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1 onding DHET regioisomers produced comparable relaxation responses.
2 g injury parameters and skeletal microvessel relaxation responses.
3 tylcholine (P < 0.01) and attenuated maximal relaxation responses and sensitivity (i.e.,-log ED50) to
4 hago-UES contractile reflex and esophago-LES relaxation response, and rapid air injection activated t
5                                              Relaxation responses for RBCs were compared with S-nitro
6 %) contractile responses as well as the anal relaxation response in both muscle layers.
7 urther addition of L-NA nearly abolished the relaxation response in the LM, but did not cause any fur
8 n W/W(V) muscles and L-NNA did not attenuate relaxation responses in W/W(V) fundus muscles.
9                                    Creep and relaxation responses indicate that for objects larger th
10               Seven weeks later, microvessel relaxation responses, myocardial perfusion, and myocardi
11 we show that such effects alter the magnetic relaxation response of local water in ways that may enab
12      We compare measurements of the Brownian relaxation response of magnetic nanobeads in suspension
13 t did not cause any further reduction in the relaxation response of the CM observed in apamin alone.
14 tile response of the LM by 30%, and the anal relaxation response of the LM and CM by about 30%.
15                                 In contrast, relaxation responses of microvessels to bFGF were not al
16                                     In vitro relaxation responses of precontracted arterioles (80 to
17                                     In vitro relaxation responses of precontracted arterioles to endo
18  microM), which did not affect the transient relaxation response recorded in control conditions.
19                                  Microvessel relaxation response to adenosine 5'-diphosphate was impr
20 ced attenuation of the endothelial-dependent relaxation response to bradykinin at day 10 postinfectio
21 2+ transient could not explain the divergent relaxation response to endothelin in myocytes expressing
22          Endothelium-dependent microvascular relaxation response to Substance P was diminished in HCC
23 d carotid arteries also demonstrated reduced relaxation responses to acetylcholine (p < 0.05) 6 h aft
24  using mesenteric arteries demonstrated that relaxation responses to acetylcholine were significantly
25                                 The post-CPB relaxation responses to ADP and substance P were signifi
26                        Hyperpolarization and relaxation responses to ATP and ADP were retained in col
27                              Contractile and relaxation responses to beta-AR stimulation with dobutam
28 nses to high molar KCl and u46619 levels and relaxation responses to bradykinin and sodium nitropruss
29 amins diet (87.7 +/- 3.0%; P = 0.1), as were relaxation responses to calcium ionophore A23187.
30 oproterenol and PGE2 (P < 0.05), whereas the relaxation responses to direct stimulation of adenylate
31 (P < 0.001) and PGE2 (P < 0.05); whereas the relaxation responses to direct stimulation of adenylate
32  terms of the [Ca2+] vs. force relationship, relaxation responses to EFS differed from responses to N
33                                              Relaxation responses to endothelium-dependent and -indep
34                                 The impaired relaxation responses to isoproterenol and PGE2 were abla
35 ntraction of the tissues with acetylcholine, relaxation responses to isoproterenol, PGE2, and forskol
36 ontractility to acetylcholine and attenuated relaxation responses to isoproterenol.
37 ed from endothelial dysfunction with similar relaxation responses to Psgl-1(+/+) or Psgl-1(-/-) mice
38     Only patients with SERD had abnormal UES relaxation responses to rapid distension with saline.
39                             It did not alter relaxation responses to sodium nitroprusside, iloprost,
40                          Post-CP reperfusion relaxation responses to the activator of intermediate an
41                                 In contrast, relaxation responses to the activator of large conductan
42 tatic tensile forcing and their viscoelastic relaxation response upon release of the stretching force
43                              The NaF-induced relaxation response was significantly greater in PHT ves
44           IJPs were reduced in amplitude and relaxation responses were absent in Sl/Sl(d) mice.
45             The distal colon contraction and relaxation responses were assessed by electrical field s
46          Rate-dependent crack nucleation and relaxation responses were obtained as a function of matr
47                                              Relaxation responses were of smaller amplitude in W/W(V)
48 od flow, and in vitro coronary microvascular relaxation responses were studied in noninstrumented con
49 ractile in response to vasoconstrictors, and relaxation responses were unimpaired.