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Cochlear blood flow (CoBF), perilymphatic partial pressure of oxygen (PL-pO2), cochlear microphonics (CMs), compound action potentials of the auditory nerve (CAPs), and auditory brainstem responses (ABRs) were studied in noise-exposed guinea pigs during and after the following treatments: intravenous infusion of isotonic saline (placebo); blood flow promoting drugs (hydroxyethyl starch = HES, pentoxifylline, betahistine, gingko biloba, naftidrofuryl); antiinflammatory agents (prednisolone, diclofenac sodium, histamine H1-receptor antagonist); isobaric oxygenation (IBO); and hyperbaric oxygenation (HBO) with and without supplements (simultaneous infusion of isotonic saline, pentoxifylline, prednisolone, or HES). It was found that PL-pO2 declined simultaneously with deterioration of CM, CAP, and ABR amplitudes after exposure to broad-band noise (bandwidth 1-12 kHz, 30 min, 106-dB SPL). CoBF decreased only 30 min after cessation of broad-band noise and progressed with cochlear hypoxia, while the hearing loss showed no further signs of deterioration and no recovery up to 3 h after exposure. Treatment (60 min) started 60 min after cessation of noise and was studied for a further 60 min. Isotonic saline did not influence the measuring parameters. Noise-induced cochlear hypoxia was compensated by IBO and more effectively by HBO with and without supplements, while other treatments had no sustained effect. A sustained therapeutic effect on noise-induced cochlear ischemia was achieved only by HES, HBO + HES, and pentoxifylline. However, the best therapeutic effect on noise-induced hearing loss was achieved with a combination of HBO and prednisolone, followed by monotherapy with prednisolone or HES with the result that not only did the CAPs and ABRs completely recover, the CMs also showed significant improvement, although full recovery did not occur. All other therapies were significantly less effective or did not improve noise-induced reduction of auditory evoked potentials.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10842597&dopt=Abstract




Br J Pharmacol. 2000 Jan;129(1):77-86.
Bradyzide, a potent non-peptide B(2) bradykinin receptor antagonist with long-lasting oral activity in animal models of inflammatory hyperalgesia.

Burgess GM, Perkins MN, Rang HP, Campbell EA, Brown MC, McIntyre P, Urban L, Dziadulewicz EK, Ritchie TJ, Hallett A, Snell CR, Wrigglesworth R, Lee W, Davis C, Phagoo SB, Davis AJ, Phillips E, Drake GS, Hughes GA, Dunstan A, Bloomfield GC.

Novartis Institute for Medical Sciences, 5 Gower Place, London, UK.

Bradyzide is from a novel class of rodent-selective non-peptide B(2) bradykinin antagonists (1-(2-Nitrophenyl)thiosemicarbazides). Bradyzide has high affinity for the rodent B(2) receptor, displacing [(3)H]-bradykinin binding in NG108-15 cells and in Cos-7 cells expressing the rat receptor with K(I) values of 0.51+/-0.18 nM (n=3) and 0.89+/-0.27 nM (n=3), respectively. Bradyzide is a competitive antagonist, inhibiting B(2) receptor-induced (45)Ca efflux from NG108-15 cells with a pK(B) of 8.0+/-0.16 (n=5) and a Schild slope of 1.05. In the rat spinal cord and tail preparation, bradyzide inhibits bradykinin-induced ventral root depolarizations (IC(50) value; 1.6+/-0.05 nM (n=3)). Bradyzide is much less potent at the human than at the rodent B(2) receptor, displacing [(3)H]-bradykinin binding in human fibroblasts and in Cos-7 cells expressing the human B(2) receptor with K(I) values of 393+/-90 nM (n=3) and 772+/-144 nM (n=3), respectively. Bradyzide inhibits bradykinin-induced [(3)H]-inositol trisphosphate (IP(3)) formation with IC(50) values of 11.6+/-1.4 nM (n=3) at the rat and 2.4+/-0.3 microM (n=3) at the human receptor. Bradyzide does not interact with a range of other receptors, including human and rat B(1) bradykinin receptors. Bradyzide is orally available and blocks bradykinin-induced hypotension and plasma extravasation. Bradyzide shows long-lasting oral activity in rodent models of inflammatory hyperalgesia, reversing Freund's complete adjuvant (FCA)-induced mechanical hyperalgesia in the rat knee joint (ED(50), 0.84 micromol kg(-1); duration of action >4 h). It is equipotent with morphine and diclofenac, and 1000 times more potent than paracetamol, its maximal effect exceeding that of the non-steroidal anti-inflammatory drugs (NSAIDs). Bradyzide does not exhibit tolerance when administered over 6 days. In summary, bradyzide is a potent, orally active, antagonist of the B(2) bradykinin receptor, with selectivity for the rodent over the human receptor. British Journal of Pharmacology (2000) 129, 77 - 86

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10694205&dopt=Abstract




J Rheumatol. 1990 Mar;17(3):295-303.
Impact of NSAIDS on murine antigen induced arthritis. II. A light microscopic investigation of antiinflammatory and bone protective effects.

de Vries BJ, van den Berg WB.

Department of Rheumatology, Academic Hospital Sint Radboud, Nijmegen, The Netherlands.

The impact of daily, orally administered nonsteroidal antiinflammatory drugs (NSAID) or a steroid on arthritic knee joints of mice with 1-3 weeks of antigen induced arthritis (AIA) was examined by light microscopy. Prophylactic drug effects on inflammatory cell infiltrate in synovium and joint cavity were evident only in mice treated with prednisolone (0.2-5.0 mg/kg). Treatment with diclofenac, piroxicam (both 0.5-7.5 mg/kg) or tiaprofenic acid (3-30 mg/kg) did not change these phlogistic features significantly. Striking, however, was the protective effect of piroxicam on bone apposition, a common trait in murine AIA. Among the other drugs, minor antiosteophyte effects were exerted only by prednisolone. Histological assessment was also performed on osteocyte death which was almost exclusively confined to menisci and tibial subchondral bone. Because of variability in occurrence and intensity, no clear picture emerged from drug effects on this lethal feature. Combined data from this and a previous pharmacological study, directed at chondroprotective effects, points to prednisolone as the best antiinflammatory and joint protective drug.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2332850&dopt=Abstract












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