Drugs online research references
J Clin Pharmacol. 1993 Oct;33(10):929-32.
Single-dose pharmacokinetics of cetirizine in patients with chronic liver disease.
Horsmans Y, Desager JP, Hulhoven R, Harvengt C.
Laboratoire de Pharmacotherapie, Universite Catholique de Louvain, Brussels, Belgium.
The pharmacokinetics of the H1-receptor antagonist cetirizine were studied from 0 to 72 hours after a single dose of 20 mg in 5 patients with chronic hepatocellular liver disease (group A), in 5 patients with chronic cholestatic liver disease (group B), and in 16 healthy volunteers. The renal function of patients and volunteers was normal (creatinine clearance > or = 70 mL/min). Cetirizine pharmacokinetics were similar in the two groups of patients. The elimination t1/2 was prolonged in patients (mean +/- standard deviation; group A: 14.32 +/- 2.30 hours; group B: 13.86 +/- 3.14 hours) in comparison with the values observed in volunteers (9.42 +/- 2.4 hours). A reduced apparent oral body clearance also was observed in patients (group A: .48 +/- .23 mL/min/kg; group B: .41 +/- .09 mL/min/kg) in comparison with volunteers (.74 +/- .19 mL/min/kg). No differences were observed in the mean cumulative urinary excretion between patients (group A: 69 +/- 15%; group B: 69 +/- 13%) and volunteers (70.7 +/- 7.8%).
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8227463&dopt=Abstract
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Endocrinology. 1993 May;132(5):2213-20.
Insulin/hypoglycemia-induced adrenocorticotropin and beta-endorphin release: involvement of hypothalamic histaminergic neurons.
Kjaer A, Knigge U, Madsen EL, Soe-Jensen P, Bach FW, Warberg J.
Department of Medical Physiology, Panum Institute, University of Copenhagen, Denmark.
We have previously found that histamine (HA) is involved in the mediation of restraint- and ether stress-induced release of the POMC-derived peptides ACTH and beta-endorphin (beta-END). In the present study we investigated the possible involvement of hypothalamic histaminergic neurons in the mediation of insulin/hypoglycemia-induced release of ACTH and beta-END in conscious male rats. To do so, hypoglycemia stress was performed during 1) inhibition of HA synthesis, 2) activation of inhibitory presynaptic HA H3-auto-receptors, or 3) blockade of postsynaptic HA H1- or H2-receptors. Hypoglycemia (plasma glucose, 2.2 +/- 0.3 nmol) induced by insulin (3 IU/kg, ip) caused a 3- to 5-fold increase in the plasma concentrations of ACTH and beta-END. A negative exponential correlation was found between the plasma glucose concentration and the ACTH and beta-END levels. Pretreatment of the animals with the HA synthesis inhibitor alpha-fluoromethylhistidine (1.0 mumol) intracerebroventricularly (icv) in a lateral ventricle, inhibited the ACTH and beta-END responses to insulin/hypoglycemia by 60%. When administered ip (100 mumol/kg), the synthesis inhibitor decreased the beta-END response 50%, but did not affect ACTH secretion significantly. Pretreatment of the rats with the H3-receptor agonist R(alpha)methylhistamine (50 mumol/kg, ip, twice) inhibited the secretory responses of ACTH and beta-END to insulin/hypoglycemia by 60-80%. This inhibitory effect of R(alpha)methylhistamine was reversed by prior administration of the specific H3-receptor antagonist thioperamide. Administration of the H1-antagonists mepyramine and cetirizine dose-dependently inhibited the ACTH and beta-END responses to insulin/hypoglycemia, with the highest dose (mepyramine, 350 nmol, icv; cetirizine, 40 mumol/kg, ip) inhibiting the response by 80-100%. The H1-antagonist SKF-93944 (226 nmol, icv) inhibited the ACTH response, but had no effect on the beta-END response. Administration of the H2-antagonists cimetidine (400 nmol, icv) and ranitidine (400 nmol, icv) inhibited the ACTH and beta-END responses to insulin/hypoglycemia by 50-80%. We conclude that histaminergic neurons are involved in the mediation of the insulin/hypoglycemia-induced release of ACTH and beta-END and that the effect is mediated via activation of primarily postsynaptic H1-receptors and, to a lesser extent, H2-receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8386615&dopt=Abstract
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Int Arch Allergy Immunol. 1993;102(1):87-93.
Effect of cefadroxil on antigen-induced bronchial hyperresponsiveness and eosinophil accumulation in lung from sensitized guinea pigs.
Boichot E, Richard MP, Paubert-Braquet M.
Bio-Inova Research Laboratory, Plaisir, France.
The effect of a semi-synthetic cephalosporin, Cefadroxil, on antigen-induced bronchial hyperresponsiveness and eosinophil accumulation in lungs from sensitized guinea pigs was investigated and compared to the effects of Cetirizine and Ketotifen. When aerosol-sensitized guinea pigs were pretreated 1 h before the antigen challenge with Cefadroxil (100 mg/kg i.p.) a partial but significant inhibition of the bronchial hyperresponsiveness to aerosolized acetylcholine chloride was observed. Furthermore, the treatment of guinea pigs (115 mg/kg, per os) 24 and 1 h before ovalbumin challenge also significantly reduced bronchial hyperresponsiveness. In contrast, no significant inhibition was noted when the guinea pigs were treated by a single dose of Cefadroxil (115 mg/kg per os) 1 h before challenge. Pretreatment of the guinea pigs with Cetirizine (1 mg/kg per os) or Ketotifen (0.1 mg/kg per os) completely inhibited the antigen-induced bronchial hyperresponsiveness. Cefadroxil (100 mg/kg i.p.) slightly inhibited the accumulation of eosinophils in the peribronchial area induced by antigen challenge. In contrast, no significant reduction was noted when the guinea pigs were treated per os with Cefadroxil (115 mg/kg), Cetirizine (1 or 10 mg/kg) or Ketotifen (0.1 mg/kg). These results show that Cefadroxil is effective in reducing antigen-induced bronchial hyperresponsiveness, an effect independent of a reduction in the pulmonary inflammation, namely eosinophil accumulation in lung.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8400889&dopt=Abstract
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