Drugs online research references
Ophthalmic Res. 1999;31(4):309-16.
The ocular pharmacokinetics of topical diclofenac is affected by ocular inflammation.
Palmero M, Bellot JL, Alcoriza N, Garcia-Cabanes C, Orts A.
Department of Interuniversitary Optics, University of Alicante, Spain.
The ocular pharmacokinetics of topical diclofenac sodium was studied in two experimental models of ocular inflammation and compared to physiological conditions. Keratitis or uveitis were induced by intrastromal injection of clove oil or by intravitreal lipopolysaccharide in rabbits. The control eyes were not inflamed. Simultaneously to the induction of inflammation, 30 microl of 0.1% diclofenac were applied topically in the right eye. Diclofenac levels were measured by HPLC in the cornea, aqueous humor (AH), iris/ciliary body (ICB) and plasma 30 min, 1, 3, 6 and 12 h after application. In physiological conditions, diclofenac reached a peak level in the cornea and ICB at 30 min slowly decreasing afterwards. Low levels of diclofenac were found in AH. In keratitic eyes, two peak levels which were significantly higher than in the controls were found in the cornea 30 min and 3 h after application. Diclofenac concentrations in keratitic AH and ICB were lower than in controls. In uveitic eyes, corneal and ICB levels peaked at 30 min, being significantly higher than in controls, and decreased quickly to very low levels at 1 h after application. In uveitic AH, diclofenac levels were lower than in controls. Plasma levels were very low (less than 0.1 microg/ml) in all experimental groups. It is concluded that the ocular pharmacokinetics of topical diclofenac is affected by inflammatory processes in the eye, reaching higher levels in the target tissues.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10325547&dopt=Abstract
Int J Pharm. 1999 Apr 20;181(1):11-21.
Dehydration and rehydration of a hydrate diclofenac salt at room temperature.
Fini A, Fazio G, Alvarez-Fuentes J, Fernandez-Hervas MJ, Holgado MA.
Istituto di Scienze Chimiche, Universita di Bologna, Via S. Donato 15, I-40127, Bologna, Italy.
The salt diclofenac/N-(2-hydroxyethyl) pyrrolidine crystallizes from water as a dihydrate, while it precipitates from organic solvents anhydrously: the two salts have different crystal structures. Dehydration of the dihydrate salt was carried out in a desiccator over silica gel at room temperature: the process occurs with the retention of the crystal structure. Slight changes observed in the diffractograms suggest, that soon after dehydration, a phase transition starts, slowly due to the low temperature of the process. The reaction was followed determining the loss of weight as a function of time and by thermal analysis, since the dihydrate and the dehydrate forms have different thermograms, but similar diffractograms. The reaction was complete after 24 h. The analysis of the experimental data suggests a kinetic process related to a one-dimensional diffusion of the crystallization water molecules outwards the solid particles. At room temperature, the dehydrate material rapidly back-absorbs the two molecules of crystallization water from the atmosphere moisture. The interaction with water of the different forms of the salt was discussed as a function of their solid structures as well as of the complex equilibria present in aqueous solution: these can explain previous apparently anomalous results. Copyright
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10370198&dopt=Abstract
uta.fi
OBJECTIVE: Since the effects of angiotensin II receptor antagonism on arterial function in nitric oxide (NO)-deficient hypertension are unknown, we investigated the influence of losartan therapy (20 mg kg-1 day-1) on the control of arterial tone in NG-nitro-L-arginine methyl ester (L-NAME; 20 mg kg-1 day-1)-induced hypertension. METHODS: Forty Wistar rats were divided into four groups: control, losartan, L-NAME, and losartan + L-NAME. The responses of isolated mesenteric arterial rings were examined in standard organ chambers after 8 treatment weeks. RESULTS: Losartan therapy prevented the development of L-NAME-induced hypertension and the associated impairments of endothelium-independent relaxations to nitroprusside, isoprenaline, and cromakalim, vasodilators acting via the formation of NO, activation of beta-adrenoceptors and opening of K+ channels, respectively. In addition, endothelium-dependent relaxations of noradrenaline-precontracted rings to acetylcholine during NO synthase inhibition in vitro were decreased in L-NAME rats, and clearly improved by losartan therapy. The inhibition of cyclooxygenase by diclofenac improved the responses to acetylcholine more effectively in L-NAME than losartan + L-NAME rats, but the relaxations remained decreased in L-NAME rats when compared with losartan + L-NAME rats. When hyperpolarization of smooth muscle was prevented by precontractions induced by high concentration of KCl, the responses to acetylcholine during combined NO synthase and cyclooxygenase inhibition were similar and almost abolished in all groups. Furthermore, superoxide dismutase, a scavenger of superoxide anions, enhanced the acetylcholine-induced relaxations more effectively in L-NAME than losartan + L-NAME rats, although plasma antioxidant capacity was similar in all study groups. CONCLUSION: Chronic L-NAME-induced hypertension was associated with attenuated arterial relaxation via endothelium-dependent and -independent mechanisms, both of which were improved by the losartan treatment. The mechanisms whereby losartan enhanced arterial relaxation in this model of experimental hypertension may have included enhanced hyperpolarization and increased sensitivity to NO in smooth muscle, and decreased vascular production of superoxide and vasoconstrictor prostanoids.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10533618&dopt=Abstract
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