ライフサイエンスコーパス: relaxation response

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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 Seven weeks later, microvessel relaxation responses, myocardial perfusion, and myocardi

10 we show that such effects alter the magnetic relaxation response of local water in ways that may enab

11 We compare measurements of the Brownian relaxation response of magnetic nanobeads in suspension

12 t did not cause any further reduction in the relaxation response of the CM observed in apamin alone.

13 tile response of the LM by 30%, and the anal relaxation response of the LM and CM by about 30%.

14 In contrast, relaxation responses of microvessels to bFGF were not al

15 In vitro relaxation responses of precontracted arterioles (80 to

16 In vitro relaxation responses of precontracted arterioles to endo

17 microM), which did not affect the transient relaxation response recorded in control conditions.

18 Microvessel relaxation response to adenosine 5'-diphosphate was impr

19 ced attenuation of the endothelial-dependent relaxation response to bradykinin at day 10 postinfectio

20 2+ transient could not explain the divergent relaxation response to endothelin in myocytes expressing

21 Endothelium-dependent microvascular relaxation response to Substance P was diminished in HCC

22 using mesenteric arteries demonstrated that relaxation responses to acetylcholine were significantly

23 The post-CPB relaxation responses to ADP and substance P were signifi

24 Hyperpolarization and relaxation responses to ATP and ADP were retained in col

25 Contractile and relaxation responses to beta-AR stimulation with dobutam

26 nses to high molar KCl and u46619 levels and relaxation responses to bradykinin and sodium nitropruss

27 amins diet (87.7 +/- 3.0%; P = 0.1), as were relaxation responses to calcium ionophore A23187.

28 oproterenol and PGE2 (P < 0.05), whereas the relaxation responses to direct stimulation of adenylate

29 (P < 0.001) and PGE2 (P < 0.05); whereas the relaxation responses to direct stimulation of adenylate

30 terms of the [Ca2+] vs. force relationship, relaxation responses to EFS differed from responses to N

31 Relaxation responses to endothelium-dependent and -indep

32 The impaired relaxation responses to isoproterenol and PGE2 were abla

33 ntraction of the tissues with acetylcholine, relaxation responses to isoproterenol, PGE2, and forskol

34 ontractility to acetylcholine and attenuated relaxation responses to isoproterenol.

35 ed from endothelial dysfunction with similar relaxation responses to Psgl-1(+/+) or Psgl-1(-/-) mice

36 Only patients with SERD had abnormal UES relaxation responses to rapid distension with saline.

37 It did not alter relaxation responses to sodium nitroprusside, iloprost,

38 Post-CP reperfusion relaxation responses to the activator of intermediate an

39 In contrast, relaxation responses to the activator of large conductan

40 tatic tensile forcing and their viscoelastic relaxation response upon release of the stretching force

41 The NaF-induced relaxation response was significantly greater in PHT ves

42 IJPs were reduced in amplitude and relaxation responses were absent in Sl/Sl(d) mice.

43 The distal colon contraction and relaxation responses were assessed by electrical field s

44 Relaxation responses were of smaller amplitude in W/W(V)

45 od flow, and in vitro coronary microvascular relaxation responses were studied in noninstrumented con

46 ractile in response to vasoconstrictors, and relaxation responses were unimpaired.

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