ライフサイエンスコーパス: artery dilation

1 d 1.3, respectively; P<0.05), as was femoral artery dilation.

2 e, but had no significant effect on brachial artery dilation.

3 significant effect of treatment on brachial artery dilation.

4 ted N-methyl-D-aspartate (NMDA)-induced pial artery dilation.

5 ischemic impairment of NOC/oFQ-mediated pial artery dilation.

6 ction between opioids and NO in hypoxic pial artery dilation.

7 g conduit artery constriction and resistance artery dilation.

8 opioids, in turn, contribute to hypoxic pial artery dilation.

9 sites in their contributions to hypoxic pial artery dilation.

10 2 channels contribute to opioid-induced pial artery dilation.

11 , partially restored attenuated NOC/oFQ pial artery dilation 1 h after I+R (9+/-1 and 18+/-1 vs. 3+/-

12 rtan therapy improved flow-mediated brachial artery dilation (1.4+/-0.9% to 3.2+/-0.8%, P=0.03) but h

13 Carotid artery dilation (2.5 atm) and complete endothelial denud

14 ine decreased impairment of hypotensive pial artery dilation after fluid percussion brain injury in f

15 ral channels and access for branch pulmonary artery dilation, all of which results in pulmonary arter

16 Mac-1 to a novel form of mechanical carotid artery dilation and complete endothelial denudation.

17 Endothelial-dependent coronary artery dilation and increased blood flow in healthy subj

18 diagnosis; their associations with coronary artery dilation and inflammatory markers have not been w

19 c abnormalities are associated with coronary artery dilation and laboratory evidence of inflammation

20 , MR, and aortic root dilation with coronary artery dilation and laboratory inflammatory markers.

21 e effect of H/I on Katp and Kca induced pial artery dilation and the roles of tPA and ERK during/afte

22 coronary cardiac abnormalities with coronary artery dilation and with laboratory inflammatory markers

23 othelial NO release), flow-mediated brachial artery dilation (as an index of vascular NO bioactivity)

24 diagnosis predicted greater odds of coronary artery dilation at 1 and 5 weeks after diagnosis (5-week

25 These data show that NOC/oFQ elicits pial artery dilation, at least in part, via cAMP, K(ATP), and

26 FPI blunted PGE2 pial artery dilation, but U 0126 and SP 600125 (10(-6) M) (ER

27 These data show that pial artery dilation by Kca channel activation is not mediate

28 We have shown that artery dilation by lithocholate (LC) and related cholane

29 203580 did not prevent impairment of PG pial artery dilation by NOC/oFQ.

30 Since recent studies show that pial artery dilation during a 20 or 40 min hypoxic exposure w

31 These data suggest that diminished pial artery dilation during longer hypoxic exposure results f

32 tivation and cAMP contribute to hypoxic pial artery dilation in a stimulus duration-dependent manner.

33 ) channel activation in NOC/oFQ-induced pial artery dilation in newborn pigs equipped with a closed c

34 annel activation in hypotension induced pial artery dilation in newborn pigs equipped with a closed c

35 a+2 channels and cAMP in opioid-induced pial artery dilation in newborn pigs equipped with closed cra

36 nd cAMP-dependent mechanisms to hypoxic pial artery dilation in piglets equipped with a closed crania

37 However, tPA potentiates impairment of pial artery dilation in response to hypotension after hypoxia

38 (Kca) activation contribute to hypoxic pial artery dilation in the piglet, responses to the NO relea

39 Hypotension induced pial artery dilation is prostaglandin-dependent in the newbor

40 (ca)) K channels and cAMP contribute to pial artery dilation observed during a 10-min exposure to hyp

41 eatment difference in flow-mediated brachial artery dilation of 1.7% or larger as statistically signi

42 During hypotension, pial artery dilation (PAD) was impaired more in the male than

43 of subjects and was associated with coronary artery dilation, seen in 29% (p = 0.004).

44 ating system blunted mastoparan induced pial artery dilation similar to FPI (10+/-1 and 17+/-1 vs. 2+

45 Mastoparan (10(-8), 10(-6) M) elicited pial artery dilation that was blunted by FPI and partially re

46 ize the role of vasopressin in impaired pial artery dilation to activators of the ATP sensitive K (K(

47 prostaglandins contributes to impaired pial artery dilation to the newly described opioid, nocicepti

48 hannel-dependent mechanisms in impaired pial artery dilation to the newly described opioid, nocicepti

49 FQ), which contributes to impairment of pial artery dilation to the prostaglandins (PG) PGE2 and PGI2

50 Vasopressin so administered attenuated pial artery dilation to these K(+) channel activators under c

51 of N-methyl-D-aspartate (NMDA)-induced pial artery dilation to vasoconstriction.

52 lin (10(-10), 10(-8), 10(-6) M)-induced pial artery dilation was also inhibited within 1 h of FPI, bu

53 NMDA induced pial artery dilation was attenuated by I+R or H+I+R; but such

54 Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI and MEAVP p

55 Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI, while indo

56 Nitrite-induced radial artery dilation was enhanced by administration of acetaz

57 ies in piglets show that opioid-induced pial artery dilation was impaired following fluid percussion

58 Flow-mediated brachial artery dilation was impaired in the diabetics compared w

59 sion and fluid percussion brain injury, pial artery dilation was impaired more in males.

60 Flow-mediated brachial artery dilation was measured by ultrasound.

61 eucine enkephalin and dynorphin-induced pial artery dilation were similarly altered by FPI and partia