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1 tivation of PI 3-kinase in the presence of a beta adrenergic receptor antagonist.
2 macrophages were prevented by propranolol, a beta-adrenergic receptor antagonist.
5 CHF patients have shown that treatment with beta-adrenergic receptor antagonists (betaB) improves ca
7 e expression, but pre-exposure to timolol, a beta-adrenergic receptor antagonist, delayed this effect
8 r antagonist, or propranolol, a nonselective beta-adrenergic receptor antagonist, delivered by osmoti
9 y was prevented with either LTCC blockers or beta-adrenergic receptor antagonists, demonstrating a pr
13 hese responses can be inhibited by alpha and beta-adrenergic receptor antagonists implying a bacteria
18 in precursor, or with S(-) pindolol, a 5HT1A/beta adrenergic receptor antagonist or with LY206130, a
20 s in Thy-1 mRNA levels were prevented by the beta-adrenergic receptor antagonist propranolol (10 micr
21 ug or 30 mug) or vehicle (Experiment 1), the beta-adrenergic receptor antagonist propranolol (2 mug)
22 M) blocked the effects of NA on Ito, but the beta-adrenergic receptor antagonist propranolol (20 micr
24 Healthy participants were administered the beta-adrenergic receptor antagonist propranolol or a pla
25 ntrast, treatment before hemorrhage with the beta-adrenergic receptor antagonist propranolol was asso
28 and absence of a alpha2-agonist (clonidine), beta-adrenergic receptor antagonist (propranolol), and b
30 herapies is also enhanced by administering a beta-adrenergic receptor antagonist to mice housed at 22
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