ライフサイエンスコーパス: warm ischemia

1 expression of VEGF in a mouse model of liver warm ischemia.

2 preservation of kidneys exposed to 60 min of warm ischemia.

3 pMRI, are biomarkers of kidney injury after warm ischemia.

4 ve endothelial structure and function during warm ischemia.

5 HBD), thereby improving function with longer warm ischemia.

6 roups were subjected to approximately 70 min warm ischemia.

7 use liver dysfunction after cold storage and warm ischemia.

8 an shortage, but they inherently suffer from warm ischemia.

9 volume before and after a 7-minute period of warm ischemia.

10 lipid peroxidation occurs in this model with warm ischemia.

11 to potentially damaging conditions, such as warm ischemia.

12 oblems often worsen the dangerous effects of warm ischemia.

13 = 30) sustained either minimal or 75 min of warm ischemia.

14 uctions can be performed ex situ, minimizing warm ischemia.

15 ld good results in DCD livers with prolonged warm ischemia.

16 aluate LEEDR compared to prolonged untreated warm ischemia.

17 on after circulatory deaths, with 4.5-5 h of warm ischemia.

18 on fall to less than 10% after 30 minutes of warm ischemia.

19 of kidney grafts associated with substantial warm ischemia.

20 lly relevant 2-hour cold ischemia and 1-hour warm ischemia.

21 important roles in mitigating the effects of warm ischemia.

22 ection of DCD grafts and clear definition of warm ischemia.

23 g systemic injury, hepatotoxin exposure, and warm ischemia.

24 Rats underwent bilateral renal warm ischemia (15-60 min) then reperfusion (20 or 80 min

25 ular EVLP for 2 hours after a combination of warm ischemia (20-420 min) and cold ischemia (120-600 mi

26 s, P < 0.001), with shorter functional donor warm ischemia (22 vs 31 minutes, P < 0.001) and a lower

27 l allografts were subjected to 30 minutes of warm ischemia, 3.5 hours of cold ischemia, and then perf

28 Warm ischemia (30 and 60 min) induced significant histol

29 Global warm ischemia (37 degrees C) significantly impaired comp

30 were exposed to 0, 60, or 75 min of in situ warm ischemia (37 degrees C), followed by 24 to 72 hr pr

31 role of TIM-4 signaling in a model of liver warm ischemia (90 minutes) and reperfusion.

32 WT) controls were subjected to partial liver warm ischemia (90 minutes) followed by reperfusion (1-6

33 an established mouse model of partial liver warm ischemia (90 minutes) followed by reperfusion (6 ho

34 With a partial lobar liver warm ischemia (90 minutes) model, ASC-deficient and wild

35 (PACAP) in a murine model of partial liver "warm" ischemia (90 minutes) followed by reperfusion.

36 eath leads to vascular damage as a result of warm ischemia, affecting renovascular circulating volume

37 kidney graft, revascularized after 35 min of warm ischemia, also functioned immediately.

38 underwent sham operation (n=9), or 45 min of warm ischemia and 10 min of reperfusion with U74389G (6

39 Kidneys exposed to 75 minutes of warm ischemia and 16 hours of static cold storage were i

40 After these kidneys had sustained 30 min of warm ischemia and 24 h of oxygenated HMP, they were eith

41 5% survival) in kidneys exposed to 75 min of warm ischemia and 24 hr machine perfusion.

42 suscitate porcine livers after 60 minutes of warm ischemia and 4 hours of cold preservation.

43 ce of delayed graft function attributable to warm ischemia and cold ischemia (CI).

44 awley rats were subjected to 75 min of renal warm ischemia and contralateral nephrectomy.

45 -1 (PSGL-1) in rat models of hepatic in vivo warm ischemia and ex vivo cold ischemia.

46 Porcine kidneys were retrieved after 10-min warm ischemia and flushed with 500 mL hyperosmolar citra

47 here the donor organ undergoes both cold and warm ischemia and global ischemic insult.

48 in a well-established model of liver partial warm ischemia and in situ reperfusion.

49 Criteria for matching included duration of warm ischemia and key confounders summarized in the bala

50 Median functional warm ischemia and no-flow time were 36 and 28 min, respe

51 sed in two distinct animal models of hepatic warm ischemia and orthotopic liver transplantation (hypo

52 om male Lewis rats were subjected to 1 hr of warm ischemia and preserved with 5 hr of SCS or NELP, an

53 +/-40 kg pigs were exposed to 30 minutes of warm ischemia and randomized to receive 22-hour HMP with

54 livers were exposed to 55 minutes prolonged warm ischemia and reperfused for 3 days (n = 6).

55 Hepatic warm ischemia and reperfusion (I/R) injury and inflammat

56 mucosal damage that occurs after intestinal warm ischemia and reperfusion and its recovery, little i

57 Liver injury from warm ischemia and reperfusion was attenuated with all la

58 ENT2 transcript and protein levels following warm ischemia and reperfusion.

59 cell-derived IL-22 in liver injury caused by warm ischemia and reperfusion.

60 rdiac arrest (DCD) followed by 15 minutes of warm ischemia and resuscitation on NRP.

61 ceived normal saline, the sham group without warm ischemia and the experimental groups, which receive

62 rcine livers were subjected to 60 minutes of warm ischemia and then assigned to the following groups:

63 orcine kidneys were exposed to 30 minutes of warm ischemia and then reimplanted following either 16 h

64 t the immediate-function kidneys had shorter warm ischemia and total preservation times compared with

65 C57Bl/6J mice underwent bilateral warm ischemia and were sacrificed after 30 minutes or 24

66 emia-reperfusion injury model (predominantly warm ischemia) and a kidney transplantation model (predo

67 th ischemia-reperfusion injury (IRI) (45-min warm ischemia), and rats subjected to acute cyclosporine

68 rfused hearts were subjected to 5 minutes of warm ischemia, and at 5, 10, and 15 minutes after initia

69 Vascular clamping confers warm ischemia, and attempts at renal hypothermia include

70 y of mouse liver grafts after cold ischemia, warm ischemia, and combined warm+cold ischemia.

71 Mice underwent euthanasia and 60 minutes warm ischemia, and lungs were flushed with Perfadex and

72 eservation solution extends the tolerance to warm ischemia, and may reduce the rate of ischemic chola

73 e II NKT cells in mice with partial hepatic, warm ischemia, and reperfusion injury.

74 Mean console, warm ischemia, and rewarming times were 130.8 minutes, 2

75 of AP-1 was dramatically increased following warm ischemia at 1 to 3 hours postreperfusion.

76 donors after circulatory death (DCD) suffer warm ischemia before cold storage which may prejudice gr

77 f donor liver grafts to prolonged periods of warm ischemia before procurement causes injuries includi

78 Organs were subjected to 60 min of warm ischemia before the hypothermic machine preservatio

79 ole in signalling liver tissue damage due to warm ischemia before transplantation.

80 D, pig kidneys underwent 0, 30, or 60 min of warm ischemia, before hypothermic machine perfusion.

81 erformed in 15 patients without the need for warm ischemia by utilizing pharmalogically induced hypot

82 After warm ischemia, cardiac output in EC-SOD was significantl

83 late that this is caused by a combination of warm ischemia, cold ischemia, and hypertonic citrate dur

84 g) underwent left nephrectomy with 30 min of warm ischemia, Collins C-4 flush, and 24 hr of cold stor

85 n (HPP) of kidneys subjected to preretrieval warm ischemia compared with nonischemic controls.

86 etting of a solitary kidney, every minute of warm ischemia counts and ischemia is an important modifi

87 livers were subjected to 30 min of asystolic warm ischemia (DCD), followed by 2 h of either static co

88 o (odds ratio, 0.20; P = 0.008) and arterial warm ischemia duration (odds ratio, 1.05; P = 0.008).

89 For the DCD donors, the median donor warm ischemia duration was 24 minutes.

90 undergo apoptosis after 60 to 120 minutes of warm ischemia followed by 0 to 24 hours of reperfusion.

91 Porcine kidneys were subjected to 10 min of warm ischemia followed by 18 hr of static cold storage w

92 Kidneys were subjected to 20 min warm ischemia followed by 2 or 18 hr of cold storage (n=

93 Ninety minutes of warm ischemia followed by 6 hours of reperfusion induced

94 njury induced by 90 minutes of liver partial warm ischemia followed by 6 hours of reperfusion.

95 served livers that had experienced 30 min of warm ischemia followed by a 10 hr preservation period.

96 erved tissues that had experienced 30 min of warm ischemia followed by a 5-hr preservation period wit

97 nephrectomized rats that underwent 60 min of warm ischemia followed by a 72-hr reperfusion interval w

98 Porcine kidneys were exposed to 30 min of warm ischemia followed by perfusion.

99 stem in an established murine model of liver warm ischemia followed by reperfusion.

100 from an abattoir were subjected to 30 min of warm ischemia, followed by 3 h of hypothermic oxygenated

101 After 75 min of kidney warm ischemia, four experimental groups of n = 7 underwe

102 he slight deterioration seen when increasing warm ischemia from 1 to 2 hr, significantly improving tr

103 ) in the control to 0.82 (0.1) in the 60-min warm ischemia group (P<0.01).

104 -hr preservation of kidneys not subjected to warm ischemia (heart-beating donor model), but there was

105 ctively mitigated the consequences of 9 h of warm ischemia in a swine model, improving survival, pres

106 risk profile resulting from the longer donor warm ischemia in Italy (40 versus 18 min; P < 0.001).

107 After 45 minutes of warm ischemia in oxygenated UW + PFC solution, grafts sh

108 However, all rats with 120 min (n=8) liver warm ischemia in splenic-caval shunt group survived for

109 ecipient age + 0.816 log creatinine + 0.0044 warm ischemia (in minutes) + 0.659 (if second transplant

110 reduce and limit the impact of the prolonged warm ischemia inherent to the uDCD process, and to deal

111 ury and to enhance the tolerance of liver to warm ischemia injury with portosystemic shunt.

112 In the first model (warm ischemia), IPC significantly decreased serum aminot

113 ted inflammatory responses in models of both warm ischemia (kidney clamping) and prolonged cold ische

114 Following exposure to 30 min of warm ischemia, kidneys (n = 6/group) were removed and ei

115 Following exposure to 30 min of warm ischemia, kidneys (n = 6/group) were removed and ei

116 Using a partial lobar warm ischemia model, groups of wild-type (WT), T cell-de

117 In an in vivo warm ischemia model, hepatic injury was assessed by seru

118 ponse were studied in a murine partial liver warm ischemia model.

119 to either minimal warm ischemia or 75 min of warm ischemia (n = 30 per group).

120 A total of 67% of rats with 45 min liver warm ischemia (n=6) and 100% of rats with 60 min liver w

121 mia (n=6) and 100% of rats with 60 min liver warm ischemia (n=6) died within 1 day.

122 estigated in porcine livers with minimal (no warm ischemia, n = 5) or severe injury (60 min warm isch

123 rm ischemia, n = 5) or severe injury (60 min warm ischemia, n = 5).

124 Controlled donors with a warm ischemia of <30 minutes were considered.

125 del and simulate the static cold storage and warm ischemia of a proposed model of liver cells.

126 n Lewis and Fischer 344 rats after 45 min of warm ischemia of a single kidney and with or without con

127 kidneys and assess the additional impact of warm ischemia on ex vivo kidney metabolism.

128 rcine kidneys were exposed to either minimal warm ischemia or 75 min of warm ischemia (n = 30 per gro

129 eased in human donor lungs starting from the warm-ischemia phase and were associated with increased t

130 of lipopolysaccharide in the rats with liver warm ischemia plus splenic-caval shunt.

131 After 30 min of warm ischemia, porcine kidneys were randomly assigned to

132 After 30 min of asystolic warm ischemia, porcine livers underwent 6 h of SCS follo

133 After 30 minutes of warm ischemia, porcine slaughterhouse kidneys were prese

134 ction associated with 30 min of preretrieval warm ischemia (pre-WI).

135 a +/-40 kg pig was exposed to 30 minutes of warm ischemia prior to 22 hours of HMP and autotransplan

136 vestigated in an experimental model of renal warm ischemia reperfusion injury.

137 steatotic livers in a model of total hepatic warm ischemia-reperfusion (I/R).

138 reconditioned with whole liver radiation and warm ischemia-reperfusion followed by intrasplenic trans

139 rge animals for protecting the liver against warm ischemia-reperfusion injury but not injury associat

140 hat calpain proteases play a pivotal role in warm ischemia-reperfusion injury of the rat liver throug

141 selective MMP-9 inhibition largely abolished warm ischemia-reperfusion injury.

142 rough repeated CI during torpor, followed by warm ischemia/reperfusion (WI) during interbout arousal

143 d play an important role in limiting hepatic warm ischemia/reperfusion (WI/Rp) injury, probably throu

144 the role of IL-6 in rodent models of hepatic warm ischemia/reperfusion (WI/Rp) injury.

145 characterized models of acute kidney injury; warm ischemia/reperfusion and folic acid injection were

146 meliorates fatty livers and protects against warm ischemia/reperfusion fatty liver injury, suggesting

147 nd injury in a murine model of liver partial warm ischemia/reperfusion injury (IRI).

148 Further, after warm ischemia/reperfusion injury, we show that rats expr

149 vented the susceptibility of fatty livers to warm ischemia/reperfusion injury.

150 ble to phospholipid depletion in response to warm ischemia/reperfusion than normal livers.

151 ing HPP of kidneys subjected to preretrieval warm ischemia resulted in a normalization of GFR measure

152 Both 10 and 30 min warm ischemia resulted in a rise in TACE expression whic

153 However, the risk of the warm ischemia resulting from cardiac arrest to irreversi

154 ys of C57BL/6 mice that underwent unilateral warm ischemia revealed nine miRNAs (miR-21, miR-20a, miR

155 After 30 minutes of warm ischemia, right kidneys were removed from 30-kg Yor

156 mic shunt enhances the tolerance of liver to warm ischemia through the protective role of iNOS and nu

157 Donor age >50 years, BMI >30, warm ischemia time >25 minutes, ITU stay >7 days and ALT

158 Risk factors for DGF included functional warm ischemia time >40 min, dialysis >2 y, recipient bod

159 cCrCl <60 mL/min/1.73m, PELD >25 points, and warm ischemia time >60 minutes.

160 5 days), cold ischemia time (>10 hours), and warm ischemia time (>40 minutes).

161 me (mean, 159 vs. 188 min; P<0.001), shorter warm ischemia time (2 vs. 5 min; P<0.001) and a lower in

162 ighted include the vital importance of donor warm ischemia time (DWIT) on outcome for both recipients

163 status at transplantation, donor age, donor warm ischemia time (DWIT), and cold ischemia time (CIT).

164 e additional ischemic event during the donor warm ischemia time (DWIT), DCD grafts carry an increased

165 s regarding the injury incurred during donor warm ischemia time (DWIT).

166 In patients with embolization, the warm ischemia time (from embolization to removal of the

167 ntified recipient BMI (P = 0.046), recipient warm ischemia time (odds ratio, OR, 1.032; 95% CI, 1.008

168 ent age (r = -0.27662, p = 0.0016), cold and warm ischemia time (r = -0.25204, p = 0.0082; r = -0.197

169 Warm ischemia time (WIT) and ischemia-reperfusion injury

170 the impact of MPH use in DCD procurements on warm ischemia time (WIT) and organ yield.

171 " such as cold ischemia time (CIT) recipient warm ischemia time (WIT) and the use of thrombolytic flu

172 ischemia time (CIT) at 2-hour intervals and warm ischemia time (WIT) at 10-minute intervals showed t

173 imated blood loss (EBL) greater than 500 mL, warm ischemia time (WIT) greater than 30 minutes, positi

174 In the HCV+ cohort, recipient race, warm ischemia time (WIT), and diabetes also independentl

175 ive time (210 versus 195 min; P = 0.011) and warm ischemia time (WIT; 230 versus 180 s; P < 0.001) we

176 Median operative time was 159 (54) minutes, warm ischemia time 180 (90) seconds, estimated blood los

177 sults are as follows: operative time 4.5 hr, warm ischemia time 25 min, and blood transfused (packed

178 es, estimated blood loss 344.2 +/- 690.3 mL, warm ischemia time 4.9 +/- 3.4 minutes, and donor length

179 n after circulatory death (DCD, n = 36, mean warm ischemia time = 2 min) and donation after brain dea

180 and donation after brain death (DBD, n = 76, warm ischemia time = none) were collected.

181 The donor organ was subjected to 1 hour of warm ischemia time after circulatory cessation, then flu

182 Warm ischemia time and cold ischemia times were 38 and 4

183 optimal outcomes in both DCD with prolonged warm ischemia time and ECD-DBD LT.

184 analyzed following challenge with 45 min of warm ischemia time and either 4 h of reperfusion or 24 h

185 s well as clinical factors, such as cold and warm ischemia time and HLA mismatch.

186 ed temperature profiles crucial for managing warm ischemia time and optimizing cooling rates.

187 cases showed no significant differences for warm ischemia time and other donor outcomes, delayed gra

188 um level, donor length of hospital stay, and warm ischemia time approached significance.

189 usal mediation analysis was used to evaluate warm ischemia time as a potential mediator of this assoc

190 perform this type of anastomosis may reduce warm ischemia time as well.

191 atients, retransplant recipients, donor age, warm ischemia time greater than 30 minutes and cold isch

192 , 1.23-2.83; P = 0.003); however, functional warm ischemia time had no impact (hazard ratio, 1.00; 95

193 Median functional warm ischemia time in DCD donors was 44 (39-48) min.

194 last 5 years with a nearly 50% reduction of warm ischemia time in experienced hands.

195 clinical phase, the length of the functional warm ischemia time in the donation process was inversely

196 onor-specific antibody, negative crossmatch, warm ischemia time less than 60 min, absence of recipien

197 While donor warm ischemia time may be shorter compared with controll

198 a mean estimated blood loss of 85.7 mL and a warm ischemia time of 116.0 seconds.

199 Mean warm ischemia time of the pancreas graft was 34 min.

200 greater than 30% on liver biopsy, and donor warm ischemia time over 30 minutes (P < .05).

201 in cold ischemia time and organs with donor warm ischemia time over 30 minutes (P < .05).

202 Cold as well as warm ischemia time resulted in a significant decrease in

203 no-flow time to <30 minutes, and functional warm ischemia time to <150 minutes.

204 n to asystole was 15.9+/-1.9 min and overall warm ischemia time was 12.5+/-1.0 min.

205 n, mean hospital stay was 3.2 days, and mean warm ischemia time was 123.3 seconds.

206 Mean functional warm ischemia time was 135 minutes.

207 Mean warm ischemia time was 14.7 minutes (range, 7-40 minutes

208 The warm ischemia time was 21 minutes, and the cold ischemia

209 Mean warm ischemia time was 3 minutes after laparoscopic harv

210 let isolation time was 185 (37) minutes, and warm ischemia time was 51 (62) minutes.

211 The median primary warm ischemia time was 6 min (interquartile range [IQR]:

212 Average warm ischemia time was 76 minutes.

213 Warm ischemia time was 77 minutes.

214 Warm ischemia time was longer in ROB (P 0.001) with resp

215 /-0.7 vs. 3.0+/-0.7 hours, P <0.04), whereas warm ischemia time was shorter (3:55+/-1:47 vs. 4:55+/-0

216 Warm ischemia time was shorter in the piggyback group an

217 Donor warm ischemia time was significantly shorter in the SCS

218 Per minute increase in warm ischemia time was the only significant risk factor

219 aining treatment to asystole, and functional warm ischemia time was the time from donor systolic bloo

220 hospitalization at time of OLT, and cold and warm ischemia time were independent predictors of surviv

221 s, improving renal cooling or shortening the warm ischemia time will expand its indications further.

222 creatinine excretion, TIMP-2/mOsm, and total warm ischemia time with an AUC of 0.85 (95% confidence i

223 After remaining in situ for 120 min (30-min warm ischemia time, 90-min cold ischemia time), the seco

224 rgical demographics included operative time, warm ischemia time, and estimated blood loss.

225 Graft survival is affected by donor gender, warm ischemia time, and pretransplant patient condition.

226 ewithdrawal preparation, definition of donor warm ischemia time, DCD surgical technique, combined tho

227 etwork for Organ Sharing (UNOS) status, cold/warm ischemia time, intraoperative blood loss, and occur

228 cluded operative time, islet isolation time, warm ischemia time, islet equivalent (IE) counts, estima

229 Despite prolonged warm ischemia time, Italian centers reported good outcom

230 Duration of surgery, warm ischemia time, operative blood loss, conversion, an

231 Longer cold/warm ischemia time, recipient/donor hypertension, and ha

232 sis, panel-reactive antibodies, and cold and warm ischemia time, the odds of oliguria were 1.60 (1.14

233 prove perioperative characteristics, such as warm ischemia time, to levels comparable to open surgery

234 (LPN), particularly in regards to decreased warm ischemia time.

235 system closure and hemostasis with a limited warm ischemia time.

236 transaminase, UNOS status, donor gender, and warm ischemia time.

237 h has a lengthier overall operative time and warm ischemia time.

238 also enriched in DCD donors after the first warm ischemia time.

239 quality of life, shorter operating time, and warm ischemia time.

240 ), durations of perfusion (1 and 24 hr), and warm ischemia times (15 and 45 min).

241 operative times (TOT) (324 vs. 344 min) and warm ischemia times (WIT) (28 vs. 31 min) in the 45-90 g

242 d hypothermia should be considered if longer warm ischemia times are anticipated (i.e. >25 min).

243 nephrectomy group had shorter operative and warm ischemia times by 52 minutes (P < 0.001) and 102 se

244 by lung recovery, poor HLA DR matching, and warm ischemia times differing with donor age.

245 rculatory death report good outcomes despite warm ischemia times up to 57 minutes.

246 Mean cold and warm ischemia times were 9:08 +/- 2:57 hr and 51 +/- 9 m

247 re procured from older donors and had longer warm ischemia times, and consequently achieved higher ut

248 any DCD grafts are discarded because of long warm ischemia times, and the absence of reliable measure

249 Outcomes evaluated were operative and warm ischemia times, blood loss, donor complications, le

250 ve complications, conversions, operative and warm ischemia times, blood loss, length of hospital stay

251 may be associated with shorter operative and warm ischemia times, patients undergoing laparoscopic ne

252 he open group but nonsignificantly different warm ischemia times.

253 COR-NMP than after SCS, despite longer donor warm ischemia times.

254 discarded because of older donor age or long warm ischemia times.

255 kidneys, which is susceptible to changes in warm ischemia times.

256 ime, and significantly decreased with longer warm ischemia times.

257 the first time from organ retrieval, through warm ischemia, transportation on ice, right through to c

258 o kidneys during reperfusion after 1 hour of warm ischemia using a mouse model.

259 owing a lethal 90 minutes of partial in vivo warm ischemia was examined.

260 Partial hepatic warm ischemia was induced in C57Bl/6 wild-type (WT) and

261 Local warm ischemia was induced in groups wild-type (WT) and t

262 A 30-min period of preretrieval warm ischemia was induced.

263 Partial warm ischemia was produced in hepatic lobes for 90 min f

264 METHODS.: Partial warm ischemia was produced in the left and middle hepati

265 er transplantation, livers exposed to 15' of warm ischemia were either modulated (N = 6) with a flush

266 -two porcine kidneys presenting up to 90 min warm ischemia were perfused with oxygenation at 4 degree

267 nutes (DCD70'), and 120 minutes (DCD120') of warm ischemia were studied.

268 liver tissue that has experienced 30 min of warm ischemia when compared with SCS tissues.

269 e (GFR) of kidneys subjected to preretrieval warm ischemia when measured in situ at 2 weeks after tra

270 liver tissue that has experienced 30 min of warm ischemia, when compared with simple cold storage.

271 DCD kidneys have increased caspase-1 due to warm ischemia (WI) and increased caspase-3 and apoptosis

272 ssessment of liver quality premortem, during warm ischemia (WI) and post-NRP.

273 Control of warm ischemia (WI) lesions that occur with donation afte

274 Donor lungs obtained after prolonged warm ischemia (WI) may be unsuitable for transplantation

275 on reperfusion in line with the duration of warm ischemia with a concomitant rise in the vasoconstri

276 subjected to 45, 60, 120, and 150 min liver warm ischemia with or without portosystemic shunt (splen

277 gly increased in the hepatocytes after liver warm ischemia with portosystemic shunt, compared with li

278 circulatory deaths (uDCD), with up to 4-5 h warm ischemia, without advanced cardiopulmonary resuscit

279 t kidneys were exposed to 30 minutes in situ warm ischemia, without application of heparin.