Drugs online research references
Life Sci. 1998;63(22):PL 317-22.
No development of tolerance to analgesia by repeated administration of H1 antagonists.
Ghelardini C, Galeotti N, Bartolini A.
Department of Pharmacology, University of Florence, Italy.
The effect produced by repeated administration of the H1-antihistaminics diphenhydramine, promethazine and pyrilamine on their ability to induce antinociception was evaluated in the mouse hot-plate and abdominal constriction tests. Contrary to morphine, baclofen and oxotremorine, the three H1 antagonists investigated did not promote the development of tolerance to the analgesic effect after 14 days of repeated treatment. H1 antagonists could, therefore, represent a promising pharmacological approach to the management of chronic pain.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9839549&dopt=Abstract
Br J Pharmacol. 1998 Nov;125(6):1304-12.
Unilateral injection of calcitonin gene-related peptide (CGRP) induces bilateral oedema formation and release of CGRP-like immunoreactivity in the rat hindpaw.
Bileviciute I, Stenfors C, Theodorsson E, Lundeberg T.
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
The contribution of calcitonin gene-related peptide (CGRP) to bilateral oedema formation in the rat hindpaw following an unilateral challenge with CGRP was investigated. Rats were injected into the left hindpaw with either saline, CGRP or a CGRP antagonist (CGRP8-37). All injections were given in a double blind fashion and in a volume of 100 microl. CGRP and CGRP8-37 were administered in concentrations of 75, 150 or 300 pmol. Volumes of the right and left hindpaw were measured every hour for 5 h by plethysmometry. Injection of CGRP 300 pmol into the left hindpaw resulted in a bilaterally increased hindpaw volume after 5 h as compared with the groups given saline. No changes were found in hindpaw volumes following the injection of either 75 or 150 pmol of CGRP or 75, 150 or 300 pmol of CGRP8-37 as compared with saline injection. To elucidate whether or not the bilateral oedema formation was related to a release of endogenous CGRP, microdialysis of the contralateral hindpaw was carried out, and concentrations of CGRP-like immunoreactivity (-LI) were determined by radioimmunoassay and high performance liquid chromatography. Injection of CGRP 300 pmol into the left hindpaw increased the release of CGRP-LI into the right hindpaw perfusate after 4 and 5 h. No changes in CGRP-LI were detected in the right hindpaw perfusate following challenge with saline or CGRP8-37. To study the contribution of the nervous system to the contralateral release of CGRP-LI, sciatic nerve ligated and intact sham-operated rats were used. Sciatic nerve ligation but not sham-operation on the non-injected side abolished the increased release of CGRP-LI following contralateral administration of CGRP 300 pmol. To study the spinal cord mechanisms resulting in the bilateral oedema formation following unilateral challenge with 300 pmol of CGRP, intrathecal pretreatment with either 10 nmol bicuculline (GABA(A) receptor antagonist) or 10 nmol CGRP8-37 was carried out. Bicuculline but not CGRP8-37 abolished the bilateral oedema formation induced by CGRP 300 pmol. In order to study the mechanisms by which administration of CGRP 300 pmol induces oedema, CGRP 300 pmol was administered concomitantly with either 300 pmol of CGRP8-37 (CGRP receptor antagonist), or 3 nmol of promethazine (H1 receptor antagonist), or 3 nmol of s(-)-propranolol (5-HT1 receptor antagonist), or 3 nmol of cyproheptadine (5-HT2 receptor antagonist) or 3 nmol of ICS 205-930 (5-HT3 receptor antagonist). Oedema formation was measured at 1, 5, 7 and 24 h. Injection of CGRP 300 pmol into the left hindpaw induced a bilateral oedema formation which was still significant at 24 h. Concomitant administration of either CGRP8-37, ICS 205-920 or cyproheptadine blocked the oedema formation at 24 h. No effect on oedema formation was found when CGRP 300 pmol was co-administered with either promethazine or s(-)-propranolol (H1 and 5-HT1 receptor antagonists, respectively). The results of the present study show that both the nervous system and local inflammatory processes contribute to bilateral hindpaw oedema formation following unilateral challenge with CGRP 300 pmol. Our results indicate that endogenous release of CGRP following inflammatory response may play an important role in inducing oedema formation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9863661&dopt=Abstract
Biol Pharm Bull. 1998 Dec;21(12):1243-6.
Thermodynamic studies of the charge-transfer interactions of chloranilic acid with moclobemide and promethazine hydrochloride.
Adikwu MU, Ofokansi KC, Attama AA.
Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, University of Nigeria, Nsukka.
Spectrophotometric absorption studies gave evidence for the formation of strongly bonded charge-transfer complexes between moclobemide and promethazine hydrochloride with chloranilic acid in non-aqueous media comprising chloroform and 1,4-dioxane. The transitions involved were detected at wavelengths longer than those of the single pure substances in the visible region. Equilibrium constants from the Scott equation could be measured together with other thermodynamic parameters and molar absorptivities at different temperatures. Theoretical arguments are presented as to the spontaneity of these interactions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9881631&dopt=Abstract
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