Drugs online research references
Arch Facial Plast Surg. 1999 Jan-Mar;1(1):27-32.
Comparison of topical anti-ischemic agents in the salvage of failing random-pattern skin flaps in rats.
Davis RE, Wachholz JH, Jassir D, Perlyn CA, Agrama MH.
Department of Otolaryngology, University of Miami School of Medicine, Fla., USA.
OBJECTIVE: To determine the efficacy of topical anti-ischemic drug therapy in the salvage of failing, random-pattern skin flaps. DESIGN: Prospective, randomized, placebo-controlled, therapeutic trial. SETTING: Academic medical center. SUBJECTS: Sixty-one adult male Sprague-Dawley rats. INTERVENTION: Each experimental rat underwent a caudally based random-pattern skin flap using the modified McFarlane technique. Rats were randomized to 1 of 6 treatment groups: topical nifedipine, topical trolamine salicylate, topical nitroglycerin, topical trolamine salicylate-nitroglycerin combination, topical nifedipine-trolamine salicylate-nitroglycerin combination, or inert carrier ointment (control). Treatment was initiated immediately following flap closure and continued every 6 hours for 7 days. At the end of the treatment period, animals were euthanized and flap survival was determined for each one. RESULTS: Topical anti-ischemic drug therapy resulted in a statistically significant reduction in ischemic flap necrosis for each drug (or combination) tested relative to the 44.2% mean necrosis observed in control animals. Treatment with the combination of topical nitroglycerin and topical trolamine salicylate resulted in the best salvage response (25.2% mean necrosis) with a statistically significant improvement in flap survival relative to both controls and nitroglycerin alone. CONCLUSIONS: Topical anti-ischemic agents are effective in reducing ischemic necrosis of failing, random-pattern skin flaps in the rat model. Although nitroglycerin, trolamine salicylate, and nifedipine possess unique pharmacologic mechanisms of action, each drug produced a statistically significant improvement in flap survival. The results of this study suggest that topical drug therapy may play an important role in clinical salvage of the failing skin flap. Further studies are needed to explore the potential of combination drug therapy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10937072&dopt=Abstract
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RATIONALE: Previous studies have shown that buspirone, a partial 5-HT(1A) receptor agonist, produces antinociceptive effects in rats and mice; Ca(2+) plays a critical role as a second messenger in mediating nociceptive transmission. 5-HT(1A) receptors have been proven to be coupled functionally with various types of Ca(2+) channels in neurons, including N-, P/Q-, T-, or L-type. It was of interest to investigate the involvement of extracellular/intracellular Ca(2+) in buspirone-induced antinociception. OBJECTIVES: To determine whether central serotonergic pathways participate in the antinociceptive processes of buspirone, and investigate the involvement of Ca(2+) mechanisms, particularly L-voltage-gated Ca(2+) channels and Ca(2+)/caffeine-sensitive pools, in buspirone-induced antinociception. METHODS: Antinociception was assessed using the hot-plate test (55 degrees C, hind-paw licking latency) in mice treated with either buspirone (1.25-20 mg/kg i.p.) alone or the combination of buspirone and fluoxetine (2.5-10 mg/kg i.p.), 5-HTP (25 mg/kg i.p.), nimodipine (2.5-10 mg/kg i.p.), nifedipine (2.5-10 mg/kg i.p.), CaCl(2) (25-200 nmol per mouse i.c.v.), EGTA (5-30 nmol per mouse i.c.v.), or ryanodine (0.25-2 nmol per mouse i.c.v.). RESULTS: Buspirone dose dependently increased the licking latency in the hot-plate test in mice. This effect of buspirone was enhanced by fluoxetine, 5-HTP, nimodipine, and nifedipine. Interestingly, central administration of Ca(2+) reversed the antinociceptive effects of buspirone. In contrast to these, ryanodine or EGTA administered centrally potentiated buspirone-induced antinociception. CONCLUSIONS: Decreasing neuronal Ca(2+) levels potentiated buspirone-induced antinociception; conversely, increasing intracellular Ca(2+) abolished the antinociceptive effects of buspirone. These results suggest that Ca(2+) influx from extracellular fluid and release of Ca(2+) from Ca(2+)/caffeine-sensitive microsomal pools may be involved in buspirone-induced antinociception.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12552360&dopt=Abstract
Br J Pharmacol. 1995 Jul;115(5):845-51.
BaCl2- and 4-aminopyridine-evoked phasic contractions in the rat vas deferens.
Huang Y.
Department of Physiology, Chinese University of Hong Kong, Shatin, NT.
1. The actions of BaCl2 and 4-aminopyridine, blockers of K+ channels, on the mechanical activity of the epididymal half of the rat vas deferens were investigated. 2. Both BaCl2 and 4-aminopyridine dose-dependently evoked phasic contractions. High extracellular potassium (35-40 mM) caused a tonic contraction but abolished the BaCl2- and 4-aminopyridine-induced phasic activity and reduced the BaCl2-induced sustained component of contraction, but increased the 4-aminopyridine-induced tonic contraction. 3. Omission of calcium from the extracellular medium totally abolished the 4-aminopyridine-induced response but only reduced the mean amplitude of phasic contractions induced by BaCl. 4. Procaine (10 mM), an inhibitor of internal calcium release, completely abolished the phasic activity and reduced the sustained contraction induced by BaCl2. The remaining tone was abolished by nifedipine (1 microM). 5. Tetraethylammonium (1 mM) suppressed the amplitude of the BaCl2-induced phasic contractions, and induced a biphasic increase in tonic tension. 6. The BaCl2-induced responses were resistant to prazosin (1 microM), yohimbine (3 microM), propranolol (3 microM) or atropine (3 microM); in contrast, the 4-aminopyridine-induced activity was effectively inhibited by prazosin (1 microM) attenuated by yohimbine (1 microM) and atropine (1 microM) but not by propranolol (3 microM). The 4-aminopyridine-induced response was abolished by pretreatment of the vas deferens with 6-hydroxydopamine (0.5 mM). 7. The results indicate that the BaCl2-evoked activity in the vas deferens was mainly due to blockade of Ba(2+)-sensitive K+ channels on the smooth muscle plasma membrane. Subsequent calcium entry through the depolarized plasma membrane was needed to trigger generation of phasic contractions.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8548186&dopt=Abstract
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