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

4 the NMDAR-dependent component of functional hyperemia.

5 uma, neurovascular dysfunction and transient hyperemia.

6 ins unclear which vessels mediate functional hyperemia.

7 enosis at rest and during adenosine-mediated hyperemia.

8 comatous optic nerve damage, or conjunctival hyperemia.

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

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

11 determine whether the iFR is independent of hyperemia.

12 and the pressure gradient induced by maximal hyperemia.

13 ing physiological phenomena such as reactive hyperemia.

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

15 0.75 when comparing Pd/Pa at peak and stable hyperemia.

16 decreased vision, and none had conjunctival hyperemia.

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

18 s critically on the establishment of maximal hyperemia.

19 ing the efficacy of K(+) for eliciting local hyperemia.

20 uronal activity that accounts for functional hyperemia.

21 prolonged recovery during the early phase of hyperemia.

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

23 imaging at rest and during adenosine-induced hyperemia.

24 ) in humans during pharmacologically induced hyperemia.

25 ce imaging during rest and adenosine-induced hyperemia.

26 moral mediators, and induction of intestinal hyperemia.

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

28 nsive events, such as fluid accumulation and hyperemia.

29 ocal inflammatory reaction, and conjunctival hyperemia.

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

31 ence of pharmacologically induced myocardial hyperemia.

32 flow was quantified at rest and during peak hyperemia.

33 the brachial artery in response to reactive hyperemia.

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

35 nduced prolonged joint swelling and synovial hyperemia.

36 bute to neuronal activation-induced cortical hyperemia.

37 ine bicycle exercise, and adenosine-mediated hyperemia.

38 and unravel the mechanisms of saline-induced hyperemia.

39 rent three-dimensional mapping of functional hyperemia.

40 dependent dips in O2 tension drive capillary hyperemia.

41 ance of a coronary stenosis measured without hyperemia.

42 al arteriolar dilation and heat-induced skin hyperemia.

43 t dips in tissue O2 tension elicit capillary hyperemia.

44 , during supine bicycle exercise, and during 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 netarsudil-treated patients was conjunctival hyperemia (47.9%), which was predominately mild.

50 om rest to exercise and was unchanged during hyperemia (59+/-11% vs 65+/-14% vs 57+/-18%; P=0.02 and

51 (CBF) evoked by neural activity (functional hyperemia), a vital homeostatic response in which NMDA r

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

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

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

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

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 Bulbar conjunctival hyperemia and ocular symptoms decreased and temperature

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

68 la cardiac magnetic resonance imaging during hyperemia and rest; inducible ischemia was defined as hy

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 uring rest, exercise, and adenosine-mediated hyperemia and were classified as the reference group or

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

74 generally scored as mild, with conjunctival hyperemia and/or hemorrhage appearing sporadically durin

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

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

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

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

79 antly associated with hypotony, conjunctival hyperemia, and fibrinous reaction on presentation.

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

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

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

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

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

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

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

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

88 persists when neural activity and functional hyperemia are blocked, occurred both in the tissue and i

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

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

91 Reactive hyperemia as a parameter of endothelial function and vas

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

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

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

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

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

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

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

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

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

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

102 During reactive hyperemia, blood flow velocity yielded peak velocity, ti

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

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

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

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

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

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

109 :00 hours, the incidence of mild to moderate hyperemia by biomicroscopy was 18%, 24%, and 11%, respec

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

111 The tPA deficit attenuated functional hyperemia by suppressing NMDAR-dependent nitric oxide pr

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

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

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

115 en treatment groups; in the BBFC arm, ocular hyperemia, corneal abrasion, and dysgeusia were the most

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

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

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

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

120 Under hyperemia, flow increased by 88% (95% CI, 68% to 111%).

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

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

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

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

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

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

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

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

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

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

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

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

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

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 re and flow were measured at rest and during hyperemia in both groups, before and after TAVI (group 1

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

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

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

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

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

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

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

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

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

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

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

148 thelial NMDARs (eNMDARs) regulate functional hyperemia in vivo.

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

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

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

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

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

154 .29, P=0.008) and tended to improve reactive hyperemia index (+0.30+/-0.45 versus -0.17+/-0.30, P=0.0

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

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

157 isplayed stronger correlations with reactive hyperemia index (r = -0.63 vs. r = -0.31; Meng test p =

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

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

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

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

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

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

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

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

166 Reactive hyperemia index was significantly lower in high RPR pati

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

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

169 VR displayed more severely impaired reactive hyperemia index, increased liver stiffness, lower glomer

170 thelial function was assessed using reactive hyperemia index.

171 ar function was assessed as digital reactive hyperemia index.

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

173 of the tPA in the suppression of functional hyperemia induced by Abeta and in the mechanisms of cere

174 ography under baseline conditions and during hyperemia induced by intrarenal dopamine infusion (30 mu

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

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

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

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

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

180 actor 1 signaling participated in functional hyperemia-induced neurogenesis.

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

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

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

184 he other eye: (1) ocular (e.g., conjunctival hyperemia, iris heterochromia, and buphthalmos), (2) pal

185 Background Hyperemia is a key component of acute myocarditis (AM).

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

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

188 Postocclusive hyperemia is consistently blunted in children with OSA,

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

190 in response to flickering light (functional hyperemia) is a well-known autoregulatory response drive

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

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

193 Conjunctival hyperemia, lip swelling, cold sweats, and nausea present

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

195 The hyperemia magnitude increased as a nonlinear function of

196 The hyperemia magnitude was not altered by different lightin

197 arly gadolinium uptake because of myocardial hyperemia may be quantified by using T1 mapping.

198 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

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

200 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;

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

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

203 The most common AE was conjunctival hyperemia, mostly of mild severity, with an incidence of

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

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

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

207 equent ocular adverse event was conjunctival hyperemia (netarsudil/latanoprost FDC, 53.4%; netarsudil

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

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

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

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

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

213 ny (OR, 4.2; 95% CI, 1.3-13.6), conjunctival hyperemia (OR, 2.6; 95% CI, 1.02-6.5), and anterior cham

214 ern was observed in 24 cases (96%), regional hyperemia overlapping with areas of pulmonary opacities

215 operatively (P < 0.01, GG) followed by 3-day hyperemia (P > 0.05 both groups).

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

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

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

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

220 Reactive hyperemia PAT scores following mental stress were signif

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

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

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

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

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

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

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

228 Reactive hyperemia produced a time-dependent increase in fingerti

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

230 Thermal hyperemia produced distinctly different findings: there

231 an endothelial receptor that regulates brain hyperemia provides insight into how neuronal activity co

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

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

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

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

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

237 The hyperemia response magnitude was quantified by integrati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

269 Hyperemia was induced by intravenous administration of a

270 Hyperemia was induced with an A2A receptor agonist.

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

277 Ocular hyperemia was the most common treatment-related adverse

278 Conjunctival hyperemia was the most common treatment-related adverse

279 Hyperemia was the most frequent treatment-related advers

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

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

282 For each participant during baseline and hyperemia, we fitted an adapted three-element Windkessel

283 For reactive hyperemia, we observed inverse correlations with markers

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

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

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

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

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

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

290 FR measurements were performed under maximum hyperemia with intravenous adenosine with the Navvus RXi

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 e most frequent ocular AE being conjunctival hyperemia, with an incidence of 61%, 66%, and 14%, respe

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