ライフサイエンスコーパス: venous

1 omplication among patients requiring central venous access as part of their medical care.

2 Central venous access device (CVAD)-related thrombosis (CRT) is

3 to the IASD versus a sham procedure (femoral venous access with intracardiac echocardiography but no

4 rent deep venous thrombosis, loss of central venous access, and postthrombotic syndrome.

5 odeling suggesting that Eph-B4 regulates AVF venous adaptation through an Akt1-mediated mechanism.

6 1.3 vs 19.3 +/- 2.7 cm H2O; p < 0.001), and venous admixture (0.05 +/- 0.01 vs 0.22 +/- 0.03, p < 0.

7 Venous ammonia at day 5 and length of hospital stay were

8 Fasting venous ammonia levels were estimated daily from 0 to 5 d

9 er days 1-4, but not on day 5, and decreases venous ammonia, time of recovery, and length of hospital

10 ates covered by the proposed model encompass venous and arterial thrombosis, ranging from low-shear-r

11 rich glycoprotein, specifically expressed by venous and capillary endothelium.

12 e observed that microgravity reduces central venous and intracranial pressure.

13 , with numerically stronger associations for venous and IV %IT.

14 severity of PH correlates most strongly with venous and small IV intimal thickening, similar to the p

15 nus was cannulated via subclavian or femoral venous approaches, and aspiration was done directly from

16 on, the Impella system, the TandemHeart, and venous-arterial extracorporeal membrane oxygenation-and

17 f HIT-specific complications (thromboembolic venous/arterial events, amputations, recurrent/persisten

18 ral blood (PPB) and intraoperative pulmonary venous blood (IPVB) could predict poor long-term surviva

19 in arterial, hepatic venous (HV) and portal venous blood (PV).

20 ody fat metabolism, as validated by parallel venous blood beta-hydroxybutyrate (BOHB) measurements.

21 n which inspiration-induced downward flow of venous blood due to reduced intrathoracic pressure is co

22 Concomitant analysis of brain venous blood flow indicated that CSF and venous flux act

23 mitant analyses of CSF dynamics and cerebral venous blood flow, that is, in epidural veins at cervica

24 Venous blood from human volunteers was stimulated with L

25 MPs were prepared from ECs and venous blood from patients with ACS (n=30) and from heal

26 n of circulating tumor cells from peripheral venous blood in clinical practice.

27 A venous blood sample was taken at baseline and at 6 and 1

28 Patients and controls provided venous blood samples.

29 On day 20, a venous blood specimen tested negative for Ebola virus by

30 us malformations (PAVMs) that allow systemic venous blood to bypass the pulmonary capillary bed throu

31 Arterialized venous blood was sampled for 2 h, and measured meal GI a

32 Arterialized venous blood was sampled throughout the 2-h postchalleng

33 Six ml of venous blood was taken for the measurement of serum uric

34 Baseline anemia prevalence was 58% (venous blood).

35 ailure (39.8%) and the presence of a central venous catheter (50.9%) or tracheostomy (64.8%).

36 quently initiate hemodialysis with a central venous catheter (CVC) and subsequently undergo placement

37 udy population was 2.4 episodes/1000 central venous catheter (CVC) days [95% Poisson confidence limit

38 Bedside ultrasound reduced mean central venous catheter confirmation time by 58.3 minutes.

39 sed the total number of cultures and central venous catheter cultures, without an increase in rates o

40 ilm infection when used in a CLS rat central venous catheter infection model.

41 real-time ultrasound guidance during central venous catheter insertion has become a standard of care,

42 A single-operator ultrasound-guided central venous catheter insertion is effective in verifying prop

43 Selection of central venous catheter insertion site in ICU patients could hel

44 of care use of ultrasound can reduce central venous catheter insertion to use time, exposure to radia

45 ator ultrasound-guided, right-sided, central venous catheter insertion verifies proper placement and

46 When a central venous catheter malposition exists, bedside ultrasound w

47 Fifteen studies with 1,553 central venous catheter placements were identified with a pooled

48 dside ultrasound for confirmation of central venous catheter position and exclusion of pneumothorax c

49 e bedside ultrasound confirmation of central venous catheter position.

50 graph when used to accurately assess central venous catheter positioning and screen for pneumothorax.

51 reening of pneumothorax and accurate central venous catheter positioning.

52 remains the gold standard to confirm central venous catheter tip position and rule out associated lun

53 undergone recent surgery, 73% had a central venous catheter, and 41% were receiving systemic antifun

54 oing ultrasound-assisted right-sided central venous catheterization compared with 92 serial historic

55 ization, intravascular procedures, including venous catheterization or injection.

56 The efficacy of antimicrobial central venous catheters (CVCs) remains questionable.

57 y fewer cultures were collected from central venous catheters after vs before the intervention (389 [

58 e so because of the increased use of central venous catheters and other technological advancements in

59 2 chronic hemodialysis patients with central venous catheters as vascular access had their ScvO2 moni

60 cultures and cultures collected from central venous catheters in critically ill children and to exami

61 hest radiography for confirmation of central venous catheters in sufficient detail to reconstruct 2 x

62 All had permanent central venous catheters.

63 drain excess interstitial fluid back to the venous circulation.

64 Other significant variables included venous compression from mass (SHR, 3.1; 95% CI, 1.4 to 6

65 contribution in vivo, we quantified arterial-venous concentration gradients across the human cerebral

66 oracic artery or radial artery, n=5866) or a venous conduit (n=53 566) between 2006 and 2011.

67 Two independent readers rated venous contamination as absent, mild, or moderate to sev

68 Interreader agreement on venous contamination grades was assessed by using the li

69 s isolated lymphatic maps through nulling of venous contamination, thereby simplifying diagnostic int

70 ent, exercise independently promote arterial-venous delivery gradients of intravascular nitric oxide,

71 We hypothesized that the embryonic venous determinant Eph-B4 mediates AVF maturation.

72 and non-invasive technique for evaluation of venous disease.

73 Venous doppler sonography for the evaluation of calf DVT

74 Second, the asymmetry of venous drainage in the pathological cerebral hemisphere

75 e and medium-chain fatty acids from lumen to venous effluent.

76 tics of the Bagel Sign potentially represent venous engorgement and/or acute blood products within th

77 g increases transient stop-flow arm arterial-venous equilibrium pressure and reliably detects respond

78 g increases transient stop-flow arm arterial-venous equilibrium pressure beyond the limits of precisi

79 ith severe acute lung failure receiving veno-venous extracorporeal membrane oxygenation and explore r

80 proximately 7% of adults supported with veno-venous extracorporeal membrane oxygenation for respirato

81 We included 4,988 adults supported with veno-venous extracorporeal membrane oxygenation for respirato

82 reased mortality in patients undergoing veno-venous extracorporeal membrane oxygenation for respirato

83 Adults (>/= 18 yr old) supported with veno-venous extracorporeal membrane oxygenation for respirato

84 plications in adult patients undergoing veno-venous extracorporeal membrane oxygenation for respirato

85 ife support cohorts were as follows: 1) veno-venous extracorporeal membrane oxygenation for respirato

86 All primary cases supported with veno-venous extracorporeal membrane oxygenation from 2007 to

87 re for predicting hospital mortality in veno-venous extracorporeal membrane oxygenation patients befo

88 t in prediction of hospital outcomes in veno-venous extracorporeal membrane oxygenation patients, the

89 n hundred sixty-five patients underwent veno-venous extracorporeal membrane oxygenation, 775 patients

90 During veno-venous extracorporeal membrane oxygenation, hypoxemia (o

91 For patients supported with veno-venous extracorporeal membrane oxygenation, the occurren

92 In patients who received veno-venous extracorporeal membrane oxygenation, there was no

93 sociated with an increased mortality in veno-venous extracorporeal membrane oxygenation.

94 n each heartbeat is matched to the extent of venous filling.

95 brinogen, 10 nM thrombin) under a variety of venous flow conditions was developed using the thrombin-

96 vical level 3, uniquely demonstrated CSF and venous flow to be closely communicating cerebral fluid s

97 ain venous blood flow indicated that CSF and venous flux act as closely communicating systems.

98 xtracorporeal membrane oxygenation (87% veno-venous) for medical indications (78% acute respiratory d

99 Hepatic portal venous gas (HPVG) is a rare imaging finding in children.

100 of pneumoperitoneum, fixed loop, and portal venous gas were present, and 1 point was assigned if bot

101 ed by RBC iron nitrosylhemoglobin formation (venous>arterial; P<0.05) at rest in normoxia, during hyp

102 onal citrate anticoagulation-continuous veno-venous hemodialysis during a 3-year period (n = 1,070) w

103 All patients received continuous veno-venous hemodialysis during the LT.

104 citrate accumulation during continuous veno-venous hemodialysis with regional citrate anticoagulatio

105 oxygenation cardiac arrest, continuous veno-venous hemofiltration, and hyperbilirubinemia during ext

106 d ultimately transitioned to continuous veno-venous hemofiltration.

107 The first patient received continuous veno-venous hemofiltration.

108 rations were determined in arterial, hepatic venous (HV) and portal venous blood (PV).

109 Venous valves (VVs) prevent venous hypertension and ulceration.

110 We hypothesized that pulmonary venous hypertension in heart failure (HF) leads to predo

111 ents (26 cohorts; n=4232 fistulas), and 0.03 venous hypertensive events (1 cohort; n=350 fistulas).

112 Although venous imaging-based biomarkers still have to be validat

113 Several studies have correlated the venous imaging-based biomarkers with grade of collateral

114 n (HSCT) eradicates host haemopoiesis before venous infusion of haemopoietic stem cells (HSCs).

115 sis, major procedure, spinal cord paralysis, venous injury, lower extremity fracture, pelvic fracture

116 ) or 7 days (cohort 2) before CHMI by direct venous inoculation (DVI) of 3200 aseptic, purified, cryo

117 We assessed immunization by direct venous inoculation of aseptic, purified, cryopreserved,

118 %IT (control, 4.9; HF-PH, 14.9; PVOD, 31.1), venous %IT (control, 14.0; HF-PH, 24.9; PVOD, 43.9), and

119 arterial %IT (r=0.35) but more strongly with venous %IT (r=0.49) and IV %IT (r=0.55) (P<0.0001 for al

120 current in sporadically occurring multifocal venous malformation: both cause ligand-independent activ

121 dural CV development in mammals and describe venous malformations in humans with craniosynostosis and

122 duals with sporadically occurring multifocal venous malformations.

123 acterized by numerous cutaneous and internal venous malformations; gastrointestinal lesions are patho

124 cells (ECs), which ectopically expressed the venous marker Coup-TFII.

125 the DA by promoting arterial and suppressing venous marker expression.

126 le in the CV, because expression of arterial-venous markers in CV ECs was not as dramatically affecte

127 e that an early proinflammatory state in the venous milieu, orchestrated by the HIF-induced NLRP3 inf

128 Venous neointimal hyperplasia (VNH) at the outflow vein

129 The finding of a human CSF-venous network with upward CSF net movement opens new cl

130 ns from the skull and dura establish optimal venous networks independent from arterial influences.

131 ilution), forearm vascular conductance (FVC, venous occlusion plethysmography) and cutaneous vascular

132 e no benefit from IAT, whereas patients with venous opacification (COVES >0) were shown to benefit fr

133 of fluid wall shear stress (WSS) typical of venous or arterial flow inhibit taxis.

134 Associations between PASP and venous or IV %IT remained significant after adjusting fo

135 ent hospitalization, and presence of central venous or urinary catheters were independently associate

136 Hemoglobin concentration and arterial-venous oxygen content difference have large effects that

137 cially hemoglobin concentration and arterial-venous oxygen content difference) should enhance appropr

138 a gradients reflecting consumption (arterial>venous; P<0.05) were accompanied by RBC iron nitrosylhem

139 Successful CRT using coronary venous pacing depends on appropriate patient selection,

140 In a rat venous patch angioplasty model, control patches develope

141 arterial pattern, and pattern D was the more venous pattern.

142 Mean +/- SEM pre- and postfilter venous plasma citrate concentrations were 1 +/- 0.1 and

143 Mean +/- SEM pre- and postfilter venous plasma glucose concentrations in the aggregate gr

144 current measurements of retinal arterial and venous PO 2 , tPO2 through the retinal depth, inner reti

145 ifferentiating regions, and continues in the venous pole, which gives rise to the SV.

146 T (p = 0.069) and an increased rate of giant venous pouch in children in whom no mutation was identif

147 eripheral venous pressure (PVP) with central venous pressure (CVP), as well as other invasive hemodyn

148 We sought to compare peripheral venous pressure (PVP) with central venous pressure (CVP)

149 Whilst lying in the supine posture, central venous pressure (supine, 7 +/- 3 vs. microgravity, 4 +/-

150 omes included greater intraoperative central venous pressure and greater transfusion volumes.

151 eractions: patients without elevated jugular venous pressure and those without ascites showed directi

152 ngenital heart disease with elevated central venous pressure complicated by PLE.

153 ssessed whether guiding therapy with hepatic venous pressure gradient (HVPG) monitoring may improve s

154 ated cirrhosis, portal hypertension (hepatic venous pressure gradient [HVPG] >/=6 mm Hg), and body ma

155 gnificant portal hypertension (CSPH, hepatic venous pressure gradient [HVPG] 10 mmHg or greater), des

156 nt with rifaximin did not reduce the hepatic venous pressure gradient or improve systemic hemodynamic

157 Rifaximin had no effect on hepatic venous pressure gradient, mean 16.8 +/- 3.8 mm Hg at bas

158 METHODS AND PVP-HF (Peripheral Venous Pressure Measurements in Patients With Acute Deco

159 and 0.53+/-0.20; P=0.0004), higher pulmonary venous pressure relative to left ventricular transmural

160 Increased pulmonary venous pressure secondary to left heart disease is the m

161 variation, stroke volume variation, central venous pressure, and end-expiratory occlusion test obtai

162 aortic pressure, both subtracted by central venous pressure.

163 ongenital heart disease and elevated central venous pressure.

164 Venous production of TxA2 was higher in OZR than LZR and

165 gly associated with hemorrhage than cortical venous reflux (CVR) in patients with lateral sinus dural

166 for hemodialysis; however, the mechanism of venous remodeling in the fistula environment is not well

167 of pulmonary veins and that the severity of venous remodeling is associated with the severity of pul

168 on of Akt1 function abolishes Eph-B-mediated venous remodeling suggesting that Eph-B4 regulates AVF v

169 :ADP, ATP:AMP and energy charge after portal venous reperfusion, respectively.

170 by combining: (i) pharmacokinetic data (280 venous samples) from a phase I single (50 mg) dose study

171 Systemic venous sampling and positron emission tomography confirm

172 ants and creatinine can replace conventional venous sampling in daily routine.

173 unilateral primary aldosteronism by adrenal venous sampling who had undergone a total adrenalectomy,

174 y adhered to a fibrin matrix over a range of venous shear rates (46-184 s(-1)) for upwards of 30 min,

175 CPyV encephalopathy associated with cerebral venous sinus thrombosis and disseminated primary JCPyV i

176 hy of these vessels, running alongside dural venous sinuses, recapitulates the meningeal lymphatic sy

177 ia model simulations of RBC flow through the venous slits of the human spleen.

178 (PDGF-BB)-stimulated proliferation of human venous smooth muscle cells (SMC) was measured by a DNA-b

179 and CV morphogenesis, by regulating arterial-venous specification of DA ECs to ensure proper separati

180 crease) when longer echo times were used for venous suppression, but it did not subjectively degrade

181 arcinoma (HCC) cells often invade the portal venous system and subsequently develop into portal vein

182 BMP signaling in development of the cerebral venous system.

183 icity and allows more accurate assessment of venous thombosis.

184 creasing inflammatory vascular remodeling of venous thrombi in vivo, and the potential therapeutic ap

185 Small arterial, venous thrombi, thrombotic depositions on damaged endoth

186 , which were more strongly incorporated into venous thrombi.

187 nfidence interval, 1.4-21.1]); male sex; and venous thromboemboli.

188 alists systematically identified symptomatic venous thromboembolic events in both trials.

189 ), stroke (11 more cases [95% CI, 2 to 23]), venous thromboembolism (11 more cases [95% CI, 3 to 22])

190 (876 more cases [95% CI, 606 to 1168]), and venous thromboembolism (21 more cases [95% CI, 12 to 33]

191 t pooled for hypertension (I(2) = 95.0%) and venous thromboembolism (I(2) = 82.3%).

192 (RR, 0.71; 95% CI, 0.51-0.99), 33 vs 38 for venous thromboembolism (RR, 0.85; 95% CI, 0.54-1.34), an

193 ne the risk factors for 30-day postdischarge venous thromboembolism (VTE) after bariatric surgery and

194 ely stratify risk or provide prophylaxis for venous thromboembolism (VTE) among surgical patients.

195 WAS) have confirmed known risk mutations for venous thromboembolism (VTE) and identified a number of

196 The annual number of US venous thromboembolism (VTE) events, the number of poten

197 The incidence of pediatric venous thromboembolism (VTE) has been increasing signifi

198 r for predicting initial, but not recurrent, venous thromboembolism (VTE) in cancer, a setting in whi

199 rmed a meta-analysis to evaluate the risk of venous thromboembolism (VTE) in pregnant women with esse

200 Venous thromboembolism (VTE) is common in patients with

201 agulation in patients with cancer-associated venous thromboembolism (VTE) is unknown.

202 ening for cancer in patients with unprovoked venous thromboembolism (VTE) often is considered, but cl

203 superior to unfractionated heparin (UH) for venous thromboembolism (VTE) prophylaxis in patients wit

204 al patients individually risk stratified for venous thromboembolism (VTE) using Caprini scores.

205 e, no study has assessed whether the risk of venous thromboembolism (VTE) varies with blunt or penetr

206 as been associated with an increased risk of venous thromboembolism (VTE), but the association can be

207 Venous thromboembolism (VTE), caused by altered hemostas

208 pulmonary embolism are collectively known as venous thromboembolism (VTE), which is a common vascular

209 nal cardiovascular disease risk factors with venous thromboembolism (VTE).

210 , stroke, and transient ischemic attack) and venous thromboembolism (VTE).

211 dentify ENTPD1 polymorphisms associated with venous thromboembolism (VTE).

212 Cancer patients have an increased risk of venous thromboembolism (VTE).

213 s) regarding serious adverse events, such as venous thromboembolism (VTE).

214 vitamin K antagonists (VKA) in patients with venous thromboembolism (VTE).

215 herosclerosis may be associated with risk of venous thromboembolism (VTE).

216 Venous thromboembolism (which comprised events of pulmon

217 een suggested to have a protective effect on venous thromboembolism (which includes deep vein thrombo

218 boprophylaxis to prevent clinically apparent venous thromboembolism after knee arthroscopy or casting

219 We compared the incidence of symptomatic venous thromboembolism after these procedures between pa

220 ere the cumulative incidences of symptomatic venous thromboembolism and major bleeding within 3 month

221 with rosuvastatin having the lowest risk on venous thromboembolism compared with other statins 0.57

222 rapy with rosuvastatin significantly reduced venous thromboembolism compared with other statins.

223 t to which statins are associated with first venous thromboembolism events.

224 Among patients with venous thromboembolism in equipoise for continued antico

225 (F5(L) ) is a common genetic risk factor for venous thromboembolism in humans.

226 The reported incidence of venous thromboembolism is 1.5-3.4% of infected patients,

227 Oral anticoagulant therapy for venous thromboembolism is very effective.

228 Venous thromboembolism occurred in 10 of the 719 patient

229 Venous thromboembolism occurred in 5 of the 731 patients

230 Venous thromboembolism occurs in up to one-third of pati

231 primary outcome was a composite of recurrent venous thromboembolism or major bleeding during the 12 m

232 espect to the composite outcome of recurrent venous thromboembolism or major bleeding.

233 orted associations between statins and first venous thromboembolism outcomes were identified from MED

234 ive APEX trial substudy (Acute Medically Ill Venous Thromboembolism Prevention With Extended Duration

235 Although many patients with venous thromboembolism require extended treatment, it is

236 se results indicate that platelet APP limits venous thromboembolism through a negative regulation of

237 ncer who had acute symptomatic or incidental venous thromboembolism to receive either low-molecular-w

238 hase 3 study, we assigned 3396 patients with venous thromboembolism to receive either once-daily riva

239 In observational studies, the pooled RR for venous thromboembolism was 0.75 (95% CI 0.65-0.87; p<0.0

240 In RCTs, the RR for venous thromboembolism was 0.85 (0.73-0.99; p=0.038) whe

241 The rate of recurrent venous thromboembolism was lower but the rate of major b

242 th complicated recoveries (death, infection, venous thromboembolism) were matched with 12 cases with

243 ical applications within atherosclerosis and venous thromboembolism, and explores the potential for m

244 plications, such as urinary tract infection, venous thromboembolism, and myocardial infarction, on th

245 was symptomatic recurrent fatal or nonfatal venous thromboembolism, and the principal safety outcome

246 S) is an autoimmune disease characterized by venous thromboembolism, arterial thrombosis, and obstetr

247 has been suggested as a new risk factor for venous thromboembolism, but its prognostic value is uncl

248 tor (older than 65 years, male sex, previous venous thromboembolism, cancer, autoimmune disease, thro

249 nrolled patients with atrial fibrillation or venous thromboembolism, compared a novel oral anticoagul

250 ncer, while non-pulmonary conditions include venous thromboembolism, coronary artery disease, congest

251 assessed the association of statin use with venous thromboembolism, deep vein thrombosis, or pulmona

252 lacebo or no treatment and collected data on venous thromboembolism, deep vein thrombosis, or pulmona

253 site of major bleeding, INR of 4 or greater, venous thromboembolism, or death.

254 risk of major bleeding, INR of 4 or greater, venous thromboembolism, or death.

255 emic attack, renal insufficiency or failure, venous thromboembolism, pulmonary embolism, and operativ

256 the standard treatment for cancer-associated venous thromboembolism.

257 suggest a beneficial effect of statin use on venous thromboembolism.

258 n both patients with atrial fibrillation and venous thromboembolism.

259 ion in atrial fibrillation and management of venous thromboembolism.

260 effective for the prevention of symptomatic venous thromboembolism.

261 owing outcomes: acute cardiac event; stroke; venous thromboembolism; hypertension; and diabetes melli

262 parin (40 mg once daily for 10+/-4 days) for venous thromboprophylaxis.

263 t of lipid lowering on the incidence of deep venous thrombosis (DVT) is controversial.

264 Deep venous thrombosis (DVT) remains a common and serious car

265 ) in liver cirrhosis complicated with portal venous thrombosis (PVT) has been mainly treated with tra

266 ascular complications, including arterial or venous thrombosis and bleeding.

267 troversial because of its potential risks on venous thrombosis and breast cancer.

268 s a useful imaging tool for the detection of venous thrombosis and for the estimation of a complete b

269 (APS) is characterized by recurrent arterial/venous thrombosis and miscarriages in the persistent pre

270 rial injury and that platelets contribute to venous thrombosis has prompted trials comparing anticoag

271 complimentary technique for the detection of venous thrombosis in such of cases.

272 Venous thrombosis is a multicausal disease involving int

273 t failure, atrial fibrillation, stroke, deep venous thrombosis, cardiovascular death, and total morta

274 T include pulmonary embolism, recurrent deep venous thrombosis, loss of central venous access, and po

275 Using an established model of venous thrombosis, we here show that systemic hypoxia ac

276 ants for primary and secondary prevention of venous thrombosis.

277 , arrhythmias, arteriosclerosis, stroke, and venous thrombosis.

278 inferior vena cava (IVC) ligation to induce venous thrombosis.

279 ilter, whether in the presence or absence of venous thrombosis.

280 etical data sets on the effect of OC use and venous thrombosis.

281 ssary for grade 1 and 2 arterial and grade 1 venous thrombosis.

282 of PCSK9 is associated with protection from venous thrombosis.

283 a in individuals with clinically established venous thrombosis.

284 anemias, and malaria, with both arterial and venous thrombosis.

285 iciency is associated with increased risk of venous thrombosis.

286 roteinase inactivation, increase the risk of venous thrombosis.

287 with ischemic stroke, and 1 (0.1%) with deep venous thrombosis; 28 patients (2.4%) died for cardiovas

288 The incidence of major venous-thrombotic events during the study was 1.22 per 1

289 ical agonist of p53, quinacrine, accelerates venous thrombus resolution in a p53-dependent manner, ev

290 Despite the clinical importance of venous thrombus resolution, the cellular and molecular m

291 differences were demonstrable in arterial or venous tortuosity, diameter or branch density.

292 ST-elevation myocardial infarction and sinus venous tract thrombosis occurred as a complication of tr

293 ed using optic nerve sheath diameter (ONSD), venous transcranial Doppler (vTCD) of straight sinus sys

294 Venous valves (VVs) prevent venous hypertension and ulce

295 lantation, and confirmed Prox1 expression in venous valves.

296 tic reactions are characterized by pulmonary venous vasodilatation and fluid extravasation, which are

297 n identified, but the mechanisms controlling venous vessel growth have been obscure.

298 a high flow state and/or increased pulmonary venous volume.

299 MCs were present in the venous wall, and the number of granule-containing MCs de

300 tion of arterial hypervascularity and portal venous washout.