simultaneously administered drugs are not known. In this paper, the influence of rhein, danthron, sennidins A/B, sennosides A/B, and senna leaf infusion was investigated on the permeability of furosemide, ketoprofen, paracetamol, propranolol, verapamil, digoxin, and Rhodamine 123 across Caco-2 monolayers. The effects on monolayer integrity ([(14)C]mannitol permeability, TEER) were also determined. The in vitro absorption of highly permeable drugs was not strongly affected during co-administration of the laxatives. Furosemide permeability was enhanced by rhein and danthron (3.6 and 3.0-fold), which may partly be due to opening of the paracellular spaces and/or effects on active efflux. However, the secretory permeability of digoxin and Rho 123 was not strongly affected by rhein and danthron, suggesting that inhibition of MDR1 was not responsible for the increased permeation of furosemide. The absorptive permeability of digoxin was decreased by rhein and danthron, offering evidence for effects on apical membranes. The effects on monolayer integrity were detectable, but reversible. According to presented experiments, daily use of laxatives with well-absorbing drugs would seem unlikely to affect drug permeability, but the effects on the absorption of poorly permeable drugs cannot be excluded.
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Testosterone BA was less than 10% by ID, IC, and IPV routes, due to high hepatic extraction, consistent with its high systemic clearance (63 ml x min(-1) x kg(-1)) and short terminal plasma half-life (23 min). The IPV BA of amoxicillin was 95%+/-6% indicating the absence of hepatic extraction in the rat, but with an ID BA of approximately 39% suggesting incomplete GI absorption to be the main barrier to bioavailability. Absorption was poor from the colon, demonstrating site-dependence consistent with literature reports of site-dependent absorption. Low oral BA of propranolol was due in part to first-pass hepatic extraction (IPV BA of 36%). The IPV BA of propranolol was dose-dependent, most likely due to saturation of the P450 enzymes. Atenolol was incompletely bioavailable due to incomplete intestinal absorption, with no contribution of hepatic first-pass metabolism. Antipyrine was highly bioavailable by all routes.
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Nicorandil is a drug with both nitrate-like and ATP-sensitive potassium-channel (K+ ATP) activating properties. By virtue of this dual mechanism of action, the drug acts as a balanced coronary and peripheral vasodilator and reduces both preload and afterload. The K+ ATP channel has been shown to be involved in the phenomenon of myocardial preconditioning, and studies in animal models of ischaemia-reperfusion-induced myocardial stunning or infarction indicate that nicorandil has cardio-protective effects. Studies in patients undergoing percutaneous transluminal coronary angioplasty (PTCA) have shown that the administration of nicorandil reduces ST-segment elevation during ischaemia. Nicorandil significantly improved the results of exercise tolerance tests versus baseline in patients with stable effort angina pectoris in early noncomparative trials. The drug also improved the results of exercise tolerance tests relative to placebo in early randomised, double-blind, placebo-controlled trials. In randomised, double-blind comparative studies in patients with angina pectoris, nicorandil has demonstrated equivalent efficacy, as measured by exercise tolerance testing, to isosorbide di- and mononitrate, metoprolol, propranolol, atenolol, diltiazem, amlodipine and nifedipine. The effects of nicorandil on various aspects of myocardial recovery from ischaemic damage caused by acute myocardial infarction have been investigated in the short term. Regional left ventricular (LV) wall motion, a marker of myocardial function, was significantly improved in nicorandil recipients relative to control. The main adverse event associated with nicorandil as treatment for angina pectoris is headache. This can be minimised by commencing nicorandil at a low dose in patients prone to headache. There have been infrequent case reports of mouth ulcers in patients receiving nicorandil; causality has not been conclusively established, but product prescribing information indicates that an alternative treatment should be considered if persistent aphthous or severe mouth ulceration occurs. Thus, nicorandil remains a useful background therapy for patients with angina pectoris. The drug has also demonstrated potential cardioprotective effects when used as part of an intervention strategy directly after acute myocardial infarction in high-risk patients. Further large scale longer term studies of nicorandil in this latter indication are awaited with interest.
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Improvements in glucose and lipid metabolism mediated by vasodilating beta-blockers may help reduce coronary artery disease risk among high-risk patients with hypertension.
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To reveal heterogeneity of mitochondrial function on the single-mitochondrion level we have studied the spatiotemporal dynamics of the mitochondrial Ca2+ signaling and the mitochondrial membrane potential using wide-field fluorescence imaging and digital image processing techniques. Here we demonstrate first-time discrete sites--intramitochondrial hotspots--of Ca2+ uptake after Ca2+ release from intracellular stores, and spreading of Ca2+ rise within the mitochondria. The phenomenon was characterized by comparison of observations in intact cells stimulated by ATP and in plasma membrane permeabilized or in ionophore-treated cells exposed to elevated buffer [Ca2+]. The findings indicate that Ca2+ diffuses laterally within the mitochondria, and that the diffusion is limited for shorter segments of the mitochondrial network. These observations were supported by mathematical simulation of buffered diffusion. The mitochondrial membrane potential was investigated using the potentiometric dye TMRM. Irradiation-induced fluctuations (flickering) of TMRM fluorescence showed synchronicity over large regions of the mitochondrial network, indicating that certain parts of this network form electrical syncytia. The spatial extension of these syncytia was decreased by 2-aminoethoxydiphenyl borate (2-APB) or by propranolol (blockers of nonclassical mitochondrial permeabilities). Our data suggest that mitochondria form syncytia of electrical conductance whereas the passage of Ca2+ is restricted to the individual organelle.