Drugs online research references
Otolaryngol Head Neck Surg. 1993 Oct;109(4):634-45.
Mucociliary function and endothelins 1, 2, and 3.
Amble FR, Lindberg SO, McCaffrey TV, Runer T.
Department of Otorhinolaryngology-Head and Neck Surgery, Mayo Clinic, Rochester, MN 55905.
Endothelins are recently discovered peptides that cause vasoconstriction and bronchoconstriction. The significance to the mucociliary system of endothelins (ET) 1, 2 and 3 in upper as well as lower airways has not yet been clarified. Effects of these active peptides were investigated, combining both in vitro and in vivo rabbit models of mucociliary activity from the maxillary sinus and the trachea. The studies were performed using computerized photometric microscopy. Immunohistologic staining procedures were used to determine the presence of endothelins in sinus and trachea epithelium. Significant effects on mucociliary activity were noted for ET-1, -2, and -3 in vitro as well as in vivo. All endothelins were noted to accelerate mucociliary activity of both sinus and tracheal mucosa. The effects of endothelins were greater in the sinus than in the trachea. In vitro studies using the calcium blocker nifedipine and the cyclooxygenase inhibitor diclofenac indicated that the mechanism of action involves an intermediary prostaglandin pathway but is independent of release of intracellular calcium. These results were confirmed using ET-1 in vivo. Immunohistochemical staining showed endothelin to be present in both maxillary and tracheal epithelium of the rabbit. We conclude that endothelins have significant mucociliary stimulatory effects and that the presence of endothelins in normal mucosa indicates a potentially important role in respiratory homeostasis as well as inflammatory conditions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8233498&dopt=Abstract
Nippon Yakurigaku Zasshi. 1981 Sep;78(3):173-84.
[Study of platelet aggregation by the filtration pressure method (author's transl)]
[Article in Japanese]
Matsubara I.
Using Hornstra's "filter loop" technique, effects of prostaglandins and vasodilators on ADP-induced platelet aggregation were studied in anaesthetized dogs. ADP-induced platelet aggregation was observed as a transient, reversible elevation of pressure before filter. This pressure change was reproducible and dose-related. PGI2 and PGE1 suppressed the elevation of pressure induced by ADP and decreased the spontaneous elevation of pressure. Thus, it was reconfirmed that PGI2 and PGE1 not only suppressed ADP-induced platelet aggregation but also produced a disaggregation of aggregated platelets. AFter indomethacin, ADP-induced platelet aggregation was potentiated and sometimes became exceedingly protracted, indicating that anti-aggregatory prostaglandin was always present in the circulating blood. Close-injection of bradykinin did not suppress ADP-induced platelet aggregation, while intravenous injection did produce a suppression. After indomethacin, this inhibitory effect was greatly attenuated, indicating a release of anti-aggregatory prostaglandin (PGI2?) by bradykinin. Coronary vasodilators, such as dipyridamole and nifedipine did not inhibit ADP-induced platelet aggregation, nor did sulfinpyrazone. It is concluded that the "filter loop" technique is a useful method that allows aggregation and disaggregation reactions to be followed continuously and quantitatively in the blowing blood. The effects of drugs on platelet aggregation can be assessed in connection with hemodynamic changes such as blood pressure and heart rate induced by systemic administration of the drugs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7035311&dopt=Abstract
Kidney Int Suppl. 1998 Sep;67:S202-4.
Preventive strategies in endothelin-induced renal failure.
Hermann M, Schulz E, Ruschitzka F, Muller GA.
Department of Nephrology/Rheumatology, Center of Internal Medicine, University of Gottingen, Germany.
The endothelial vasoconstrictor endothelin (ET) can induce acute renal failure when fibrinolysis and vasodilatory prostanoids (PGs) are inhibited. This study compares therapeutic agents preventing ET-induced acute renal failure in anesthetized female pigs. We investigated the effect of four ET boli (1.5 microg/kg, i.v.) after pretreatment with indomethacin (2 mg/kg) and epsilon-aminocaproicacid (100 + 50 mg/kg) alone (controls, group 1) or during additional nifedipine (10 microg/kg/h; group 2), hirudin (0.5 mg/kg; group 3), or enalapril (2 x 0.15 mg; group 4) on coagulation, PGs, and renal function. The ET-induced blood pressure increase was lower in groups 2 to 4 (lowest in group 3, P < 0.05). PG synthesis was blocked in all groups. The initial hypercoagulability (controls) resulted in disseminated intravascular coagulation that was prevented by hirudin and was attenuated in groups 2 and 4. At the end of the experiment, creatinine clearance was significantly (P < 0.05) decreased. The recovery of renal function two hours after the last ET bolus was most pronounced in the hirudin group. All therapeutic drugs attenuated ET-induced impairment of renal function. Hirudin seems to be the most potent protective drug. Prevention of further ET release evoked by ET-mediated secretion of thrombin might explain this. These results suggest three important pathways for ET's hemodynamic and renal effects.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9736290&dopt=Abstract
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