ライフサイエンスコーパス: hyperemia

1 normal; 3, mild; 4, moderate; and 5, severe hyperemia).

2 p (all mild-moderate except 1 case of severe hyperemia).

3 ins unclear which vessels mediate functional hyperemia.

4 enosis at rest and during adenosine-mediated hyperemia.

5 comatous optic nerve damage, or conjunctival hyperemia.

6 (Pr) pressure at baseline, peak, and stable hyperemia.

7 rding to Pa and Pd change at peak and stable hyperemia.

8 determine whether the iFR is independent of hyperemia.

9 and the pressure gradient induced by maximal hyperemia.

10 ing physiological phenomena such as reactive hyperemia.

11 es weakly with FFR and is not independent of hyperemia.

12 0.75 when comparing Pd/Pa at peak and stable hyperemia.

13 decreased vision, and none had conjunctival hyperemia.

14 ma in the acute phase possibly due to global hyperemia.

15 s critically on the establishment of maximal hyperemia.

16 uronal activity that accounts for functional hyperemia.

17 prolonged recovery during the early phase of hyperemia.

18 and unravel the mechanisms of saline-induced hyperemia.

19 ibitor SC-560 blocked the photolysis-induced hyperemia.

20 imaging at rest and during adenosine-induced hyperemia.

21 ) in humans during pharmacologically induced hyperemia.

22 ce imaging during rest and adenosine-induced hyperemia.

23 moral mediators, and induction of intestinal hyperemia.

24 lation (FMD) in response to forearm reactive hyperemia.

25 nsive events, such as fluid accumulation and hyperemia.

26 dependent dips in O2 tension drive capillary hyperemia.

27 ocal inflammatory reaction, and conjunctival hyperemia.

28 P) were measured at baseline and during peak hyperemia.

29 ence of pharmacologically induced myocardial hyperemia.

30 ance of a coronary stenosis measured without hyperemia.

31 the brachial artery in response to reactive hyperemia.

32 ronary papaverine (20 mg) was used to induce hyperemia.

33 nduced prolonged joint swelling and synovial hyperemia.

34 bute to neuronal activation-induced cortical hyperemia.

35 er Doppler fluxmetry in response to reactive hyperemia.

36 icrocirculatory disease and impaired maximal hyperemia.

37 ous bolus injections of BR14 during coronary hyperemia.

38 wire with intracoronary adenosine to induce hyperemia.

39 al arteriolar dilation and heat-induced skin hyperemia.

40 t dips in tissue O2 tension elicit capillary hyperemia.

41 , during supine bicycle exercise, and during hyperemia.

42 age of patients with "none/trace" amounts of hyperemia.

43 rent three-dimensional mapping of functional hyperemia.

44 uma, neurovascular dysfunction and transient hyperemia.

45 oup were eye irritation (1.9%), conjunctival hyperemia (1.1%), and worsening bacterial conjunctivitis

46 327.7 +/- 5.1 mOsm/L, P = .03), conjunctival hyperemia (1.3 +/- 0.1 vs 1.6 +/- 0.1, P = .05), and cor

47 .1 versus 6.5+/-7.2 mL/min), during reactive hyperemia (191.4+/-100.7 versus 260.3+/-138.7 mL/min), d

48 dema (5%), blepharoptosis (5%), and forehead hyperemia (2%).

49 the initial peak, but during early reactive hyperemia (5 minutes of reperfusion), 1 hour of intracor

50 bution of CRP, IL-6, and sICAM-1 to reactive hyperemia above and beyond known risk factors suggests t

51 responses for conjunctival congestion, iris hyperemia, AC cells, flare, and fibrin and declined over

52 responses for conjunctival congestion, iris hyperemia, AC cells, flare, fibrin, and corneal clouding

53 stance (FVR) at baseline and during reactive hyperemia after 5 minutes of forearm ischemia.

54 Mean reactive hyperemia after cuff deflation was similar in the two gr

55 ane exhibited a 33% inhibition of functional hyperemia after L-NAME administration.

56 M and 20 control patients at rest and during hyperemia, allowing calculation of wave intensity.

57 During hyperemia alone, LCx probe and microsphere flows and MCE

58 e FFR is measured under conditions of stable hyperemia, although the FFR value at this point may be n

59 ide dose-dependently inhibited CO(2)-induced hyperemia and at 100 nmol/L inhibited CO(2)-induced intr

60 study suggest that maximal adenosine-induced hyperemia and CFR in humans are constrained by neurally

61 relationship between endothelial response to hyperemia and circulating progenitor cells (CPCs) and en

62 dary to acute lung injury by reducing airway hyperemia and edema formation and mediating bronchodilat

63 t predictor of impaired dipyridamole-induced hyperemia and flow reserve in our study, whereas outflow

64 Increased hyperemia and increased hypoxia, two important physiolog

65 odynamics, resulted in worsening of cerebral hyperemia and intracranial hypertension in patients with

66 hial artery diameter in response to reactive hyperemia and nitroglycerin, respectively.

67 Bulbar conjunctival hyperemia and ocular symptoms decreased and temperature

68 earing, foreign body sensation, conjunctival hyperemia and photophobia.

69 a were collected at baseline, hyperemia, and hyperemia and stenosis.

70 Funduscopic examination revealed hyperemia and swelling of the optic nerve, macular edema

71 lume and osmolality may affect the degree of hyperemia and therefore diagnostic performance.

72 coffee attenuates adenosine-induced coronary hyperemia and, consequently, the detection of perfusion

73 yielded by searches using the terms "ocular hyperemia" and "vomiting" exceeded the data mining thres

74 y density during postocclusive peak reactive hyperemia) and during venous occlusion (venous congestio

75 Anterior chamber cells, flare, iris hyperemia, and conjunctival congestion were seen as earl

76 tival congestion, AC cells and flare, iridal hyperemia, and fibrin within 6 hours.

77 Data were collected at baseline, hyperemia, and hyperemia and stenosis.

78 re conjunctival hemorrhage, eye pain, ocular hyperemia, and increased intraocular pressure, whereas c

79 imaging features of osteoid osteoma (edema, hyperemia, and nidus vascularization) were considered at

80 engorgement of venous structures, pituitary hyperemia, and sagging of the brain (mnemonic: SEEPS).

81 hial artery flow-mediated dilation, reactive hyperemia, and serum concentrations of C-reactive protei

82 ements in corneal and conjunctival staining, hyperemia, and TBUT than the PA group (P</=0.03).

83 g to accelerate coronary flow increased with hyperemia, and the magnitude of change was proportional

84 ictors of changes in MBF and CVR during peak hyperemia, and, thus, they should not be used to assess

85 s of the vascular response during functional hyperemia are governed by astrocytic Kir for the fast on

86 receptor activity to nitric oxide-dependent hyperemia are poorly understood.

87 Reactive hyperemia as a parameter of endothelial function and vas

88 scular resistance was calculated during peak hyperemia as pressure divided by flow, measured either w

89 Taking adenosine-induced maximal hyperemia as reference, intracoronary infusion of saline

90 iated dilatation in response to postischemic hyperemia as well as to heating, as shown by the lesser

91 ependence of compound 48/80-induced synovial hyperemia, as measured by laser Doppler imaging, and joi

92 n (flow-mediated dilation [FMD] and reactive hyperemia) assessed at a subsequent examination (mean in

93 At imaging, the edema and hyperemia associated with osteoid osteoma gradually disa

94 thermodilution induces steady-state maximal hyperemia at a flow rate >/=15 mL/min.

95 Coronary reserve was calculated as hyperemia/basal coronary flow velocity.

96 stioned the role of astrocytes in functional hyperemia because of the slow and sparse dynamics of the

97 edicted by BA diameter (p < 0.001), reactive hyperemia blood flow (p < 0.001), high-density lipoprote

98 eactions were ocular side effects, including hyperemia, blurred vision, allergic-type reactions, and

99 FMD (N-ANP, PAI-1, CRP, renin), and reactive hyperemia (BNP, PAI-1, CRP, renin, urine albumin-creatin

100 This response, named functional hyperemia, brings oxygen and nutrients to active neurons

101 Retinal blood flow had a reactive hyperemia, but choroidal blood flow did not (e.g., 14 +/

102 stematically precede the onset of functional hyperemia by 1-2 s, reestablishing astrocytes as potenti

103 umflex coronary artery stenoses that reduced hyperemia by 40% to 60% and 70% to 90% (mild and severe

104 dings suggest that Ang II impairs functional hyperemia by activating AT1 receptors and inducing ROS p

105 :00 hours, the incidence of mild to moderate hyperemia by biomicroscopy was 18%, 24%, and 11%, respec

106 er degranulating mast cells induced synovial hyperemia by PAR-2 activation.

107 igate activation-induced hypermetabolism and hyperemia by using a multifrequency (4, 8, and 16 Hz) re

108 modynamic parameters, because achievement of hyperemia can be cumbersome in daily clinical practice.

109 During maximal hyperemia, capillaries provide the greatest resistance t

110 es in angiogenic factor levels and prolonged hyperemia characterize the soft tissue response.

111 LAD stenosis during hyperemia decreased LCx probe flow (125+/-62 versus 110+

112 cium elevations in astrocytes and functional hyperemia depended on astrocytic metabotropic glutamate

113 of the digital pulse volume during reactive hyperemia divided by that at baseline.

114 of the digital pulse volume during reactive hyperemia divided by that at rest.

115 unction involving both ischemia and reactive hyperemia during tissue reperfusion.

116 With exercise and hyperemia, efficiency of perfusion improved in the healt

117 MT and brachial artery responses to reactive hyperemia (endothelium-dependent vasodilation) and to su

118 larity, phenol red thread test, conjunctival hyperemia, fluorescein tear break-up time, corneal fluor

119 larity, phenol red thread test, conjunctival hyperemia, fluorescein tear film break-up time, Schirmer

120 widely used to achieve conditions of stable hyperemia for measurement of FFR.

121 B irradiation subsides, small areas of focal hyperemia form and were seen to persist and expand long

122 i-inflammatory agent, celecoxib, to suppress hyperemia formation during photocarcinogenesis.

123 exhibited unchanged, worsened, and improved hyperemia from baseline, respectively; 77.9 %, 12.9 %, a

124 es), while causing no significant changes in hyperemia from baseline.

125 ischemia (SRi) and gradient during reactive hyperemia (Grad).

126 cruitment during postocclusive peak reactive hyperemia had an odds ratio for albuminuria of 2.27 (95%

127 orts and refutes a role for NO in functional hyperemia have been presented.

128 Conjunctival hyperemia, hemorrhage, and edema were common after the S

129 hy, myocardial blood flow at rest and during hyperemia (hMBF), and myocardial fibrosis were assessed

130 MBF at rest and during intravenous adenosine hyperemia in 11 long-term survivors of a Mustard repair

131 y (MPS) was used to assess adenosine-induced hyperemia in 30 patients before (baseline) and after cof

132 unctival hemorrhage in 8 patients and ocular hyperemia in 5 patients.

133 essor testing (CPT), and during dipyridamole hyperemia in 54 postmenopausal women without coronary ar

134 hial artery diameter in response to reactive hyperemia in adolescents age 13 to 16 years who were eit

135 multaneously assessed at rest and at maximal hyperemia in an unobstructed coronary artery in 27 patie

136 n important mechanism of functional coronary hyperemia in conscious, instrument-implanted diabetic do

137 d and that subtended by the stenosis (during hyperemia in dogs without critical stenosis and during r

138 wer retinal arteriolar %-dilation and skin %-hyperemia in fully adjusted models (for glycohemoglobin

139 Odor-evoked functional hyperemia in glomerular capillaries was highly correlate

140 ith (13)N-ammonia and PET at rest and during hyperemia in patients with coronary risk factors but wit

141 can be safely performed during exercise and hyperemia in patients with severe aortic stenosis.

142 Adjusted analyses showed a lower %-hyperemia in prediabetes (B=-46 [-163 to 72]) with furth

143 flow velocity were measured at baseline and hyperemia in proximal and distal segments of both nontar

144 ng peptide or prostaglandin E2; (iv) gastric hyperemia in response luminal capsaicin; (v) a clinical

145 data regarding skin blood flow and reactive hyperemia in response to pressure, could provide insight

146 istributed hemoglobin content reflecting the hyperemia in synovial tissue in metacarpophalangeal (MCP

147 ry physiological changes during exercise and hyperemia in the healthy heart and in patients with seve

148 ing between synaptic activity and functional hyperemia in the olfactory bulb.

149 These results indicate that functional hyperemia in the retina is driven primarily by active di

150 w velocity were measured at rest and maximal hyperemia in undiseased vessels in 15 patients with AS b

151 echanical stimulation to induce oligemia and hyperemia, in surgically prepared cats and rats, using l

152 henomena observed experimentally: functional hyperemia, in which neural activity triggers astrocytic

153 echanism observed in this unit is functional hyperemia, in which the microvasculature dilates in resp

154 n indexes accurately depicted stress-induced hyperemia (increased upslope, from 6.7 sec(-1)+/-2.3 to

155 nesis in liver cirrhosis leads to splanchnic hyperemia, increased portal inflow, and portosystemic co

156 .29, P=0.008) and tended to improve reactive hyperemia index (+0.30+/-0.45 versus -0.17+/-0.30, P=0.0

157 hs was associated with increases in reactive hyperemia index (0.38 +/- 0.14, p = 0.009) and subendoca

158 asodilation (beta = 0.1, p = 0.03), reactive hyperemia index (beta = 0.23, p < 0.001), pulse wave vel

159 ral arterial tonometry) detected by reactive hyperemia index (RHI) and EPCs and CPCs by flow cytometr

160 l artery tonometry to determine the reactive hyperemia index (RHI), and microvascular function and ox

161 ndothelial function was assessed by reactive hyperemia index after upper arm cuff occlusion.

162 ficant negative correlation between reactive hyperemia index and P2Y12 reaction unit (r=-0.32; P=0.00

163 stic regression analysis identified reactive hyperemia index as an independent and significant determ

164 dothelial function was expressed as reactive hyperemia index using reactive hyperemia peripheral arte

165 ay, and body mass index, enrollment reactive hyperemia index was associated with a 4-fold increased r

166 c oxide bioavailability measured as reactive hyperemia index was significantly higher at enrollment i

167 Reactive hyperemia index was significantly lower in high RPR pati

168 The primary outcome, change in reactive hyperemia index, a validated measurement of endothelial

169 -mediated dilatation, microvascular reactive hyperemia index, aortic hemodynamics, pulse wave velocit

170 ar function was assessed as digital reactive hyperemia index.

171 cond intervals for 4 minutes during reactive hyperemia induced by 5-minute forearm cuff occlusion.

172 tamine-atropine stress test is not less than hyperemia induced by dipyridamole.

173 5) coronary artery, both at rest and during hyperemia induced by intravenous dipyridamole.

174 tion of 300 mL of 20% intralipids (n = 3) or hyperemia induced by intravenous infusion of the adenosi

175 Recent studies have shown hyperemia induced by the standard dobutamine-atropine st

176 -pass perfusion imaging was performed during hyperemia (induced by a 4-minute infusion of adenosine a

177 ipped guidewires during baseline and maximal hyperemia, induced by an intracoronary bolus of adenosin

178 Endothelium-dependent (hyperemia-induced flow-mediated dilatation [FMD]) and -i

179 endothelial dysfunction assessed by reactive hyperemia-induced flow-mediated dilation (FMD).

180 icant fall in distal perfusion pressure with hyperemia-induced vasodilatation (fractional flow reserv

181 d, Caesarea, Israel), or Doppler measures of hyperemia], inflammatory markers (interleukin-1beta, int

182 triamine pentaacetic acid at rest and during hyperemia (intravenous adenosine).

183 lial function, measured as ischemic reactive hyperemia (IRH) and related biomarkers, were followed fo

184 Brachial artery ultrasound during reactive hyperemia is a noninvasive method of assessing periphera

185 pulse amplitude augmentation in response to hyperemia is a novel measure of peripheral vasodilator f

186 stimulus elongation suggests that functional hyperemia is an integrative process that involves the en

187 Postocclusive hyperemia is consistently blunted in children with OSA,

188 rms that spatiotemporally coupled functional hyperemia is not present during these early stages of po

189 ynamic Vessel Analyzer), heat-induced skin %-hyperemia (laser-Doppler flowmetry), and glucose metabol

190 The ensuing hyperemia, leak of plasma proteins, and recruitment of l

191 hanges in brachial artery diameter, reactive hyperemia, low-density lipoprotein cholesterol, and the

192 The hyperemia magnitude increased as a nonlinear function of

193 The hyperemia magnitude was not altered by different lightin

194 Increase of total LV blood flow during hyperemia (mean value, 89.6+/-6%; range, 17% to 233%) wa

195 1.37 vs. mean, 1.19; 95% CI, 0.75-1.63), and hyperemia (mean, 0.71; 95% CI, 0.41-1.02 vs. 1.14; 95% C

196 significantly influenced by the induction of hyperemia: mean +/- SD iFR at rest was 0.82 +/- 0.16 ver

197 1.29-2.08 vs. mean, 2.47; 95% CI, 2.07-2.88; hyperemia: mean, 1.95; 95% CI, 1.63-2.26 vs. mean, 2.84;

198 the consequences of this lack of functional hyperemia, measurements of oxidative metabolism via flav

199 Artificial tears combined with CC reduced hyperemia more than other treatments (P <0.05).

200 epithelial defect (n = 2), and conjunctival hyperemia (n = 1).

201 3), stenosis (n=7), mesenteric signs such as hyperemia (n=9), fibrofatty proliferation (n=8) and lymp

202 agnetic resonance included imaging of edema, hyperemia, necrosis, and fibrosis using semiquantitative

203 Hyperemia nutrient blood flow in treated muscles was inc

204 nd HO dependence of glutamatergic functional hyperemia observed in the newborn cerebrovascular circul

205 modynamic changes associated with functional hyperemia occurring at the capillary level.

206 It is well known that reactive hyperemia occurs following a period of ischemia.

207 Although functional hyperemia occurs rapidly, within seconds, such rapid sig

208 The incidence of hyperemia of the eye was slightly lower with brinzolamid

209 ) and is characterized by pain, swelling and hyperemia of the hemi-scrotum.

210 was 0.82 +/- 0.16 versus 0.64 +/- 0.18 with hyperemia (p < 0.001).

211 ated vasodilation and microvascular reactive hyperemia (p < 0.05 for all).

212 ncreased FVR at baseline (P<0.01) and during hyperemia (P<0.001).

213 sed from 1.14+/-7 at rest to 0.92+/-7 during hyperemia (P<0.005), and subendocardial CVR (1.43+/-3) w

214 ividuals without CP (P = 0.03 after reactive hyperemia; P = 0.05 after sublingual nitrate).

215 Reactive hyperemia PAT scores following mental stress were signif

216 Ocular hyperemia, patient preference, and self-projected adhere

217 Wall motion abnormalities (WMAs) at rest, hyperemia perfusion defect (PD), late gadolinium enhance

218 all thickness, loss of mural stratification, hyperemia, periappendiceal fat inflammation, periappendi

219 We investigated the value of reactive hyperemia peripheral arterial tonometry (RH-PAT) as a no

220 d as reactive hyperemia index using reactive hyperemia peripheral arterial tonometry.

221 ndent endothelial function by using reactive hyperemia-peripheral arterial tonometry (RH-PAT) and ass

222 Reactive hyperemia-peripheral arterial tonometry (RH-PAT), a noni

223 Hyperemia (primary endpoint) was graded at baseline, wee

224 Reactive hyperemia produced a time-dependent increase in fingerti

225 tudy assessed the occurrence and severity of hyperemia produced by bimatoprost 0.01 %, and its effica

226 Thermal hyperemia produced distinctly different findings: there

227 ditions of peak (r=0.75; P<0.001) and stable hyperemia (r=0.83; P<0.001).

228 flow (MBF) at rest, during adenosine-induced hyperemia (reflecting primarily endothelium-independent

229 ions of CRP, IL-6, and sICAM-1 with reactive hyperemia remained significant.

230 n induced 6%, 46%, 111%, and 112% of maximal hyperemia, respectively.

231 The pattern of thermal hyperemia response in low-flow POTS subjects during sali

232 The hyperemia response magnitude was quantified by integrati

233 inal blood flow has a postocclusive reactive hyperemia response modulated by occlusion duration and m

234 achial index had (1) a more delayed reactive hyperemia response time, manifesting as an increase in t

235 of adenosine and enhance adenosine-mediated hyperemia responses in a dog model.

236 Reactive hyperemia (RH) in the forearm circulation is an importan

237 were no statistically significant shifts in hyperemia severity in either group, or in subgroups base

238 hirmer test, tear breakup time, conjunctival hyperemia, staining of the cornea and conjunctiva, and a

239 neal and conjunctival staining, conjunctival hyperemia, tear film breakup time (TBUT), tear osmolarit

240 d flow and oxygen saturation during reactive hyperemia than by conventional static measurements.

241 detail spatiotemporal changes in subclinical hyperemia that occur during experimental cutaneous carci

242 LDF revealed decreased perfusion followed by hyperemia that persisted for 1 month (P </=0.05).

243 lood pressure increases, leading to cortical hyperemia that resembles adult positive BOLD responses.

244 most frequent adverse event was conjunctival hyperemia, the incidence of which ranged from 50% (126/2

245 Conjunctival hyperemia, the most commonly reported adverse event, occ

246 tival hemorrhage, eye pain, and conjunctival hyperemia; the majority of these events were mild in int

247 oup B), we evaluated endothelial response to hyperemia through digital tonometry (peripheral arterial

248 transporters also contributed to functional hyperemia through mechanisms independent of calcium rise

249 ression significantly enhances the umbilical hyperemia through NO-dependent mechanisms during a subse

250 e coupled to cerebral arterioles (functional hyperemia) through Ca2+ signals in astrocytes.

251 ion, expressed as the time to peak occlusive hyperemia (Tmax), were examined.

252 t 1 subject exhibited transient conjunctival hyperemia to some degree in the 8-hour period after morn

253 re drop across an epicardial stenosis during hyperemia to that value at rest).

254 CBF responses to neural activity (functional hyperemia), topical application of vasodilators, and dec

255 The failure of DIP to augment exercise hyperemia under these conditions suggests that ADO conce

256 l arteries at rest and during post-occlusion hyperemia using magnetic resonance imaging.

257 Intravitreous VEGF was associated with disc hyperemia, vascular dilatation and tortuosity, and fluor

258 al increase in blood flow, termed functional hyperemia, via several mechanisms, including calcium (Ca

259 Skin %-hyperemia was (mean+/-standard deviation) 1235+/-810 in

260 odilatation measured in response to reactive hyperemia was 150 times greater in pixel count than that

261 The average time from baseline to stable hyperemia was 68.2+/-38.5 seconds, when both DeltaPa and

262 Postprandial hyperemia was accompanied by a marked increase in HVPG i

263 the endocardial/epicardial MBF ratio during hyperemia was associated with inducible regional dysfunc

264 e animal model of hyperdynamic sepsis, renal hyperemia was associated with preserved cortical oxygena

265 Lower regional myocardial blood flow during hyperemia was associated with reduced regional left vent

266 Hyperemia was induced by intravenous administration of a

267 Maximal hyperemia was induced in 9 dogs using adenosine.

268 Hyperemia was induced to create flow mismatch in the dog

269 Hyperemia was induced with an A2A receptor agonist.

270 Hyperemia was not induced in dogs with reduced resting c

271 No reactive hyperemia was observed during early reperfusion.

272 BIM were 31% and 39%, respectively; moderate hyperemia was observed in 2% of patients receiving BIM.

273 though a higher incidence of moderate ocular hyperemia was observed with BIM.

274 Post-occlusion reactive hyperemia was observed.

275 y of a healthy volunteer undergoing reactive hyperemia was performed.

276 ed dilation was similar, but the duration of hyperemia was prolonged after sildenafil administration

277 od flow at rest and during adenosine-induced hyperemia was quantified by contrast-enhanced magnetic r

278 Conjunctival hyperemia was the most common treatment-related adverse

279 Ocular hyperemia was the most common treatment-related adverse

280 Hyperemia was the most frequent treatment-related advers

281 unction; RH-PAT index, a measure of reactive hyperemia, was calculated as the ratio of the digital pu

282 therapy; RH-PAT index, a measure of reactive hyperemia, was calculated as the ratio of the digital pu

283 ressure and flow velocity information during hyperemia, was superior to all other parameters (area un

284 For reactive hyperemia, we observed inverse correlations with markers

285 d PF timolol patients reporting conjunctival hyperemia were 4.4% vs 1.2% (nominal P = .016).

286 digital pulse volume changes during reactive hyperemia were assessed in 94 patients without obstructi

287 in brachial artery diameter during reactive hyperemia were measured by high-resolution ultrasound.

288 The major safety finding was ocular hyperemia, which was more common for both concentrations

289 y nitroprusside produced equivalent coronary hyperemia with a longer duration ( approximately 25%) co

290 ssessed during rest, peak CPT, and adenosine hyperemia with a saturation-recovery gradient-echo pulse

291 eries and veins during cuff-induced reactive hyperemia with magnetic resonance imaging-based oximetry

292 Conjunctival hyperemia with onset later than 2 days after the injecti

293 easured at rest and during adenosine-induced hyperemia with positron emission tomography and 15O-labe

294 The incidences of mild ocular hyperemia with TRAV and BIM were 31% and 39%, respective

295 ported adverse event was conjunctival/ocular hyperemia, with a combined incidence of 52%, 57%, and 16

296 ities in microvascular responses to reactive hyperemia, with a reduction in area under the curve adju

297 of no-flow ischemia with subsequent reactive hyperemia within the femoral region and underwent in viv

298 w phenomenon, can produce sustained coronary hyperemia without detrimental systemic hemodynamics.

299 The observed transient hyperemia would suggest that intravenous (IV) chemothera

300 se within the femoral artery during reactive hyperemia yielded substantial release of nitric oxide, s