Drugs online research references
Life Sci. 1994;54(12):799-812.
Comparable beneficial effects of defibrotide and nifedipine in calcium induced atherosclerosis.
Porta R, Conz A, Conto A, Pescador R, Mantovani M, Ferro L.
Crinos Biological Research Laboratories, Villa Guardia (Como), Italy.
The present study demonstrates the antiatherosclerotic property of Defibrotide (DFT) in an experimental model in which the pathology is secondary to calcium deposition in the vessel wall and various organs. Rats were treated by gavage for 21 consecutive days with Vitamin D3 and/or, twice a day, with DFT or Nifedipine (N). The calcium contents of aorta, heart and kidney were determined by atomic absorption spectrometry. Specimens of these tissues were examined histologically. DFT or N administered alone did not modify the calcium contents of aorta, heart or kidney. On the contrary, Vitamin D3 caused a huge increase in the calcium concentration in the aorta and in the kidney, whereas the heart content was only double that of control animals. In rats treated with Vitamin D3, contemporaneous administration of DFT or N sharply and highly significantly reduced the aorta calcium concentration and there were less striking, although still significant, reductions in the other two tissues. Histological examination paralleled these data; the effect of DFT or N in reducing the mineralization of aorta and heart was very evident, and more pronounced for DFT. These results confirm that DFT, even though not belonging to the class of the calcium antagonists, has comparable antiatherosclerotic properties, possibly due to its endothelial protective efficacy, as evidenced by the lesser amount of calcium in the aortic tissue.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8121243&dopt=Abstract
Int J Clin Pharmacol Ther. 2001 Dec;39(12):517-28.
Screening for inhibitory effects of antineoplastic agents on CYP3A4 in human liver microsomes.
Baumhakel M, Kasel D, Rao-Schymanski RA, Bocker R, Beckurts KT, Zaigler M, Barthold D, Fuhr U.
Clinical Pharmacology, Institute for Pharmacology, University of Koln, Germany.
BACKGROUND: The human cytochrome P450 enzyme CYP3A4 is involved in the metabolism of many anticancer drugs. Since these drugs are usually administered in a polychemotherapy regimen, the objective of this study was to examine their inhibitory potency on CYP3A4 with regard to possible mutual drug interactions. METHOD: CYP3A4 activities in human liver microsomes from 2 donors were determined using the oxidation of the dihydropyridine denitronifedipine, a specific CYP3A4 substrate, at a concentration of 50 microM (= KM). Formation of the pyridine metabolite was measured using HPLC. Inhibitor concentrations used were 0.5, 5 and 50 microg/ml, except for cyclophosphamide and ifosfamide (0.5, 2.5 and 5 mg/ml) and for paclitaxel (0.05, 0.15, 0.5, 1.5 and 5 microg/ml). RESULTS: The following substances showed an inhibitory effect on CYP3A4 (IC50 values for the 2 microsome samples are parenthesized): cyclophosphamide (12.3/9.2 mmol/l), mafosfamide generated 4-OH-cyclophosphamide (152/163 [micromol/l), ifosfamide (3.6/2.5 mmol/l), vinblastine sulfate (20/44 micromol/l), vincristine sulfate (67/176 micromol/l), daunorubicin hydrochloride (206/200 micromol/l), doxorubicin hydrochloride (160/215 micromol/l), teniposide (64/84 micromol/l) and docetaxel (6.4/12.7 micromol/l). No inhibitory effect on CYP3A4 was observed with epirubicin, etoposide, paclitaxel, cytarabine, 5-FU, 6-mercaptopurine, methotrexate, cisplatin, carboplatin, bleomycin, busulfan, chlorambucil and mitomycin. CONCLUSION: Comparing IC50 values with plasma concentrations present during antineoplastic therapy, the agents cyclophosphamide, ifosfamide, vinblastine, teniposide and docetaxel could possibly cause clinical drug interactions by inhibition of CYP3A4. Some recently described clinical interactions with antineoplastic agents may be explained by these results.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11770832&dopt=Abstract
J Pharmacol Exp Ther. 1992 Nov;263(2):690-7.
Hemodynamic and sedative effects of dexmedetomidine in dog.
Bloor BC, Frankland M, Alper G, Raybould D, Weitz J, Shurtliff M.
UCLA School of Medicine.
This study investigated hemodynamic and sedative effects of a single dose of the selective alpha-2 adrenoceptor agonist dexmedetoimidine (DMED) in isoflurane-anesthetized dogs. DMED (20 micrograms/kg i.v. 2-min infusion) was given to all dogs. In Group 1 the effects of DMED (time control; N = 10) were studied over 4 hr. In Group 2 (N = 11) glycopyrrolate (40 micrograms/kg initial dose followed by 20 micrograms/kg repeated every 30 min) was used to modulate the DMED-induced vagally mediated changes in heart rate. In Group 3 (N = 8), two doses of nifedipine were used to offset the DMED-induced increase in arterial blood pressure, low dose nifedipine = 10 micrograms/kg bolus followed by 2.5 micrograms/kg/min infusion for 20 min, high dose nifedipine = 20 micrograms/kg bolus followed by 5 micrograms/kg/min infusion for 20 min. DMED administration reduced isoflurane anesthetic requirements by 89% at 30 min and by 50% at 4 hr. Maximum increase in mean arterial blood pressure (MABP) +67 mm Hg occurred 1 min after DMED. MABP remained significantly elevated throughout the 4 hr studied (about +20%). Concomitant with the transient peak in MABP, heart rate (129 +/- 6 to 60 +/- 8 bpm) and cardiac output (3.5 +/- 0.3 to 0.9 +/- 0.1 l/min) decreased, whereas systemic vascular resistance (2460 +/- 210 to 14,700 +/- 1330 dynes.sec.cm-5) and left ventricular end diastolic pressure (4 +/- 1 to 27 +/- 4 mm Hg) increased.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1359110&dopt=Abstract
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