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1 is effect was blocked by the HRH1 antagonist pyrilamine.
2 dilatation was unaffected in the presence of pyrilamine.
3 P combined with 10 mm L-NAME plus 500 microm pyrilamine.
4 of L-NAME and the combination of L-NAME plus pyrilamine.
5 e, and the H1 histamine receptor antagonist, pyrilamine.
10 of H1 and H2 histamine receptor antagonists (pyrilamine and famotidine, respectively) greatly diminis
12 d the histamine 1 and 2 receptor antagonists pyrilamine and ranitidine, respectively, did not signifi
13 duced by histamine was inhibited by both H1 (pyrilamine) and H3 (thioperamide) but not H2 (ranitidine
14 In the H1 antagonist studies, CVC in l-NAME, pyrilamine, and combined l-NAME plus pyrilamine sites wa
15 n or celecoxib (cyclo-oxygenase inhibitors), pyrilamine, aprepitant (a neurokinin 1 receptor antagoni
16 istamine H1 antagonists, diphenhydramine and pyrilamine, at neurotensin (NT)-mediated hypothermia and
17 ment with histamine receptor H(1) antagonist pyrilamine blocked the increased sensory neuron excitabi
20 the much more potent histamine H1 antagonist pyrilamine did not affect antinociception mediated by NT
22 athing slices in medium containing 10 microM pyrilamine (H1 antagonist) blocked this stimulation-indu
23 systemically-administered antagonists of H1 (pyrilamine), H2 (zolantidine), H3 (GT-2016), or opioid (
27 tes were significantly reduced compared with pyrilamine only sites (P < 0.05) but no significant diff
29 acin), agents that interfere with histamine (pyrilamine or cromolyn), or a neurokinin antagonist (spa
31 inistering either an H1 receptor antagonist (pyrilamine) or an H2 receptor antagonist (cimetidine) de
32 1 receptor antagonist), or indomethacin with pyrilamine significantly reduced vascular leakage associ
33 l-NAME, pyrilamine, and combined l-NAME plus pyrilamine sites was significantly reduced compared with