Drugs online research references
Eur J Pharmacol. 1985 May 8;111(2):167-76.
Antagonism of the amphetamine cue by both classical and atypical antipsychotic drugs.
Nielsen EB, Jepsen SA.
Rats were trained to discriminate the stimulus properties of 1 mg/kg of d-amphetamine sulphate (AMPH) from saline in a two-lever task in which correct responding was reinforced with water under a fixed ratio (FR 32) schedule. Classical antipsychotic drugs from different chemical classes were all able to block the AMPH cue. Doses (mg/kg) inhibiting the cueing effect to 50% (ID50) were 0.035 (haloperidol), 0.04 (spiroperidol), 0.09 (cis(Z)-flupenthixol), 0.12 (trifluperazine), 0.15 (perphenazine), 0.92 (chlorpromazine) and 1.40 (pimozide). The AMPH cue was also antagonized by antipsychotic drugs that are considered atypical due to their relative lack of activity in conventional animal models or inability to produce extrapyramidal symptoms in the clinic. The following ID50 values were obtained: 0.88 (molindone), 1.22 (clozapine), 5.48 (metoclopramide), 15.4 (thioridazine) and 52.8 [-)-sulpiride). In addition, the AMPH cue was blocked by the D-1 selective dopamine (DA) antagonist, SCH 23390 (ID50 = 0.014 mg/kg). The abilities of these drugs to block the AMPH cue were unrelated to the drugs' effect upon the rate of responding. For example, some drugs (e.g. haloperidol, spiroperidol and SCH 23390) blocked the AMPH cue completely without any effect on the response rate. Furthermore, the non-antipsychotic phenothiazine, promethazine (2.5-12.5 mg/kg) failed to affect the AMPH cue although the drug strongly suppressed the response rate. However, the potent DA agonists, apomorphine (0.05-0.33 mg/kg) and lisuride (0.02-0.08 mg/kg), and the DA and norepinephrine agonist, DPI (0.4 and 0.8 mg/kg), did not mimic the AMPH cue or did so only partially. These results suggest that the 1 mg/kg AMPH cue depends on (DA) systems other than those involved in the stereotyped motor behavior commonly produced by high doses of AMPH or DA agonists. Low-dose AMPH discrimination may thus serve as a new model for studying antipsychotic drug action.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2862045&dopt=Abstract
Ann Emerg Med. 1991 Mar;20(3):258-61.
Treatment of pyelonephritis in an observation unit.
Ward G, Jorden RC, Severance HW.
Division of Emergency Medicine, University of Mississippi, Jackson.
STUDY OBJECTIVE: To determine the feasibility of managing patients with acute pyelonephritis as outpatients after initial treatment with IV antibiotics in an emergency department observation unit. DESIGN: Prospective and uncontrolled. SETTING: ED observation unit. TYPE OF PARTICIPANTS: Nonpregnant female patients 14 years old or older without immunocompromise or serious underlying disease and no evidence of septic shock. INTERVENTIONS: All patients received two IV doses of trimethoprim/sulfamethoxazole at a 12-hour dosing interval and promethazine and acetaminophen as needed for nausea and fever, respectively. Baseline laboratory data, urinalysis, and urine and blood cultures were obtained. MEASUREMENTS AND MAIN RESULTS: Patients were observed for signs of septic shock, nausea, vomiting, and the ability to tolerate an oral intake. At the end of the observation period, 43 of 44 patients were discharged on oral trimethoprim/sulfamethoxazole. One additional patient who was doing well clinically was recalled and admitted because of a positive blood culture. CONCLUSION: Patients with acute pyelonephritis, despite significant fever or nausea and vomiting, can be treated effectively as outpatients after a brief period of observation and IV antibiotics.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1996820&dopt=Abstract
Life Sci. 1986 Sep 8;39(10):911-22.
Possible role of calmodulin in the control of histamine release from human basophil leukocytes.
Marone G, Columbo M, Poto S, Giugliano R, Condorelli M.
We investigated the possible role of calmodulin (CaM) in the control of histamine release from human basophil leukocytes using several CaM antagonists. Trifluoperazine (TFP) (10(-6)-2 X 10(-5) M), pimozide (10(-6)-1.5 X 10(-5) M), chlorpromazine (CPZ) (10(-5)-10(-4) M) and promethazine (PMZ) (2 X 10(-5)-10(-4) M) inhibited in vitro histamine secretion from human basophils induced by several immunological (antigen, anti-IgE, and formyl-L-methionyl-L-leucyl-L-phenylalanine: f-met peptide) and nonimmunological (Ca2+ ionophore A23187 and the tumor promoter 12-0-tetradecanoyl-phorbol-13-acetate: TPA) stimuli. Trifluoperazine sulfoxide (TFP-S) and chlorpromazine sulfoxide (CPZ-S), which have very low affinity to CaM, had practically no inhibitory effect on histamine release from human basophils. The inhibitory effect of TFP could be made irreversible by irradiating the cells with UV light. A sulfonamide derivative, the compound N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7) (2.5 X 10(-5)-2 X 10(-4) M), which selectively binds to CaM, inhibited the release of histamine from basophils. In contrast, the chloride deficient analogue, W-5, which interacts only weakly with CaM, had practically no inhibiting effect. The IC50 for enzyme release by a series of eight CaM antagonists was closely correlated (r = 0.91; p less than 0.001) with the CaM specific binding, supporting the concept that these agents act by binding to CaM and thereby inhibiting histamine release. TFP and W-7 inhibited histamine release in the absence and in the presence of increasing concentrations of extracellular Ca2+. These results emphasize the possible role of CaM in the control of histamine secretion from human basophils.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2427907&dopt=Abstract
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