Drugs online research references
Gastroenterology. 1995 Aug;109(2):524-30.
A nitric oxide-releasing nonsteroidal anti-inflammatory drug accelerates gastric ulcer healing in rats.
Elliott SN, McKnight W, Cirino G, Wallace JL.
Intestinal Disease Research Unit, University of Calgary, Alberta, Canada.
BACKGROUND & AIMS: Nonsteroidal anti-inflammatory drugs (NSAIDs) have well-characterized inhibitory effects on gastric ulcer healing. A new class of gastrointestinal-sparing, nitric oxide-releasing NSAID derivatives has been recently described. This study was performed to determine if one of these compounds (nitrofenac) would influence healing of a preexisting ulcer. METHODS: Seven days after induction of gastric ulcer with serosal acetic acid, daily oral treatment with antiinflammatory doses of diclofenac, nitrofenac, or vehicle was started. After 7 days of treatment, the ulcer area was measured. The effects of misoprostol and two drugs that show in vitro selectivity for inhibiting cyclooxygenase 2 (nabumetone and L745,337) were also assessed. RESULTS: Diclofenac, nabumetone, and L745,337 had no effect on ulcer healing when compared with vehicle. Only diclofenac significantly decreased hematocrit and weight gain. On the other hand, nitrofenac significantly accelerated healing. Glyceryl trinitrate also significantly and dose dependently accelerated healing. Nitrofenac suppressed cyclooxygenase 1 activity to a similar extent as diclofenac. CONCLUSIONS: These results show that an NO-releasing NSAID derivative and an NO donor could accelerate ulcer healing, whereas a standard NSAID, misoprostol, and two inhibitors of cyclooxygenase 2 had no effect. In addition to sparing the gastrointestinal tract, NO-releasing NSAIDs, despite suppressing cyclooxygenase activity, are capable of accelerating tissue repair.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7615202&dopt=Abstract
Jpn J Pharmacol. 1994 Feb;64(2):71-8.
Effect of diclofenac, a non-steroidal anti-inflammatory drug, on lipid peroxidation caused by ischemia-reperfusion in rat liver.
Takayama F, Egashira T, Yamanaka Y.
Department of Pharmacology, Oita Medical University, Japan.
The present study investigated the effects of diclofenac sodium (Dic Na) on lipid peroxidation (LPO) and liver injury in ischemia-reperfused rat. LPO was estimated from the levels of phosphatidylcholine hydroperoxide (PCOOH), a primary peroxidative product of phosphatidylcholine. Hepatic ischemia-reperfusion induced significant elevation of plasma PCOOH and caused liver injury in rats. Rats were treated daily with Dic Na or alpha-tocopherol (alpha-toc.), p.o., for 5 days and once at 1 hr prior to induction of ischemia. Both substances prevented LPO from decreasing the plasma PCOOH level, and they significantly suppressed the elevation of serum GOT and LDH, in a dose-dependent manner. Dic Na was able to scavenge the stable free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH), but did not show radical-trapping ability for superoxide anion (O2-) or hydroxyl radicals (.OH), nor a suppressive ability for the NADPH-dependent LPO of microsomes. In contrast, alpha-toc. trapped both DPPH and O2-, but not .OH, and it inhibited the NADPH dependent LPO in vitro. These results suggest that Dic Na may suppress liver injury caused by ischemia-reperfusion through stable radical scavenging and the inhibition of superoxide production in activated phagocytes, both of which may restrain the induction and progression of oxidative stress.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8028232&dopt=Abstract
J Pharmacokinet Biopharm. 1997 Feb;25(1):63-77.
Serum protein binding of nonsteroidal antiinflammatory drugs: a comparative study.
Borga O, Borga B.
Office of Clinical Pharmacology and Biopharmaceutics, Center for Drug Evaluation and Research, Food and Drug Administration, Rockville, Maryland 20857, USA.
The unbound fraction in serum, fu, is a critical parameter in describing and understanding the pharmacokinetics of NSAIDs. We compared fu for 6 different NSAIDs using ultrafiltration of pooled serum at pH 7.4 and 24C. Measurements covered a wide concentration range in order to define binding affinity and number of binding sites. HPLC was used to measure drug concentrations in serum and ultrafiltrate. Direct injection of ultrafiltrate and serum (diluted 250 x) permitted quantitation down to approximately 70 nM for most of the NSAIDs, i.e., approximately 15-20 ng/ml. Assuming binding only to albumin, the data were fitted to a model of two classes of binding sites with dissociation constants K1 and K2. The lowest K1 (highest affinity) was found with flurbiprofen, 0.0658 microM, the highest with ketoprofen, 5.23 microM, an 80-fold difference. At low drug concentrations, fu becomes virtually constant and approaches a lower limit, fumin. The following fumin values were calculated: diclofenac 0.21%; fenoprofen 0.25%, flurbiprofen 0.022%, ketoprofen 0.52%, naproxen 0.039%, and tolmetin 0.37%. Thus the least bound NSAID, ketoprofen, had a value 24-fold that of the most highly bound, flurbiprofen. The NSAIDs also differed widely with regard to the extent of variation in fu within the range of therapeutic concentrations, and hence with regard to their potential as displacers of other drugs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9353694&dopt=Abstract
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