ライフサイエンスコーパス: hyperaemia

1 o be a significant contributor to functional hyperaemia.

2 e, old fit muscle achieves adequate exercise hyperaemia.

3 may be an important contributor to exercise hyperaemia.

4 bolished the contribution of PGs to exercise hyperaemia.

5 nation with l-NAME abolished the majority of hyperaemia.

6 nd modestly to the plateau phases of thermal hyperaemia.

7 e (NO) and prostanoids to cutaneous reactive hyperaemia.

8 Neither is a recognized feature of exercise hyperaemia.

9 ve a vasodilatory role in cutaneous reactive hyperaemia.

10 inhibition would synergistically reduce the hyperaemia.

11 contribute independently to forearm exercise hyperaemia.

12 ponsible for the initial contraction-induced hyperaemia.

13 dent's t test) indicating localised reactive hyperaemia.

14 and promotes the full expression of exercise hyperaemia.

15 he test was repeated during post-contraction hyperaemia.

16 denosine receptor does not affect functional hyperaemia.

17 es a significant, consistent contribution to hyperaemia, (2). PGs contribute modestly and transiently

18 with improved coronary flow or postischaemic hyperaemia; (2) increased MnSOD protein expression is no

19 Functional hyperaemia (9-fold increase in blood flow during contrac

20 tely 60% of the plateau in cutaneous thermal hyperaemia, a large portion of the response remains unkn

21 , while twitch contractions produce a larger hyperaemia, adenosine acting via A(2A)-receptors plays a

22 ed NO-PG inhibition reduces hypoxic exercise hyperaemia and abolishes hypoxic vasodilatation at rest.

23 ajor roles in the EDHF component of reactive hyperaemia and appear to work partly independent of each

24 ship between postischaemic coronary vascular hyperaemia and infarct size across sexes or exercise tra

25 tigating the contribution of ADO to exercise hyperaemia and possible differences between responders a

26 control fetuses at rest, during vasodilatory hyperaemia, and during hyperaemia plus increased aortic

27 influences to the total contraction-induced hyperaemia appears greatest for low to moderate intensit

28 ibution to muscle and systemic peak exercise hyperaemia appears to be minimal in comparison to the ef

29 ties identifying the mechanisms for exercise hyperaemia are especially disappointing due to the essen

30 coronary blood flow and coronary functional hyperaemia are reduced with age, and endothelium-depende

31 Demonstrations in reactive hyperaemia assessments of blood flow and hydration analy

32 denosine makes a greater contribution to the hyperaemia associated with isometric tetanic than isomet

33 A(2A)-receptors plays a greater role in the hyperaemia associated with tetanic contraction.

34 ow that BK does not contribute ot functional hyperaemia associated with twitch contraction at 3 Hz wh

35 ow that BK does not contribute to functional hyperaemia associated with twitch contraction at 3 Hz wh

36 BK plays no role in hyperaemia associated with twitch contraction of oxidati

37 ted with lower exercise blood flow (exercise hyperaemia), but the vascular mechanisms mediating this

38 ediate the development of acute inflammatory hyperaemia, but nitrergic mechanisms may supervene subse

39 older humans inhibition of NO would decrease hyperaemia, but that inhibition of PGs would increase hy

40 8-bromo-cGMP, l-NAME did not affect exercise hyperaemia, but ZM241385 still significantly reduced the

41 L-NAME reduced steady-state exercise hyperaemia by 12 +/- 3% in older subjects (P<0.01), wher

42 but ZM241385 still significantly reduced the hyperaemia by 25%.

43 O and PGs during exercise decreases exercise hyperaemia by approximately 20 and approximately 12%, re

44 a, but that inhibition of PGs would increase hyperaemia by blocking vasoconstrictor PGs.

45 ted that breathing 100% O(2) limits exercise hyperaemia by generating O(2)(-), which inactivates nitr

46 lthough modest hyperoxia attenuates exercise hyperaemia by improving O(2) supply, limiting the releas

47 res sympatholysis and improves post-exercise hyperaemia (Doppler ultrasound).

48 NO or PGs would have less impact on exercise hyperaemia due to less vasodilatation from these signals

49 hat ADO receptor antagonism blunted exercise hyperaemia during heavy rhythmic handgripping, but vasod

50 ontribution that adenosine makes to exercise hyperaemia; efflux of inorganic phosphate and its contri

51 have investigated the contribution of NO to hyperaemia evoked by isometric twitch contractions in it

52 osine, contributes significantly to exercise hyperaemia, for muscle vasodilatation induced by intralu

53 The role of adenosine in exercise hyperaemia has been controversial.

54 eyelid changes and mild bulbar conjunctival hyperaemia in a third of cases.

55 ansporter blockade had no effect on exercise hyperaemia in either subgroup.

56 nitrate improves neither sympatholysis, nor hyperaemia in healthy controls.

57 ronal NOS (nNOS)-derived NO regulates tissue hyperaemia in healthy subjects, particularly during exer

58 Exercise hyperaemia in hypoxia is augmented relative to the same

59 Lower exercise hyperaemia in older humans may be mediated in part by le

60 contribution of adenosine to coronary active hyperaemia in the dog denervated heart by using adenosin

61 Biomicroscopy showed conjunctival hyperaemia in the left eye with a slight elevation, sugg

62 lowing administration of HOE 140, functional hyperaemia in the soleus muscle was unaffected (blood fl

63 lowing administration of HOE 140, functional hyperaemia in the soleus muscle was unaffected (blood fl

64 Inflammatory hyperaemia in the vehicle group was attenuated in the in

65 endothelial function as measured by reactive hyperaemia index, or on retinopathy.

66 jor role in the coronary active (functional) hyperaemia induced by atrial pacing to a high rate in th

67 The mechanism for exercise hyperaemia is a century old enigma.

68 The early phase of exercise hyperaemia is attributable to K(+) released from contrac

69 )-receptors, but the role for NO in exercise hyperaemia is controversial.

70 Interestingly, post-handgrip hyperaemia is greater in women than men and is, in part,

71 Exercise hyperaemia is partly mediated by adenosine A(2A)-recepto

72 Additionally, this enhanced hypoxic exercise hyperaemia is proportional to the hypoxia-induced fall i

73 the relative contribution of NO to exercise hyperaemia is reduced approximately 45% (22 +/- 4 versus

74 Reactive hyperaemia is the increase in blood flow following arter

75 peripheral contributors to exercise-induced hyperaemia is unclear.

76 d only for approximately 5% of peak exercise hyperaemia.Likewise, thigh compressions alone or in comb

77 est a portion of the NO component of thermal hyperaemia may be due to activation of TRPV-1 channels.

78 our hypothesis, despite attenuated exercise hyperaemia of approximately 30%, inhibition of KIR chann

79 view considers the contributions to exercise hyperaemia of substances released into the interstitial

80 different between groups at baseline, during hyperaemia, or with hyperaemia plus increased aortic pre

81 oups at baseline, during hyperaemia, or with hyperaemia plus increased aortic pressure.

82 , during vasodilatory hyperaemia, and during hyperaemia plus increased aortic pressure.

83 Post-occlusive reactive hyperaemia (PORH) in the skin microcirculation was asses

84 low-flow-mediated constriction, and reactive hyperaemia proximal to the area of ischemia were determi

85 related to the extent of contraction-induced hyperaemia (R(2) = 0.725), but not capillary swelling.

86 adenosine receptor subtype in the functional hyperaemia response during muscle contraction.

87 adenosine receptor subtype to the functional hyperaemia response evoked by muscle contraction in anae

88 , can contribute up to 30% of the functional hyperaemia response in the hindlimb of anaesthetized cat

89 r can contribute up to 30% of the functional hyperaemia response in the hindlimb of anaesthetized cat

90 rostaglandins (PGs) would not alter exercise hyperaemia significantly, but combined inhibition would

91 e from physiological neurovascular coupling (hyperaemia) to pathological inverse coupling (hypoperfus

92 et vasodilatation (ROV) initiates functional hyperaemia upon skeletal muscle contraction and is atten

93 Forearm hyperaemia was matched across all conditions.

94 Forearm hyperaemia was matched across all vasodilatating conditi

95 Reactive hyperaemia was reduced throughout recovery (p<0.05).

96 and 4) a significant cardio-acceleration and hyperaemia was seen.

97 The plateau phase of thermal hyperaemia was significantly attenuated in capsazepine (

98 Exercise hyperaemia was significantly reduced (32%) by l-NAME and

99 ould thus be informed on the level of muscle hyperaemia when the metabolic rate varies.

100 nd PGs have little role in normoxic exercise hyperaemia whereas combined NO-PG inhibition reduces hyp

101 rteriolar response that underlies functional hyperaemia will require further exploration.

102 le for the 30% reduction in exercise-induced hyperaemia with age.