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1 and promotes the full expression of exercise hyperaemia.
2 he test was repeated during post-contraction hyperaemia.
3 denosine receptor does not affect functional hyperaemia.
4  after phacoemulsification due to functional hyperaemia.
5  may be an important contributor to exercise hyperaemia.
6 o be a significant contributor to functional hyperaemia.
7 e, old fit muscle achieves adequate exercise hyperaemia.
8 bolished the contribution of PGs to exercise hyperaemia.
9 nation with l-NAME abolished the majority of hyperaemia.
10 nd modestly to the plateau phases of thermal hyperaemia.
11 ng hyperpolarization, but contributes to the hyperaemia.
12 e (NO) and prostanoids to cutaneous reactive hyperaemia.
13  Neither is a recognized feature of exercise hyperaemia.
14 ve a vasodilatory role in cutaneous reactive hyperaemia.
15  inhibition would synergistically reduce the hyperaemia.
16 contribute independently to forearm exercise hyperaemia.
17 ponsible for the initial contraction-induced hyperaemia.
18 dent's t test) indicating localised reactive hyperaemia.
19 desaturation and speed of reperfusion during hyperaemia 2 h post-sitting, with no effects of flavanol
20 es a significant, consistent contribution to hyperaemia, (2). PGs contribute modestly and transiently
21 with improved coronary flow or postischaemic hyperaemia; (2) increased MnSOD protein expression is no
22                                   Functional hyperaemia (9-fold increase in blood flow during contrac
23 tely 60% of the plateau in cutaneous thermal hyperaemia, a large portion of the response remains unkn
24 , while twitch contractions produce a larger hyperaemia, adenosine acting via A(2A)-receptors plays a
25 ed NO-PG inhibition reduces hypoxic exercise hyperaemia and abolishes hypoxic vasodilatation at rest.
26 ajor roles in the EDHF component of reactive hyperaemia and appear to work partly independent of each
27 ship between postischaemic coronary vascular hyperaemia and infarct size across sexes or exercise tra
28 tigating the contribution of ADO to exercise hyperaemia and possible differences between responders a
29                                    Diaphragm hyperaemia and regional blood flow distribution are impa
30 test product with regards to the severity of hyperaemia and to the velocity of remission of ocular di
31 control fetuses at rest, during vasodilatory hyperaemia, and during hyperaemia plus increased aortic
32  influences to the total contraction-induced hyperaemia appears greatest for low to moderate intensit
33 ibution to muscle and systemic peak exercise hyperaemia appears to be minimal in comparison to the ef
34 ties identifying the mechanisms for exercise hyperaemia are especially disappointing due to the essen
35  coronary blood flow and coronary functional hyperaemia are reduced with age, and endothelium-depende
36                   Demonstrations in reactive hyperaemia assessments of blood flow and hydration analy
37 denosine makes a greater contribution to the hyperaemia associated with isometric tetanic than isomet
38  A(2A)-receptors plays a greater role in the hyperaemia associated with tetanic contraction.
39 ow that BK does not contribute ot functional hyperaemia associated with twitch contraction at 3 Hz wh
40 ow that BK does not contribute to functional hyperaemia associated with twitch contraction at 3 Hz wh
41                          BK plays no role in hyperaemia associated with twitch contraction of oxidati
42  for the reduced vasodilatation and exercise hyperaemia at HA remains unknown.
43 P = 0.03) and augmented the exercise-induced hyperaemia at most intensities (80% saline: Delta3818+/-
44 ted with lower exercise blood flow (exercise hyperaemia), but the vascular mechanisms mediating this
45 ediate the development of acute inflammatory hyperaemia, but nitrergic mechanisms may supervene subse
46 older humans inhibition of NO would decrease hyperaemia, but that inhibition of PGs would increase hy
47 8-bromo-cGMP, l-NAME did not affect exercise hyperaemia, but ZM241385 still significantly reduced the
48         L-NAME reduced steady-state exercise hyperaemia by 12 +/- 3% in older subjects (P<0.01), wher
49 but ZM241385 still significantly reduced the hyperaemia by 25%.
50 O and PGs during exercise decreases exercise hyperaemia by approximately 20 and approximately 12%, re
51 a, but that inhibition of PGs would increase hyperaemia by blocking vasoconstrictor PGs.
52 ted that breathing 100% O(2) limits exercise hyperaemia by generating O(2)(-), which inactivates nitr
53 lthough modest hyperoxia attenuates exercise hyperaemia by improving O(2) supply, limiting the releas
54 Nevertheless, COX inhibition attenuated peak hyperaemia by ~30% in WE, BA men and WE women, indicatin
55 ered and diminished WSR response to reactive hyperaemia compared to young people, but reduced WSR alo
56 ered and diminished WSR response to reactive hyperaemia compared to younger people [e.g. WSR peak: 62
57 res sympatholysis and improves post-exercise hyperaemia (Doppler ultrasound).
58 NO or PGs would have less impact on exercise hyperaemia due to less vasodilatation from these signals
59 hat ADO receptor antagonism blunted exercise hyperaemia during heavy rhythmic handgripping, but vasod
60 ontribution that adenosine makes to exercise hyperaemia; efflux of inorganic phosphate and its contri
61  have investigated the contribution of NO to hyperaemia evoked by isometric twitch contractions in it
62          Our findings indicate that exercise hyperaemia following rhythmic contractions at 60% maximu
63 osine, contributes significantly to exercise hyperaemia, for muscle vasodilatation induced by intralu
64            The role of adenosine in exercise hyperaemia has been controversial.
65 emoral artery diameter (FAD) and PLM-induced hyperaemia (HYP) were reduced by 7.3% and 34.3%, respect
66  eyelid changes and mild bulbar conjunctival hyperaemia in a third of cases.
67  and accumulation of dilators, while blunted hyperaemia in BAs may reflect lower oxidative capacity a
68 ansporter blockade had no effect on exercise hyperaemia in either subgroup.
69  nitrate improves neither sympatholysis, nor hyperaemia in healthy controls.
70 ronal NOS (nNOS)-derived NO regulates tissue hyperaemia in healthy subjects, particularly during exer
71                                     Exercise hyperaemia in hypoxia is augmented relative to the same
72 nic adrenergic signalling restrains exercise hyperaemia in lowlanders acclimatizing to HA.
73                               Lower exercise hyperaemia in older humans may be mediated in part by le
74 contribution of adenosine to coronary active hyperaemia in the dog denervated heart by using adenosin
75            Biomicroscopy showed conjunctival hyperaemia in the left eye with a slight elevation, sugg
76 lowing administration of HOE 140, functional hyperaemia in the soleus muscle was unaffected (blood fl
77 lowing administration of HOE 140, functional hyperaemia in the soleus muscle was unaffected (blood fl
78                                 Inflammatory hyperaemia in the vehicle group was attenuated in the in
79 endothelial function as measured by reactive hyperaemia index, or on retinopathy.
80 jor role in the coronary active (functional) hyperaemia induced by atrial pacing to a high rate in th
81                   The mechanism for exercise hyperaemia is a century old enigma.
82                  The early phase of exercise hyperaemia is attributable to K(+) released from contrac
83 ribution of prostaglandins (PGs) to exercise hyperaemia is controversial.
84 )-receptors, but the role for NO in exercise hyperaemia is controversial.
85                 Interestingly, post-handgrip hyperaemia is greater in women than men and is, in part,
86        The vasodilatory response to reactive hyperaemia is impaired with advancing age, but it is unc
87        The vasodilatory response to reactive hyperaemia is impaired with age, but it is unknown wheth
88                                     Exercise hyperaemia is partly mediated by adenosine A(2A)-recepto
89 Additionally, this enhanced hypoxic exercise hyperaemia is proportional to the hypoxia-induced fall i
90  the relative contribution of NO to exercise hyperaemia is reduced approximately 45% (22 +/- 4 versus
91                                     Reactive hyperaemia is the increase in blood flow following arter
92  peripheral contributors to exercise-induced hyperaemia is unclear.
93 d only for approximately 5% of peak exercise hyperaemia.Likewise, thigh compressions alone or in comb
94 est a portion of the NO component of thermal hyperaemia may be due to activation of TRPV-1 channels.
95  our hypothesis, despite attenuated exercise hyperaemia of approximately 30%, inhibition of KIR chann
96 view considers the contributions to exercise hyperaemia of substances released into the interstitial
97 he eye appeared proptotic, with chemosis and hyperaemia of the conjunctiva.
98 different between groups at baseline, during hyperaemia, or with hyperaemia plus increased aortic pre
99 oups at baseline, during hyperaemia, or with hyperaemia plus increased aortic pressure.
100 , during vasodilatory hyperaemia, and during hyperaemia plus increased aortic pressure.
101 cs at rest and after post-occlusive reactive hyperaemia (PORH) in the hands and feet of 52 healthy pe
102                      Post-occlusive reactive hyperaemia (PORH) in the skin microcirculation was asses
103 low-flow-mediated constriction, and reactive hyperaemia proximal to the area of ischemia were determi
104 related to the extent of contraction-induced hyperaemia (R(2) = 0.725), but not capillary swelling.
105 adenosine receptor subtype in the functional hyperaemia response during muscle contraction.
106 adenosine receptor subtype to the functional hyperaemia response evoked by muscle contraction in anae
107 , can contribute up to 30% of the functional hyperaemia response in the hindlimb of anaesthetized cat
108 r can contribute up to 30% of the functional hyperaemia response in the hindlimb of anaesthetized cat
109 ted using Doppler ultrasound during reactive hyperaemia (RH), passive leg movement (PLM) and rapid-on
110 rostaglandins (PGs) would not alter exercise hyperaemia significantly, but combined inhibition would
111  reflect a loss of precision in the reactive hyperaemia stimulus-response relationship.
112 ing the WSR-FMD response when using reactive hyperaemia to assess vascular function, as well as givin
113 ing the WSR-FMD response when using reactive hyperaemia to assess vascular function.
114 e from physiological neurovascular coupling (hyperaemia) to pathological inverse coupling (hypoperfus
115 et vasodilatation (ROV) initiates functional hyperaemia upon skeletal muscle contraction and is atten
116 < 0.05), while the magnitude of the exercise hyperaemia was attenuated by 73% (P = 0.012) in line wit
117                                      Forearm hyperaemia was matched across all conditions.
118                                      Forearm hyperaemia was matched across all vasodilatating conditi
119                                     Reactive hyperaemia was reduced throughout recovery (p<0.05).
120 and 4) a significant cardio-acceleration and hyperaemia was seen.
121                 The plateau phase of thermal hyperaemia was significantly attenuated in capsazepine (
122                                     Exercise hyperaemia was significantly reduced (32%) by l-NAME and
123 ould thus be informed on the level of muscle hyperaemia when the metabolic rate varies.
124 nd PGs have little role in normoxic exercise hyperaemia whereas combined NO-PG inhibition reduces hyp
125 rteriolar response that underlies functional hyperaemia will require further exploration.
126 le for the 30% reduction in exercise-induced hyperaemia with age.

 
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