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The AHS/AAN and Canadian guidelines are recommended for use on the basis of the AGREE-II quality assessment. Recommendations for the future development of clinical practice guidelines in migraine are provided. In particular, efforts should be made to ensure that guidelines are regularly updated and that guideline developers strive to locate and incorporate unpublished clinical trial evidence.
On-line capillary electrophoresis-electrospray ionization mass spectrometry (CE-ESI-MS) has been employed for the determination of racemic mixtures of the chiral drugs, terbutaline, ketamine, and propranolol. Separation of the different chiral forms has been achieved by introducing cyclodextrins (CDs), which act as chiral selectors, into the CE operating electrolytes. Cyclodextrins function as chiral selectors in CE because of their ability to form host-guest complexes (inclusion complexes) of varying stability with an array of chiral drugs and other compounds. Derivatized forms of beta-CD (i.e., dimethyl-beta-cyclodextrin and hydroxypropyl-beta-cyclodextrin) were used in this study due to their higher solubilities in the aqueous methanolic operating electrolyte than native beta-CD. Addition of minor quantities of methanol to the aqueous-based CE operating electrolytes improved the stability of electrospray ionization conditions and further enhanced CE resolution of the enantiomeric pairs relative to purely aqueous systems. Introduction of the CDs into the CE operating electrolytes caused suppression of analyte signals in ESI-MS, and the dependence of analyte signal intensities on the solution concentrations of the derivatized beta-CDs was examined. Under optimized conditions, the different enantiomeric forms of the compounds under investigation were successfully separated and detected by CE-ESI-MS.
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Prolongation of LBct could protect against N2 narcosis and it could plausibly be achieved with the oral administration of a beta-blocker, such as propranolol, prior to deep submarine escape. Animal experiments should be conducted to validate this pharmacological approach.
The RP4 neuron showed spontaneous firing of action potentials. Extracellular application of ropivacaine (900 microM) reversibly elicited bursts of potential in the RP4 neuron. The bursts of potential elicited by ropivacaine were not blocked after administration of: (1) prazosin, propranolol, atropine, d-tubocurarine; (2) calcium-free solution; and (3) pretreatment with H89 or chelerythrine. The bursts of potential elicited by ropivacaine were blocked by pretreatment with U73122 (30 microM) or by adding neomycin (3.5 mM) or high-magnesium solution (30 mM).
The hypotensive effects of A. muricata are not mediated through muscarinic, histaminergic, adrenergic and nitric oxide pathways, but through peripheral mechanisms involving antagonism of Ca(2+).
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Randomized controlled trials of variceal bleeding prophylaxis demonstrate beta-blocker (BB) withdrawal rates of about 15%. We aimed to evaluate the dosing and tolerance of BBs achievable in a specialized, nurse-run BB titration clinic with non-trial participants.
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In vitro, ketamine preconditions isolated human myocardium, at least in part, via activation of adenosine triphosphate-sensitive potassium channels and stimulation of alpha- and beta-adrenergic receptors.
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Our hypothesis is that leptin release is controlled neurohormonally. Conscious, male rats bearing indwelling, external, jugular catheters were injected with the test drug or 0.9% NaCl (saline), and blood samples were drawn thereafter to measure plasma leptin. Anesthesia decreased plasma leptin concentrations within 10 min to a minimum at 120 min, followed by a rebound at 360 min. Administration (i.v.) of lipopolysaccharide (LPS) increased plasma leptin to almost twice baseline by 120 min, and it remained on a plateau for 360 min, accompanied by increased adipocyte leptin mRNA. Anesthesia largely blunted the LPS-induced leptin release at 120 min. Isoproterenol (beta-adrenergic agonist) failed to alter plasma leptin but reduced LPS-induced leptin release significantly. Propranolol (beta-receptor antagonist) produced a significant increase in plasma leptin but had no effect on the response to LPS. Phentolamine (alpha-adrenergic receptor blocker) not only increased plasma leptin (P < 0.001), but also augmented the LPS-induced increase (P < 0.001). alpha-Bromoergocryptine (dopaminergic-2 receptor agonist) decreased plasma leptin (P < 0.01) and blunted the LPS-induced rise in plasma leptin release (P < 0.001). We conclude that leptin is at least in part controlled neurally because anesthesia decreased plasma leptin and blocked its response to LPS. The findings that phentolamine and propranolol increased plasma leptin concentrations suggest that leptin release is inhibited by the sympathetic nervous system mediated principally by alpha-adrenergic receptors because phentolamine, but not propranolol, augmented the response to LPS. Because alpha-bromoergocryptine decreased basal and LPS-induced leptin release, dopaminergic neurons may inhibit basal and LPS-induced leptin release by suppression of release of prolactin from the adenohypophysis.
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Pretreatment of cultured endothelial cells from human umbilical veins (HUVECs) with different concentrations of the non-selective beta-blocker propranolol, the beta 1-blocker metoprolol and the beta 1-blocker and beta 2-agonist celiprolol (all 10(-7)-10(-4) mol L-1) was found to reduce ET-1 production. This ET-1-reducing effect was even more pronounced in thrombin-stimulated cells (10(-5) mol L-1 of propranolol, metoprolol and celiprolol: 19% +/- 5.8%, 25% +/- 4% and 37% +/- 5.2% respectively).
Norepinephrine (NE) causes hypertrophic growth of cardiac myocytes via stimulation of alpha1-adrenergic receptors (alpha1-AR). Reactive oxygen species (ROS) can act as signaling molecules for cell growth. Accordingly, we tested the hypothesis that ROS mediate alpha1-AR-stimulated hypertrophic growth in adult rat ventricular myocytes (ARVM). NE increased the level of intracellular ROS as assessed by lucigenin chemiluminescence or cytochrome c reduction, and this effect was prevented by the superoxide dismutase (SOD)-mimetic MnTMPyP. NE also caused the induction of MnSOD mRNA. alpha1-AR stimulation with NE (1 microM) in the presence of propranolol (2 microM) for 48-96 h caused a hypertrophic growth phenotype characterized by a 36+/-3% increase in 3H-leucine incorporation, a 49+/-14% increase in protein accumulation, a six-fold induction of atrial natriuretic peptide mRNA, actin filament reorganization, and the induction of MnSOD mRNA. These responses were all prevented by pretreatment with the alpha1-AR-selective antagonist prazosin (100 n M) or the SOD-mimetics MnTMPyP (50 microM) and Euk-8 (100 microM). MnTMPyP had no effect on alpha1-AR-stimulated 3H-inositol phosphate turnover or the hypertrophic phenotype caused by the protein kinase C activator phorbol-12-myristate-13-acetate. Thus, ROS play a critical role in mediating the hypertrophic growth response to alpha1-AR-stimulation in ARVM.
In hyperthyroid men, HSD, DE, PE, and ED prevalence was 17.6, 2.9, 50, and 14.7%, whereas in hypothyroid men, the prevalence of HSD, DE, and ED was 64.3% and of PE was 7.1%. After thyroid hormone normalization in hyperthyroid subjects, PE prevalence fell from 50 to 15%, whereas DE was improved in half of the treated hypothyroid men. Significant changes were found in the subdomains of the International Index of Erectile Function; ejaculation latency time doubled after treatment of hyperthyroidism (from 2.4 +/- 2.1 to 4.0 +/- 2.0 min), whereas for hypothyroid men it declined significantly, from 21.8 +/- 10.9 to 7.4 +/- 7.2 (P < 0.01 for both). TSH and thyroid hormone levels normalized rapidly after treatment, and changes in circulating sex steroids partially reflected the changes in SHBG levels.
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The records of 53 patients who underwent treatment after a diagnosis of abdominal migraine were retrospectively reviewed. Responses to treatment were graded as excellent (cessation of recurrent abdominal pain), fair (persistence of symptoms but milder and less frequent), or poor (no response). Follow-up data were available in 38 patients. Twenty-four patients were treated with propranolol and 12 with cyproheptadine. Four were not treated because of mild and infrequent symptoms.