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antitussives/infarction
Veza se sprema u međuspremnik
6 rezultatima
Cerebral infarct after an overdose of anti-cold medicines.
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Ameliorating effects of cloperastine on dysfunction of the urinary bladder caused by cerebral infarction in conscious rats.
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We investigated the effects of the centrally acting antitussives dextromethorphan and cloperastine on urinary bladder dysfunction 24 h after cerebral infarction in rats using the cystometry technique. First, cystometrography was performed in conscious male Sprague-Dawley rats. Cerebral infarction
Comparison of stably expressed rat UGT1.1 and UGT2B1 in the glucuronidation of opioid compounds.
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Prijava Registriraj se
Opioids are important drugs used as analgesics, antitussives, antidiarrheals, and in the therapy of myocardial infarctions, and as antagonists of opioid intoxication. The glucuronidation of these compounds, catalyzed by UDP-glucuronosyltransferases (UGTs), is well known to be a primary step in their
Neuroprotection by dextromethorphan in acute experimental subdural hematoma in the rat.
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Experimental acute subdural hematoma in the rat has been shown to produce a zone of apparent infarction under the clot, and excitatory amino acid toxicity appears to play a role in the damage observed. We report the effect of dextromethorphan, a commonly used antitussive and a noncompetitive
[Is the GIRK channel a possible target in the development of a novel therapeutic drug of urinary disturbance?].
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Clinically, both overactive bladder (OAB) and dysuria are known to occur in patients with cerebral infarction (CI). A few anticholinergic drugs are used to treat OAB in such patients, although the effect is not satisfactory. On the other hand, little or no therapeutic drug is available for dysuria
Dimemorfan protects rats against ischemic stroke through activation of sigma-1 receptor-mediated mechanisms by decreasing glutamate accumulation.
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Dimemorfan, an antitussive and a sigma-1 (sigma(1)) receptor agonist, has been reported to display neuroprotective properties. We set up an animal model of ischemic stroke injury by inducing cerebral ischemia (for 1 h) followed by reperfusion (for 24 h) (CI/R) in rats to examine the protective
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