ライフサイエンスコーパス: pulmonary edema

1 s of respiratory mechanics, blood gases, and pulmonary edema.

2 t (n=2), and acute RV dysfunction with flash pulmonary edema.

3 oxia-treated mice die within days from acute pulmonary edema.

4 penia, and vascular leakage leading to acute pulmonary edema.

5 ult, halted LPS-induced vascular leakage and pulmonary edema.

6 t may be valuable for diagnosing reperfusion pulmonary edema.

7 hypoxemia, cardiopulmonary dysfunction, and pulmonary edema.

8 ockade has been shown to prevent and resolve pulmonary edema.

9 lung syndrome and sepsis, prime the lung for pulmonary edema.

10 ed with impaired wound repair and subsequent pulmonary edema.

11 ith intraluminal purulent exudate, BOOP, and pulmonary edema.

12 e (LVSV) and aortic stiffness predict future pulmonary edema.

13 lial barrier function and the development of pulmonary edema.

14 me overload in vivo pig model of hydrostatic pulmonary edema.

15 attenuated VILI-induced albumin leakage and pulmonary edema.

16 vacaftor is a novel therapeutic approach for pulmonary edema.

17 ften present with cardiogenic shock or acute pulmonary edema.

18 nosine receptor ligands can be used to treat pulmonary edema.

19 stinguishing cardiogenic from noncardiogenic pulmonary edema.

20 with an important role in hyperoxic ALI and pulmonary edema.

21 nt of plasma into the alveolar space causing pulmonary edema.

22 ma fluid is increased in adults with ALI and pulmonary edema.

23 tiating between hydrostatic and permeability pulmonary edema.

24 ive pulmonary disease, and acute cardiogenic pulmonary edema.

25 o maintain alveolar fluid homeostasis during pulmonary edema.

26 riction, lung inflammation, and protein-rich pulmonary edema.

27 ained from control patients with hydrostatic pulmonary edema.

28 corpion venom causes respiratory failure and pulmonary edema.

29 , which increased to 4.6, reflective of mild pulmonary edema.

30 subjects, regardless of the etiology of the pulmonary edema.

31 nfluent opacities, a finding consistent with pulmonary edema.

32 s confirm that SIPE is a form of hemodynamic pulmonary edema.

33 n, mortality, RRT, cardiovascular events, or pulmonary edema.

34 nt approach for inflammation-induced ALI and pulmonary edema.

35 olar fluid clearance, which in turn leads to pulmonary edema.

36 P had significantly enhanced lung damage and pulmonary edema.

37 spiratory distress syndrome from cardiogenic pulmonary edema.

38 MA), as a therapeutic strategy for treating pulmonary edema.

39 rome and 15 patients (11.4%) had cardiogenic pulmonary edema.

40 SCs on both survival and the accumulation of pulmonary edema.

41 -/-) mice showed increased susceptibility to pulmonary edema.

42 linical signs associated with HPS, including pulmonary edema.

43 mmation with relevance for clinical study of pulmonary edema.

44 ng O2 sensing and preventing hypoxia-induced pulmonary edema.

45 ing pulmonary inflammation can contribute to pulmonary edema.

46 oxygen toxicity include vascular leakage and pulmonary edema.

47 osis surrounded by hemorrhagic effusions and pulmonary edema.

48 itial fibrosis, left atrial hypertrophy, and pulmonary edema.

49 eal body weight could detect weaning-induced pulmonary edema.

50 tery catheter for diagnosing weaning-induced pulmonary edema.

51 lial cell surface, leading to persistence of pulmonary edema.

52 g systolic) treated with vasopressors (18%), pulmonary edema (14%), and hyponatremia<130 mmol/L (14%)

53 decrease in excess lung water, a measure of pulmonary edema (145 +/- 50 vs 87 +/- 20 microl; p < 0.0

54 increased only in cases with weaning-induced pulmonary edema (25% +/- 23%).

55 pro-B-type natriuretic peptide, (2) clinical pulmonary edema, (3) radiologic pulmonary congestion or

56 ; most of the patients had acute cardiogenic pulmonary edema (48.6% of the nasal mask group and 42.8%

57 ), 39% in 28 patients with acute cardiogenic pulmonary edema, 68% in nine patients with non-COPD hype

58 increased only in cases with weaning-induced pulmonary edema (9% +/- 3%, 9% +/- 4%, 21% +/- 23%, resp

59 When measured early after the onset of acute pulmonary edema, a BNP level of <250 pg/mL supports the

60 cell (EC) permeability and may culminate in pulmonary edema, a devastating complication of acute lun

61 decreased pulmonary gas exchange, increased pulmonary edema, abnormal lung compliance, and extensive

62 d the ability of Sph 1-P to prevent regional pulmonary edema accumulation in clinically relevant rode

63 e lung strategy to reduce the development of pulmonary edema, acute lung injury and pneumonia, and to

64 on cohort of consecutive patients with acute pulmonary edema admitted to three intensive care units.

65 ay prove valuable for diagnosing reperfusion pulmonary edema after pulmonary endarterectomy and had p

66 hydrostatic (TACO) and permeability (TRALI) pulmonary edema after transfusion is difficult, in part

67 spiratory distress syndrome from cardiogenic pulmonary edema alone or no edema (area under the receiv

68 ity of USA300 to cause severe lung necrosis, pulmonary edema, alveolar hemorrhage, hemoptysis, and de

69 taneous breathing trial with weaning-induced pulmonary edema and 15 without.

70 ted to the respiratory tract and resulted in pulmonary edema and acute lung injury with hyaline membr

71 tions where oxidative stress occurs, such as pulmonary edema and acute lung injury.

72 y in critically ill patients, in particular, pulmonary edema and acute lung injury.

73 Histopathology revealed pulmonary edema and airway obstruction as the morphologi

74 thelium that leads to impaired resolution of pulmonary edema and also facilitates accumulation of pro

75 with respiratory failure due to cardiogenic pulmonary edema and chronic obstructive pulmonary diseas

76 lung water (EVLW) correlate to the degree of pulmonary edema and have substantial prognostic informat

77 ribution of PBF was similar in patients with pulmonary edema and healthy subjects, regardless of the

78 bronchiolitis, diffuse alveolar damage with pulmonary edema and hemorrhage, and interstitial and air

79 e microvascular leakage, resulting in severe pulmonary edema and hemorrhage.

80 ndings included diffuse alveolar damage with pulmonary edema and hyaline membrane formation associate

81 of fluid in the alveoli, which causes severe pulmonary edema and impaired oxygen uptake.

82 type in Ent2(-/-) mice, including attenuated pulmonary edema and improved gas exchange during ALI in

83 cellular adenosine generation show increased pulmonary edema and inflammation after ventilator-induce

84 Markers of pulmonary edema and inflammation indicated that only 40

85 d protein, and cytokines were used to assess pulmonary edema and inflammation.

86 e respiratory failure that result from acute pulmonary edema and inflammation.

87 The latter causes hydrostatic pulmonary edema and is commonly referred to as transfusi

88 Pulmonary edema and lung function parameters were derive

89 mplicated HIF1A-stabilization in attenuating pulmonary edema and lung inflammation during ALI in vivo

90 treatment of patients with acute cardiogenic pulmonary edema and may reduce mortality.

91 nants of systemic anaphylaxis and associated pulmonary edema and might be beneficial targets for anap

92 e proinflammatory cytokine TNF, showing both pulmonary edema and mortality at subthreshold S1P doses.

93 Anxa2(+/+) controls, Anxa2(-/-) mice develop pulmonary edema and neutrophil infiltration in the lung

94 this setting is essential for resolution of pulmonary edema and recovery of left ventricular functio

95 nts with severe preeclampsia associated with pulmonary edema and renal failure.

96 om room air controls despite the presence of pulmonary edema and severe histologic injury.

97 We also demonstrate that pulmonary edema and TGF-beta activity are similarly redu

98 potential therapeutic approach for reducing pulmonary edema and the severity of HPS following ANDV i

99 ardiac dysfunction as the principal cause of pulmonary edema and therefore help in the diagnosis of a

100 oleic acid acted synergistically to increase pulmonary edema and to worsen gas exchange and hemodynam

101 accompanying brain death leads to neurogenic pulmonary edema and triggers development of systemic and

102 ology of the lung tissues revealed extensive pulmonary edema and vascular damage following infection,

103 virus 71-induced brainstem encephalitis with pulmonary edema and/or neurogenic shock (stage 3B) is as

104 e 1-week mortality of enterovirus 71-induced pulmonary edema and/or neurogenic shock without adverse

105 9 patients with ALI, 7 patients with non-ALI pulmonary edema, and 7 healthy subjects.

106 Clinical presentations included chest pain, pulmonary edema, and cardiogenic shock.

107 mpact on outcome and treatment of neurogenic pulmonary edema, and considerations for organ donation.

108 vascular permeability, interleukin-2-induced pulmonary edema, and delayed-type hypersensitivity (DTH)

109 tion of P326TAT attenuated vascular leakage, pulmonary edema, and endothelial apoptosis in the lungs

110 gas exchange and lung compliance, increased pulmonary edema, and extensive airway obstruction.

111 clude acute mountain sickness, high-altitude pulmonary edema, and high-altitude cerebral edema.

112 ious effects, including necrotizing colitis, pulmonary edema, and hydropericardium.

113 y disease exacerbations or acute cardiogenic pulmonary edema, and in immunocompromised patients, as w

114 gas exchange and lung compliance, increased pulmonary edema, and inflammatory indices, such as inter

115 attenuates cardiac hypertrophic remodeling, pulmonary edema, and interstitial fibrosis and prevents

116 Hypoxemia, pulmonary edema, and levels of BALF alveolar macrophages

117 y of proinflammatory cytokines, high-protein pulmonary edema, and neutrophilic lung inflammation.

118 ocardial infarction, myocarditis, neurogenic pulmonary edema, and nonischemic cardiomyopathy.

119 ications (respiratory failure, reintubation, pulmonary edema, and pneumonia) within 3 days of surgery

120 a, bleeding, patient discomfort, reexpansion pulmonary edema, and pneumothorax.

121 une response, capillary leak, noncardiogenic pulmonary edema, and shock in humans.

122 noninfectious etiologies (e.g., atelectasis, pulmonary edema, and shock).

123 tantially less lung injury and inflammation, pulmonary edema, and tissue bacterial burden than did in

124 tration in the pulmonary vasculature, severe pulmonary edema, and tissue oxidation, yet at an equal d

125 es a new PCV2 disease syndrome, called acute pulmonary edema (APE), which, unlike other PCVAD syndrom

126 ding the cytokine release syndrome and flash pulmonary edema, are well recognized in the transplant c

127 dicted development of clinically significant pulmonary edema (area under the receiver-operating chara

128 impaired carotid body O2 sensing and develop pulmonary edema as a consequence of poor ventilatory ada

129 ute respiratory distress syndrome (ARDS) and pulmonary edema associated with the accumulation of neut

130 controls and patients with acute cardiogenic pulmonary edema, baseline protein-C levels were low and

131 et: severe hyperkalemia, metabolic acidosis, pulmonary edema, blood urea nitrogen level higher than 1

132 Fio2 ratios from 6 to 24 hrs, p < .01 each), pulmonary edema (bloodless wet-to-dry-weight ratio; p =

133 ty in DNI patients with COPD and cardiogenic pulmonary edema but not in patients with post-extubation

134 cells but not vascular endothelium, induces pulmonary edema by acute tight junction opening.

135 P (10 cm H(2)O) would diminish the degree of pulmonary edema by attenuating injury to the alveolar ep

136 elium, including enhancing the resolution of pulmonary edema by up-regulating sodium-dependent alveol

137 brupt progression to cardiac dysfunction and pulmonary edema by using an animal model.

138 resolution of alveolar edema in cardiogenic pulmonary edema can be rapid, the rate of edema resoluti

139 Pulmonary edema, cardiac enlargement, and left ventricul

140 t outcomes (death, congestive heart failure, pulmonary edema, cardiogenic shock, stroke, myocardial i

141 gressing abruptly to cardiac dysfunction and pulmonary edema causes rapid death within several hours.

142 eeded to treat=16, with survival improved in pulmonary edema, chronic obstructive pulmonary disease e

143 r performance, reduced fibrosis, and reduced pulmonary edema comparable to or better than metoprolol

144 igher mortality but similar infarct size and pulmonary edema compared with BM(+/+) mice.

145 e wet-to-dry lung weight ratio, a measure of pulmonary edema, compared with mice that received LPS al

146 Rates of congestive heart failure and pulmonary edema declined in both populations: STEMI, -9

147 predictive markers of clinically significant pulmonary edema (defined as acute respiratory distress s

148 dy were hypovolemic or euvolemic at the time pulmonary edema developed.

149 ollapse, acute left ventricular failure with pulmonary edema, disseminated intravascular coagulation,

150 "pulmonary edema," "experimental neurogenic pulmonary edema," "donor brain death," and "donor lung i

151 Acute pulmonary edema during HPS may be caused by capillary le

152 me patients are at risk for death from flash pulmonary edema during rapid fluid remobilization.

153 l, 26 patients (84%) experienced reperfusion pulmonary edema during the first 72 hours after pulmonar

154 All patients with pulmonary edema during the study were hypovolemic or euv

155 rms "neurogenic" with "pulmonary oedema" or "pulmonary edema," "experimental neurogenic pulmonary ede

156 nts (77%); eight of these patients developed pulmonary edema, five of whom died.

157 oxygenase-2 mRNA and PGE2-inducing factor in pulmonary edema fluid and accounts for the differential

158 ations of surfactant proteins A and D in the pulmonary edema fluid and higher concentrations in the p

159 surfactant proteins A and D were measured in pulmonary edema fluid and in plasma.

160 s and protein concentration were measured in pulmonary edema fluid and in plasma.

161 Undiluted pulmonary edema fluid and plasma samples were collected

162 Undiluted pulmonary edema fluid and plasma were collected within 1

163 he Fas/FasL system was assessed in undiluted pulmonary edema fluid and simultaneous plasma.

164 human alveolar type II cells exposed to ALI pulmonary edema fluid compared with plasma (0.02 +/- 0.0

165 at concentrations close to that detected in pulmonary edema fluid from ALI patients.

166 In this study, we tested the hypothesis that pulmonary edema fluid from patients with ALI might reduc

167 inally, NRG-1 was detectable and elevated in pulmonary edema fluid from patients with ALI.

168 Pulmonary edema fluid from subjects with acute lung inju

169 e have reported that IL-1beta is elevated in pulmonary edema fluid in those with ALI and mediates an

170 nsistent with the experimental results, high pulmonary edema fluid levels of IL-8 (>4000 pg/ml) were

171 Pulmonary edema fluid obtained from patients with ALI or

172 oluble FasL were significantly higher in the pulmonary edema fluid of the patients with ALI or ARDS c

173 These results demonstrate that reduced pulmonary edema fluid surfactant protein D and elevated

174 In contrast, pulmonary edema fluid surfactant protein D, but not surf

175 to identify fibroblast mitogenic factors in pulmonary edema fluid, and second to examine the human l

176 Following exposure to ALI pulmonary edema fluid, the gene copy number for the majo

177 ast's gene expression profile in response to pulmonary edema fluid.

178 almeterol 10 (-6) M attenuated the degree of pulmonary edema following acid-induced lung injury.

179 implication in the treatment of cerebral and pulmonary edema following ischemic stroke.

180 d lipopolysaccharide-induced lung injury and pulmonary edema following Klf4 depletion.

181 d increase in lung vascular permeability and pulmonary edema following transient overexpression of th

182 holamines to prevent cardiac dysfunction and pulmonary edema for increasing survival rate.

183 nockout mice had increased vascular leak and pulmonary edema formation after endotracheal LPS, and in

184 We evaluated the role of TNF signaling in pulmonary edema formation in a clinically relevant mouse

185 ce, Sphk1(-/-) mice showed markedly enhanced pulmonary edema formation in response to lipopolysacchar

186 ung injury through enhanced PMN recruitment, pulmonary edema formation, and endothelial and myeloid c

187 ess ET increases lung VEGF levels, promoting pulmonary edema formation, and that hypoxia exaggerates

188 Endothelin (ET) may contribute to pulmonary edema formation, particularly under hypoxic co

189 treatment on LPS-induced PMN recruitment and pulmonary edema formation.

190 itantly with VE-cadherin internalization and pulmonary edema formation.

191 itially seen with acute flaccid paralysis or pulmonary edema had significantly greater frequencies of

192 al parameters in patients with high-altitude pulmonary edema (HAPE) and high-altitude pulmonary hyper

193 om eleven unbiased studies for high altitude pulmonary edema (HAPE) and respiratory distress syndrome

194 The pathogenesis of high-altitude pulmonary edema (HAPE) is considered an altered permeabi

195 ressure and vascular injury in high-altitude pulmonary edema (HAPE).

196 xide synthase (NOS3) in HA adaptation and HA pulmonary edema (HAPE).

197 roxidase activity, endothelial permeability (pulmonary edema), immune cell infiltrate (histological a

198 583 treatment was associated with attenuated pulmonary edema, improved histologic lung injury, and da

199 mplicated 19.4% of ongoing pregnancies, with pulmonary edema in 16.7% and sustained arrhythmias in 2.

200 kness occurred in 314 (23.7%), high-altitude pulmonary edema in 22 (1.7%), and high-altitude cerebral

201 in 4 (7%), and autonomic dysregulation with pulmonary edema in 4 (7%).

202 luid clearance in normal lungs and b) reduce pulmonary edema in acid aspiration-induced lung injury b

203 F plays a central role in the development of pulmonary edema in ALI through activation of p55-mediate

204 o patients, pericardial effusion in one, and pulmonary edema in another; in the group that underwent

205 risk of clinically significant postoperative pulmonary edema in at-risk surgical patients.

206 l mechanisms that regulate the resolution of pulmonary edema in both the normal and the injured lung.

207 injection, providing >60% protection against pulmonary edema in endotoxin-challenged mice (vs <6% pro

208 lightly to improved oxygenation during early pulmonary edema in humans.

209 uch perfusion redistribution occurs in acute pulmonary edema in humans.

210 itrite formation, endothelial apoptosis, and pulmonary edema in lungs of hyperoxic mice.

211 tion of circulating histamine and associated pulmonary edema in mice, were significantly attenuated b

212 anging from respiratory tract irritation and pulmonary edema in severe cases to constrictive bronchio

213 , decompensated heart failure and death from pulmonary edema in TG9 mice.

214 , and VEGF overexpression in the lung causes pulmonary edema in vivo.

215 (neutrophil infiltration) and wet-dry ratio (pulmonary edema) in the lungs of animals subjected to Gr

216 on of proinflammatory cytokines, more severe pulmonary edema, increased neutrophil extracellular trap

217 agnosis between hydrostatic and permeability pulmonary edema, invasive techniques such as right heart

218 e alveolar epithelium to prevent and resolve pulmonary edema is a crucial determinant of morbidity an

219 Pulmonary edema is a serious condition following brain i

220 Reperfusion pulmonary edema is a specific complication of pulmonary

221 Pulmonary edema is an under-recognized and potentially s

222 Neurogenic pulmonary edema is an underrecognized and underdiagnosed

223 (BNP) in critically ill patients with acute pulmonary edema is controversial.

224 Pulmonary edema is the hallmark of acute respiratory dis

225 Chronic kidney disease, pulmonary edema, left ventricular ejection fraction <20%

226 y dynamic strain (VT 825+/-424 mL) developed pulmonary edema (lung weight from 334+/-38 to 658+/-99 g

227 y contribute to the development of hyperoxic pulmonary edema, lung injury, and respiratory failure.

228 li pneumonia with a significant reduction in pulmonary edema, lung vascular permeability, and bactere

229 omparable levels of physiological injury and pulmonary edema, measured by respiratory system mechanic

230 ents with HF are severely ill as a result of pulmonary edema, myocardial ischemia, or cardiogenic sho

231 : acute reversible renal failure (n = 2) and pulmonary edema (n = 2).

232 ompared to control patients with hydrostatic pulmonary edema (n = 40; soluble Fas, 12 ng/ml; soluble

233 respectively, for patients with cardiogenic pulmonary edema (n = 97), acute exacerbation of chronic

234 In patients with acute cardiogenic pulmonary edema, noninvasive ventilation induces a more

235 No pulmonary edema occurred and the rats survived for more

236 thmia, heart, liver or renal dysfunction, or pulmonary edema, occurred in both groups to a similar ex

237 ctomy is closely associated with reperfusion pulmonary edema occurrence in the next 48 hours (area un

238 Neurogenic pulmonary edema occurs as a complication of acute neurol

239 lmonary rales, cardiomegaly, interstitial or pulmonary edema on chest radiograph, S(3) heart sound, t

240 .008), as well as increased diuretic use and pulmonary edema on first chest x-ray, which resolved wit

241 art rate, arterial oxygenation, evidence for pulmonary edema on initial chest x-ray, or rearrest.

242 case report, we described fast resolution of pulmonary edema on treatment with the tyrosine kinase in

243 resent a degree of subclinical high-altitude pulmonary edema or a functional limitation in pulmonary

244 one or more of the following complications: pulmonary edema or embolism, myocardial infarction, stro

245 evels were only moderately increased, and no pulmonary edema or mortality occurred.

246 otension, and/or hypoxemia) or severe (acute pulmonary edema or need for mechanical ventilation) reac

247 3 per quintile; 95% CI, 1.0 to 1.7; P=0.03), pulmonary edema (OR, 2.1 per quintile; 95% CI, 1.6 to 2.

248 dosage (OR: 0.47; 95% CI: 0.25 to 0.87), and pulmonary edema (OR: 3.41; 95% CI: 1.53 to 7.60).

249 Severe presentation (cardiogenic shock, pulmonary edema, or cardiac arrest) was noted in 91% pre

250 estigator-reported congestive heart failure, pulmonary edema, or cardiac failure (hazard ratio for th

251 underlying heart disease and congestive HF, pulmonary edema, or cardiogenic shock.

252 no weight loss, hypoxemia, lung dysfunction, pulmonary edema, or pulmonary inflammation over a 6-day

253 isk for clinically significant postoperative pulmonary edema, particularly resulting from the acute r

254 rgic stress may serve as a marker for future pulmonary edema (PE).

255 rate is a risk factor for ventilator-induced pulmonary edema, possibly because it amplifies lung visc

256 l O2 saturation (hypoxemia), lung pathology, pulmonary edema, reduced lung compliance, increased basa

257 erapeutic intervention for the prevention of pulmonary edema related to inflammatory injury and incre

258 Pulmonary edema--secondary to increased pulmonary vascul

259 ng ischemia/reperfusion, tumor angiogenesis, pulmonary edema, sepsis, and acute lung injury.

260 et a therapeutic option for the treatment of pulmonary edema, several experimental studies have repor

261 All 4 patients with pulmonary edema (severe disease) demonstrated dorsal bra

262 S is characterized by increased permeability pulmonary edema, severe arterial hypoxemia, and impaired

263 Swimming-induced pulmonary edema (SIPE) occurs during swimming or scuba d

264 fatal myocardial infarction, cardiac events, pulmonary edema, stroke, thromboembolism, renal failure,

265 es virus (ANDV) causes a highly lethal acute pulmonary edema termed hantavirus pulmonary syndrome (HP

266 ARDS is caused by protein-rich pulmonary edema that causes severe hypoxemia and impaire

267 ung injury (TRALI), a form of noncardiogenic pulmonary edema that develops during or within 6 h after

268 During ascent to high altitude and pulmonary edema, the alveolar epithelial cells (AEC) are

269 e of PLY, a mediator of pneumococcal-induced pulmonary edema, this binding stabilizes the ENaC-PIP2-M

270 The median time from the onset of pulmonary edema to BNP testing was 3 hrs.

271 inflammatory and hypersensitivity disorders, pulmonary edema, traumatic lung injury, cerebral edema r

272 ide, TRALI causes hypoxia and noncardiogenic pulmonary edema, typically within 6 hours of transfusion

273 00A10, failed to demonstrate hypoxia-induced pulmonary edema under the same conditions.

274 lish-language articles concerning neurogenic pulmonary edema using the search terms "neurogenic" with

275 respiratory distress syndrome or cardiogenic pulmonary edema) using area under the receiver-operating

276 eta1-mediated acute lung injury by promoting pulmonary edema via regulation of actin cytoskeleton dyn

277 The prevalence of pulmonary edema was 20% among piglets ventilated with lo

278 Development of pulmonary edema was assessed by measurement of wet and d

279 Weaning-induced pulmonary edema was defined by the association of signs

280 Pulmonary edema was due to increased permeability, which

281 Interestingly, pulmonary edema was evident only in NTg mice, and no evi

282 Pulmonary edema was first detected ultrastructurally on

283 Hydrostatic pulmonary edema was induced in pigs by acute volume over

284 evident only in NTg mice, and no evidence of pulmonary edema was observed in the eNOS TG mice.

285 In 45/0, pulmonary edema was overt and rapid, with survival less

286 Alveolar/interstitial pulmonary edema was similar with HBOC and HEX, but Po2 w

287 acteristics curves to detect weaning-induced pulmonary edema were 0.89 (95% CI, 0.78-0.99) for extrav

288 nd measures of acidosis, renal function, and pulmonary edema were followed prospectively.

289 mechanisms responsible for the formation of pulmonary edema were identified by 1980, the mechanisms

290 he mechanisms that explain the resolution of pulmonary edema were not well understood at that time.

291 nic obstructive pulmonary disease, and acute pulmonary edema), whereas others were observed only in C

292 syndrome are characterized by noncardiogenic pulmonary edema, which can be assessed by measurement of

293 right ventricular strain and noncardiogenic pulmonary edema, which may potentially alter concentrati

294 an or equal to 14% diagnosed weaning-induced pulmonary edema with a sensitivity of 67% (95% CI, 43-85

295 Chest radiographs showed mild pulmonary edema with a small right pleural effusion.

296 HAPE is a form of hydrostatic pulmonary edema with altered alveolar-capillary permeabi

297 Acid aspiration produced pulmonary edema with significant alveolar epithelial dys

298 otoxin into the distal airspaces resulted in pulmonary edema with the loss of alveolar epithelial flu

299 severe respiratory disease characterized by pulmonary edema, with fatality rates of 35 to 45%.

300 Primary outcome was the occurrence of pulmonary edema within 54 hours.

301 ermore, we hypothesized that the I/R-induced pulmonary edema would be significantly attenuated in rat