ライフサイエンスコーパス: hemorrhagic shock

1 l inflammatory response following injury and hemorrhagic shock.

2 ted to the surgical intensive care unit with hemorrhagic shock.

3 rimary product for resuscitating patients in hemorrhagic shock.

4 both increased and decreased NO levels after hemorrhagic shock.

5 iac and renal function in a porcine model of hemorrhagic shock.

6 and coagulopathy in the rat model of severe hemorrhagic shock.

7 ning clinical acceptance in the treatment of hemorrhagic shock.

8 ate with PATD CO in a piglet model of severe hemorrhagic shock.

9 ry response and may reduce lung injury after hemorrhagic shock.

10 c arterial pressure (SAP) time series during hemorrhagic shock.

11 may permit identification of casualties with hemorrhagic shock.

12 n in vivo models of endotoxemia, sepsis, and hemorrhagic shock.

13 adrenal insufficiency seen in patients with hemorrhagic shock.

14 in preventing organ injury following trauma/hemorrhagic shock.

15 morrhage volume in a porcine model of lethal hemorrhagic shock.

16 swine due to an increased susceptibility to hemorrhagic shock.

17 dynamic variables in porcine model of severe hemorrhagic shock.

18 e threshold, on hemodynamic variables during hemorrhagic shock.

19 o vascular failure and early mortality after hemorrhagic shock.

20 and chronic inflammatory diseases, including hemorrhagic shock.

21 c that significantly protects against lethal hemorrhagic shock.

22 d receptor antagonist, improves tolerance to hemorrhagic shock.

23 ovel therapeutic approach for the therapy of hemorrhagic shock.

24 renal dysfunction and liver injury caused by hemorrhagic shock.

25 effect on the organ injury/failure caused by hemorrhagic shock.

26 S), associated with trauma in a rat model of hemorrhagic shock.

27 clearance by catecholamines after prolonged hemorrhagic shock.

28 o different stimuli such as inflammation and hemorrhagic shock.

29 is swine model of liver injury with profound hemorrhagic shock.

30 fluid clearance by catecholamines following hemorrhagic shock.

31 that intra-abdominal organ pH varies during hemorrhagic shock.

32 o be more vulnerable to hypoxic insult after hemorrhagic shock.

33 eptibility to subsequent sepsis after severe hemorrhagic shock.

34 ls is a lifesaving therapy for patients with hemorrhagic shock.

35 on of the inflammatory response occurring in hemorrhagic shock.

36 in initiating the inflammatory signaling of hemorrhagic shock.

37 ated leukocyte-endothelium interaction after hemorrhagic shock.

38 25 mg/kg iv) and maintained (10 mg/hr) after hemorrhagic shock.

39 eficial effects in a porcine model of severe hemorrhagic shock.

40 all intestine of wild-type mice subjected to hemorrhagic shock.

41 ctin in the recruitment of leukocytes during hemorrhagic shock.

42 iple organ failure and decrease mortality in hemorrhagic shock.

43 eted hemorrhagic shock and a volume-targeted hemorrhagic shock.

44 %) and hemodynamics consistent with class II hemorrhagic shock.

45 %) with hemodynamics consistent with class I hemorrhagic shock.

46 and organ damage during experimental trauma/hemorrhagic shock.

47 %) with hemodynamics consistent with class I hemorrhagic shock.

48 flammatory responses in organs in mice after hemorrhagic shock.

49 ) with hemodynamics consistent with class II hemorrhagic shock.

50 o effective small-volume fluid for traumatic hemorrhagic shock.

51 the RBC changes observed after actual trauma-hemorrhagic shock.

52 ated microcirculatory blood flow behavior in hemorrhagic shock.

53 of injury, such as myocardial infarction and hemorrhagic shock.

54 the role of fibrinogen in resuscitation from hemorrhagic shock.

55 bias of -11+/-27 (+/-2 SD) mL/min/kg during hemorrhagic shock, 1.3+/-20.4 (+/- 2 SD) mL/min/kg durin

56 ed cardiac output compared with LiDCO during hemorrhagic shock (2.25 vs. 0.78 L/min).

57 C) or mild hypothermia (33-34 degrees C from hemorrhagic shock 20 mins to resuscitation time 12 hrs).

58 to laparotomy (i.e., soft tissue trauma) and hemorrhagic shock (35 +/- 5 mm Hg for 90 mins, resuscita

59 to laparotomy (i.e., soft tissue trauma) and hemorrhagic shock (35 +/- 5 mm Hg for 90 minutes, then r

60 otensin-converting enzyme inhibitors) before hemorrhagic shock, 4) shocked mice treated with angioten

61 Male rats underwent laparotomy and hemorrhagic shock (40 mm Hg for 90 minutes), followed by

62 -Dawley rats underwent a 5-cm laparotomy and hemorrhagic shock (40 mm Hg for approximately 90 minutes

63 To produce hemorrhagic shock, 45% to 47% of the estimated blood vol

64 -sham shock plus lymph duct ligation, trauma-hemorrhagic shock (90 mins of shock at 30 mm Hg), and tr

65 Head and neck injuries and hemorrhagic shock account for most maternal deaths secon

66 During hemorrhagic shock, acute B2 receptor blockade significan

67 atory collapse during fluid resuscitation of hemorrhagic shock after traumatic brain injury.

68 Then, C3H/HeN mice were subjected to hemorrhagic shock, after which they received either a ca

69 al venules compared with either hypoxemia or hemorrhagic shock alone.

70 onist) was studied using a pressure-targeted hemorrhagic shock and a volume-targeted hemorrhagic shoc

71 gans are differentially altered after trauma-hemorrhagic shock and acute resuscitation in the rat.

72 on indicator technique (LiDCO) during severe hemorrhagic shock and after fluid resuscitation in dogs.

73 of vasopressin vs. high-dose epinephrine in hemorrhagic shock and cardiac arrest on bone marrow bloo

74 Starting at 20 mins of hemorrhagic shock and continuing through the resuscitati

75 row blood flow may not be predictable during hemorrhagic shock and drug therapy.

76 predominantly affecting the frontal lobes, 1 hemorrhagic shock and encephalopathy, 1 acute hemorrhagi

77 el pH responded most rapidly to the onset of hemorrhagic shock and had the largest change in tissue p

78 of their beneficial effects in patients with hemorrhagic shock and multiple-system trauma, hypertonic

79 end-organ dysfunction associated with severe hemorrhagic shock and prolongs short-term survival.

80 stinal barrier function in rats subjected to hemorrhagic shock and resuscitation (HS/R).

81 n could improve survival in rodent models of hemorrhagic shock and resuscitation and also down-regula

82 Hemorrhagic shock and resuscitation trigger a global isc

83 s show that alcohol intoxication exacerbated hemorrhagic shock and resuscitation-induced hypotension

84 nvestigated how alcohol intoxication impacts hemorrhagic shock and resuscitation-induced microvascula

85 leakage following alcohol intoxication plus hemorrhagic shock and resuscitation.

86 obal ischemia/reperfusion elicited by trauma/hemorrhagic shock and resuscitation.

87 were similar between the three groups during hemorrhagic shock and resuscitation.

88 cardiac output in an adult porcine model of hemorrhagic shock and resuscitation.

89 Mice subjected to hemorrhagic shock and sepsis received either Fas-, caspa

90 response is observed in patients undergoing hemorrhagic shock and sepsis.

91 of four liver lobes rapidly led to profound hemorrhagic shock and subsequent cardiac arrest at 10-13

92 let activation) in lambs subjected to severe hemorrhagic shock and that concurrent inhalation of nitr

93 re designed in a mouse model of resuscitated hemorrhagic shock and tissue trauma (HS/T).

94 , mesenteric lymph was collected from trauma-hemorrhagic shock and trauma-sham shock rats, and the bi

95 y to both the physiologic stress response of hemorrhagic shock and vasopressors given during resuscit

96 elial cell apoptosis occurs following trauma-hemorrhagic shock and, if so, the source of factors lead

97 the treatment of patients in cardiac arrest, hemorrhagic shock, and cardiovascular collapse secondary

98 uding ischemia/reperfusion, transplantation, hemorrhagic shock, and endotoxemia.

99 Recordings were made before, after 1 hr of hemorrhagic shock, and immediately and 3 hrs after infus

100 tation, family discussions, resuscitation of hemorrhagic shock, and resuscitation of septic shock.

101 In 3 dogs subjected to similar prolonged hemorrhagic shock, angiotensin II 180 ng.kg(-1).min(-1)

102 erse effects of transfusion with SRBCs after hemorrhagic shock are ameliorated by treatment with eith

103 ation and systemic inflammatory responses to hemorrhagic shock are minimally influenced by mild hypot

104 s, endotoxemia, ischemia/reperfusion injury, hemorrhagic shock, arthritis, and other inflammatory syn

105 rant further evaluation for the treatment of hemorrhagic shock as well as other acute conditions asso

106 itative fluid in brain-injured patients with hemorrhagic shock, as therapy for intracranial hypertens

107 se death (odds ratio [OR], 1.88; p < 0.001), hemorrhagic shock-associated death (OR, 2.44; p = 0.001)

108 iation with all-cause in-hospital mortality, hemorrhagic shock-associated in-hospital mortality, veno

109 Patients with hemorrhagic shock at admission were excluded.

110 dline laparotomy and approximately 90 min of hemorrhagic shock (blood pressure 35 mmHg), followed by

111 e laparotomy and approximately 90 minutes of hemorrhagic shock (blood pressure, 35 mm Hg), followed b

112 One hour after volume-targeted hemorrhagic shock, blood lactate was measured to evaluat

113 usion, sulfide treatment can be effective in hemorrhagic shock, but its effectiveness is restricted t

114 ne response in vitro and in animal models of hemorrhagic shock, but the effect on the inflammatory re

115 Lambs were subjected to 2 hours of hemorrhagic shock by acutely withdrawing 50% of their bl

116 Mice were subjected to hemorrhagic shock by blood withdrawn until the mean arte

117 lveolar epithelial transport after prolonged hemorrhagic shock by directly impairing the function of

118 apacity of the alveolar epithelium following hemorrhagic shock by inhibiting the iNOS-mediated releas

119 anesthetized pigs were subjected to profound hemorrhagic shock by withdrawal of 55% of estimated bloo

120 on will decrease acute lung injury following hemorrhagic shock, by inhibiting the release of epitheli

121 Hemorrhagic shock caused a reversible decrease in RRI co

122 Hemorrhagic shock caused decreases in RRI complexity as

123 We show that trauma/hemorrhagic shock caused lung injury in wild-type mice,

124 through the utilization of animal models of hemorrhagic shock coupled with prospective observational

125 In a rat model of hemorrhagic shock, delayed treatment with XJB-5-131 has

126 lso, 50% of massively transfused patients in hemorrhagic shock demonstrated SD physiology on admissio

127 Hemorrhagic shock did not affect SAP complexity.

128 The association of hypoxemia and hemorrhagic shock did not amplify leukocytes adhesion to

129 The association of hypoxemia and hemorrhagic shock did not further amplify leukocytes adh

130 of sublingual microcirculation in traumatic hemorrhagic shock during the first 4 days after trauma.

131 lymph obtained from rats subjected to trauma-hemorrhagic shock elicited apoptosis in cultured endothe

132 ial model of indirect ALI induced in mice by hemorrhagic shock followed 24 h later by polymicrobial s

133 murine model of indirect-acute lung injury (hemorrhagic shock followed 24 hours after with cecal lig

134 ant model of indirect ALI induced in mice by hemorrhagic shock followed 24 hours later by polymicrobi

135 Rats underwent hemorrhagic shock followed by 2 hrs of resuscitation and

136 Resuscitated hemorrhagic shock following major trauma promotes the de

137 controlled (mean arterial pressure 40 mm Hg) hemorrhagic shock for 90 mins.

138 decreased significantly during induction of hemorrhagic shock from 14.4 +/- 4.1 to 3.7 +/- 1.8 mL.10

139 ring 60 minutes to reach a PaO2 of 40 mm Hg, hemorrhagic shock group in which animals were exsanguina

140 vel of 40 mm Hg during 30 minutes, hypoxemia-hemorrhagic shock group in which PaO2 was decreased to 4

141 he fraction of perfused villi (94% +/- 2% in hemorrhagic shock group vs 100% +/- 0% in control group,

142 synergistic manner (69% +/- 3% in hypoxemia-hemorrhagic shock group vs 94 +/- 2 in hemorrhagic shock

143 xemia-hemorrhagic shock group vs 94 +/- 2 in hemorrhagic shock group, p < 0.005).

144 disorders-stroke, myocardial infarction, and hemorrhagic shock-have been disappointing.

145 In hemorrhagic shock, Hb-200 infusion may not improve oxyge

146 omposition of exudate cells was unaltered by hemorrhagic shock; however, in vivo injection of S. aure

147 Hemorrhagic shock (HS) and resuscitation leads to widesp

148 Hemorrhagic shock (HS) due to major trauma and surgery p

149 Hemorrhagic shock (HS) due to trauma remains a major cau

150 Hemorrhagic shock (HS) followed by resuscitation (HS-R)

151 organ injury and dysfunction associated with hemorrhagic shock (HS) in the rat.

152 studies of traumatic brain injury (TBI) and hemorrhagic shock (HS) models, have shown cardiorespirat

153 ods for conventional resuscitation (CR) from hemorrhagic shock (HS) often fail to restore adequate in

154 Resuscitation from hemorrhagic shock (HS) predisposes to subsequent infecti

155 Hemorrhagic shock (HS) promotes the development of syste

156 tion of survival in rats subjected to lethal hemorrhagic shock (HS), even in the absence of resuscita

157 polysaccharide(LPS)-induced shock (LPSS) and hemorrhagic shock (HS).

158 During resuscitation from near-lethal hemorrhagic shock, hyperoxia attenuated hyperinflammatio

159 During volume-targeted hemorrhagic shock, icatibant prevented blood pressure lo

160 with a number of pathologic states including hemorrhagic shock, immunosuppression, traumatic tissue i

161 impact of acute B2 receptor blockade during hemorrhagic shock in angiotensin-converting enzyme inhib

162 Trauma-hemorrhagic shock in rats was induced by laparotomy foll

163 survival time after severe volume-controlled hemorrhagic shock in rats without worsening hypotension

164 n vivo model of acute lung injury induced by hemorrhagic shock in rats.

165 d with ischemia and reperfusion injury after hemorrhagic shock in rats.

166 r cross-matching, and are ideal for treating hemorrhagic shock in remote settings.

167 fects of hyperoxia during resuscitation from hemorrhagic shock in swine with preexisting coronary art

168 Hyperoxia during resuscitation from hemorrhagic shock in swine with preexisting coronary art

169 tate (DCA) on survival in an animal model of hemorrhagic shock in the absence of fluid resuscitation.

170 can be successfully used in the treatment of hemorrhagic shock in the absence of fluid resuscitation;

171 ne) and dysfunction (kidney) associated with hemorrhagic shock in the anesthetized rat.

172 bolic, and renal recoveries following severe hemorrhagic shock in the pig compared with 7.5% NaCl alo

173 oxemia frequently occurs simultaneously with hemorrhagic shock in traumatic conditions, it can worsen

174 erebral microcirculation may be preserved in hemorrhagic shock in which systemic and buccal microcirc

175 following combined alcohol intoxication and hemorrhagic shock, in a dose-related manner.

176 well as the organ injury and dysfunction in hemorrhagic shock include 1) inhibition of calpain activ

177 ases in pressure and flow characteristics of hemorrhagic shock, including decreases in microcirculati

178 At 3 and 24 hrs, trauma-hemorrhagic shock increased endothelial cell P-selectin

179 In both rats and humans, trauma-hemorrhagic shock increased RBC adhesion to endothelium

180 RRI high-frequency power decreased with hemorrhagic shock-indicating withdrawal of vagal cardiac

181 Hemorrhagic shock induced lipid peroxidation, neutrophil

182 y rats were intravascularly catheterized and hemorrhagic shock induced to a mean arterial pressure of

183 Lymph duct ligation prevented trauma-hemorrhagic shock-induced increased adhesion molecule ex

184 Trauma-hemorrhagic shock-induced increases in endothelial cell

185 senteric lymph duct ligation prevents trauma-hemorrhagic shock-induced lung injury and neutrophil act

186 molecule-1, after shock, and because trauma-hemorrhagic shock-induced lung injury appears to involve

187 at lymph duct ligation would diminish trauma-hemorrhagic shock-induced P-selectin and intercellular a

188 intestinal lymphatics triggered these trauma-hemorrhagic shock-induced RBC changes because 1) prevent

189 ic shock lymph replicated the in vivo trauma-hemorrhagic shock-induced RBC changes while 3) injection

190 zed that modifying resuscitation would alter hemorrhagic shock-induced respiratory dysfunction and co

191 Hemorrhagic shock-induced tissue hypoxia induces hyperin

192 Trauma-hemorrhagic shock induces endothelial as well as epithel

193 1) Trauma-hemorrhagic shock induces rapid RBC adhesion to endothel

194 At 3 and 24 hrs after trauma-hemorrhagic shock, intercellular adhesion molecule-1 exp

195 ced RBC changes because 1) preventing trauma-hemorrhagic shock intestinal lymph from reaching the sys

196 Ischemia-induced lethal cell swelling during hemorrhagic shock is a key mediator of resuscitation inj

197 Hemorrhagic shock is a leading cause of death in people

198 Decreased organ perfusion after hemorrhagic shock is associated with metabolic acidosis,

199 Trauma/hemorrhagic shock is associated with morbidity and morta

200 The multiple organ injury associated with hemorrhagic shock is due at least in part to ischemia (d

201 Hemorrhagic shock is known to produce immunodepression i

202 ansport across the lung epithelium following hemorrhagic shock is mediated by NO released within the

203 Fluid resuscitation following hemorrhagic shock is often problematic, with development

204 Trauma-hemorrhagic shock is one of the leading causes of acute

205 When hypoxemia was associated to hemorrhagic shock, it decreased villous RBCs velocity in

206 insufficiency occurs after severe trauma and hemorrhagic shock, it remains controversial whether adre

207 ced RBC changes while 3) injection of trauma-hemorrhagic shock lymph into naive animals recreated the

208 incubation of naive whole blood with trauma-hemorrhagic shock lymph replicated the in vivo trauma-he

209 n, trauma-hemorrhage (laparotomy, 90 minutes hemorrhagic shock, MAP 35 +/- 5 mm Hg followed by resusc

210 Patients suffering from hemorrhagic shock may receive several liters of crystall

211 In 7 dogs, prolonged hemorrhagic shock (mean arterial pressure [MAP] of appro

212 soft tissue trauma (midline laparotomy) and hemorrhagic shock (mean blood pressure 35-40 mm Hg for 9

213 of resuscitation with SRBCs after 2 hours of hemorrhagic shock, mice that received SRBCs were given a

214 itoneal adenosine, n = 6 each) with the same hemorrhagic shock model at resuscitation time 1 hr or 4

215 rthermore, in vivo study with a mouse trauma/hemorrhagic shock model showed that administration of ne

216 A three-phase, volume-controlled hemorrhagic shock model was used: hemorrhagic shock phas

217 s correlate well with PATD CO in this severe hemorrhagic shock model.

218 tor and peroxynitrite scavenger, in a severe hemorrhagic shock model.

219 Hemorrhagic shock (n = 11) was induced over 15 mins to l

220 Hemorrhagic shock not only decreased RBCs velocity in vi

221 Hemorrhagic shock often progresses to multiple organ fai

222 Severely injured patients experiencing hemorrhagic shock often require massive transfusion.

223 Using a rat model, we examined the effect of hemorrhagic shock on alpha-defensin expression.

224 However, in hemorrhagic shock or after vasopressors are given during

225 esion to the endothelium further than either hemorrhagic shock or hypoxemia alone did.

226 RBCs obtained from rats subjected to trauma-hemorrhagic shock or sham shock as well as from severely

227 At 3 or 24 hrs after trauma-hemorrhagic shock or trauma-sham shock, lung, heart, liv

228 cted to a laparotomy (trauma) and 90 mins of hemorrhagic shock or trauma/sham shock.

229 d mortality following liver transplantation, hemorrhagic shock, or major hepatic surgery.

230 r adverse reaction to liver transplantation, hemorrhagic shock, or resection.

231 pharmacological therapy for liver resection, hemorrhagic shock, or transplantation surgery.

232 r blood glucose concentrations at 90 mins of hemorrhagic shock (p <.05).

233 Fifteen hemorrhagic shock patients requiring RBC transfusion.

234 Alterations of microcirculation in traumatic hemorrhagic shock patients result from the interplay amo

235 ransfusion on sublingual microcirculation in hemorrhagic shock patients.

236 macrocirculation and the hemoglobin level in hemorrhagic shock patients.

237 terations and organ dysfunction in traumatic hemorrhagic shock patients.

238 ation after control of bleeding in traumatic hemorrhagic shock patients.

239 Eighteen traumatic hemorrhagic shock patients.

240 Therefore, in patients with hemorrhagic shock, perfusion-sensitive organs such as th

241 controlled hemorrhagic shock model was used: hemorrhagic shock phase (120 mins), resuscitation phase

242 k (90 mins of shock at 30 mm Hg), and trauma-hemorrhagic shock plus lymph duct ligation.

243 that fluid resuscitation with HS bolus after hemorrhagic shock prevents the intracranial pressure (IC

244 rol hemorrhage, and the different degrees of hemorrhagic shock produced from these models allow for f

245 highly correlated with cardiac index during hemorrhagic shock (r2 = .69, p < .01), septic shock (r2

246 Adhesion of trauma-hemorrhagic shock RBCs was mediated, at least in part, b

247 After 4 hours of hemorrhagic shock (removal of 30% of the blood volume, s

248 cally instrumented pigs underwent 3 hours of hemorrhagic shock (removal of 30% of the calculated bloo

249 Patients with hemorrhagic shock require optimal resuscitation and cess

250 velopment of remote lung injury after trauma/hemorrhagic shock requires activation of TLR4 in the int

251 t gut barrier function is impaired following hemorrhagic shock, resulting in translocation of bacteri

252 Intestinal ischemia after hemorrhagic shock results in gut barrier dysfunction and

253 Hemorrhagic shock/resuscitation (HS/R)-induced generatio

254 ation from bone marrow supports a sustained, hemorrhagic shock/resuscitation (HS/R)-primed migration

255 creased histone acetylation in kidneys after hemorrhagic shock/resuscitation was restored by valproic

256 nuclear factor-kappaB, which was induced by hemorrhagic shock/resuscitation, was eliminated by BAY11

257 and BAY11-7082 significantly attenuated the hemorrhagic shock/resuscitation-induced protein expressi

258 tory responses were significantly induced by hemorrhagic shock/resuscitation.

259 on of neutrophils in kidneys and liver after hemorrhagic shock/resuscitation.

260 Hemorrhagic shock secondary to trauma is associated with

261 ovascular dysfunction occurring after trauma-hemorrhagic shock, sepsis, and other stress states.

262 Using intravital microscopy, we found that hemorrhagic shock significantly increased the number of

263 Hemorrhagic shock suppresses bone marrow hematopoiesis a

264 entially life-threatening conditions such as hemorrhagic shock syndrome and less frequently acute hep

265 lled exosomes, secreted into ML after trauma/hemorrhagic shock (T/HS) have the potential to activate

266 In rats subjected to trauma hemorrhagic shock (T/HS) or sham shock, the role of panc

267 ride or its vehicle were subjected to trauma-hemorrhagic shock (T/HS) or trauma sham-shock (T/SS) and

268 il [PMN]) respiratory burst after trauma and hemorrhagic shock (T/HS) predisposes subjects to acute r

269 one marrow (BM) dysfunction after trauma and hemorrhagic shock (T/HS) results in a decrease in clonog

270 DL) on distant organ injury following trauma/hemorrhagic shock (T/HS) was examined.

271 Trauma with hemorrhagic shock (T/HS), has been shown to result in li

272 ow-dose albumin could protect against trauma/hemorrhagic shock (T/HS)-induced endothelial cell, lung,

273 During pressure-targeted hemorrhagic shock, the mean blood volume withdrawn was s

274 During hemorrhagic shock, the occurrence of hypoxemia considera

275 ound infection is increased after trauma and hemorrhagic shock, the underlying mechanism for this inc

276 Post-hemorrhagic shock treatment for acute traumatic coagulop

277 Trauma-hemorrhagic shock triggered endothelial cell apoptosis i

278 Furthermore, hemorrhagic shock triggered leukocytes adhesion to the v

279 fective pressor in the irreversible phase of hemorrhagic shock unresponsive to volume replacement and

280 Hemorrhagic shock was associated with an inducible NO sy

281 Hemorrhagic shock was created by graded hemorrhage in an

282 Hemorrhagic shock was induced by phlebotomy to mean arte

283 Hemorrhagic shock was induced by removing 0.025 mL of bl

284 Hemorrhagic shock was induced by withdrawing blood to a

285 Hemorrhagic shock was induced by withdrawing blood to ac

286 Hemorrhagic shock was induced in five pigs by bleeding f

287 Hemorrhagic shock was induced in rats by withdrawing 60%

288 Hemorrhagic shock was induced in young and mature rats b

289 Hemorrhagic shock was initiated by withdrawing blood ove

290 tely at the end of and 12 and 22 hours after hemorrhagic shock, we measured hemodynamics, blood gases

291 smallest changes in organ pH as a result of hemorrhagic shock were seen in the abdominal wall muscle

292 enty four patients (35 with sepsis, 239 with hemorrhagic shock) were managed.

293 y of the alveolar epithelium after prolonged hemorrhagic shock, whereas direct stimulation of adenyl

294 uted, with the exception of resuscitation of hemorrhagic shock, which occurs less frequently than the

295 thirty-five adult blunt trauma patients with hemorrhagic shock who survived beyond 48 hours after inj

296 ata suggest that resuscitation of lambs from hemorrhagic shock with autologous stored RBCs induces pu

297 and challenged the Army leadership to treat hemorrhagic shock with blood rather than plasma.

298 ive groups: unmanipulated controls (n = 12), hemorrhagic shock with laparotomy (n = 8), hemorrhagic s

299 , hemorrhagic shock with laparotomy (n = 8), hemorrhagic shock with mesenteric lymph duct ligation (n

300 We find that during hemorrhagic shock with resuscitation, an in vivo mouse m