ライフサイエンスコーパス: rewarming

1 r 72 hours, followed by spontaneous, natural rewarming.

2 yocardial infarction) followed by controlled rewarming.

3 auses Ca(2+) loading and reduced function on rewarming.

4 ere unsuitable candidates for OLT died after rewarming.

5 icrotubule network was observed after 60 min rewarming.

6 l conditions, during cortical cooling and on rewarming.

7 n = 94) followed by cardioplegic arrest and rewarming.

8 ct the brain through improved cooling and/or rewarming.

9 followed by a slight ( approximately 2-3 K) rewarming.

10 plegic arrest and subsequent reperfusion and rewarming.

11 ollowed by simulated cardioplegic arrest and rewarming.

12 dioprotection during cardioplegic arrest and rewarming.

13 rdial function after cardioplegic arrest and rewarming.

14 ion during simulated cardioplegic arrest and rewarming.

15 bjected to simulated cardioplegic arrest and rewarming.

16 ring 24 hours therapeutic hypothermia, until rewarming.

17 were obtained during cooling and again after rewarming.

18 very of normothermic homeostasis ensues upon rewarming.

19 mia, followed by a secondary increase during rewarming.

20 hypothermia and remained at this level after rewarming.

21 atures in a pig model of surface cooling and rewarming.

22 values of interleukin-10 were observed after rewarming.

23 urs followed by 12 to 24 hours of controlled rewarming.

24 in nonsurvivors (n=6) at admission and after rewarming.

25 lapse; and SEPs during hypothermia and after rewarming.

26 ents during mild therapeutic hypothermia and rewarming.

27 ests at room temperature, after cooling, and rewarming.

28 n, thereby normalizing drug metabolism after rewarming.

29 pact of hypothermia on drug metabolism after rewarming.

30 which contributes causally to the injury at rewarming.

31 ortening the time to achieve hypothermia and rewarming.

32 meters were restored to precooling levels on rewarming.

33 hese temperature conditions for 6 hrs before rewarming.

34 ter followed by release of the occluders and rewarming.

35 maintained for 24 hours followed by passive rewarming.

36 measured at the end of both hypothermia and rewarming (1 and 2 hrs after traumatic brain injury).

37 jury for 4 hours, 33 degrees C) with gradual rewarming (1 degrees C per hour) for the preservation of

38 posttraumatic hypothermia followed by rapid rewarming (15 mins) failed to decrease contusion volume,

39 re continued in both groups until the end of rewarming (2 hrs after traumatic brain injury).

40 = 8) were tested at 25 degrees C and during rewarming (30-34 degrees C).

41 In contrast to cold storage alone, rewarming (37 degrees C for 24 hr) of cold stored cells,

42 es), DHCA (120 minutes at 18 degrees C), and rewarming (40 minutes).

43 : 48 hr cold: 2+/-0.6%, 48 hr cold and 24 hr rewarming: 54+/-17%), which was confirmed by the TEM bas

44 of synaptic contacts, which are reformed on rewarming, a form of structural plasticity.

45 jugular venous desaturation can occur during rewarming after cardiopulmonary bypass surgery.

46 l application suggests that controlled graft rewarming after cold storage is a feasible and safe meth

47 The recovery of cytoplasmic Ca2+ during rewarming after rapid cooling in lactate was slower than

48 ange during mild therapeutic hypothermia and rewarming, although low values of interleukin-10 were ob

49 Specimens were harvested following rewarming and 2 hours of recovery.

50 Hands were imaged to monitor rewarming and reperfusion.

51 demographics were collected during cooling, rewarming, and posttreatment periods (8 d).

52 onary bypass, decreased significantly during rewarming, and remained depressed 6 hrs after cardiopulm

53 appropriate inotropic support, attention to rewarming, and ventilator management are key components.

54 25 degrees C, but returned to control during rewarming at 34-35 degrees C.

55 2-33 degrees C for 72 hours followed by slow rewarming at a rate compatible with maintaining intracra

56 After rewarming at approximately 12 degrees C/min and removal

57 dered and a minimum observation period after rewarming before brain death testing ensues should be es

58 creased permeability in the first hour after rewarming but had significantly increased permeability a

59 Myocyte contractility was measured after rewarming by videomicroscopy.

60 During rewarming, cardiovascular effects of dopamine at moderat

61 Cardioplegic arrest and rewarming caused a decline in steady-state myocyte short

62 Hyperkalemic cardioplegia and rewarming caused a significant reduction in myocyte velo

63 Rewarming caused retraction of pseudopods on taxol-treat

64 ming protocol using continuous arteriovenous rewarming (CAVR) or to a standard rewarming (SR) control

65 es during cardiopulmonary bypass just before rewarming commenced (hypotensive, hypothermic), after re

66 ng was reduced after cardioplegic arrest and rewarming compared with normothermic control (37 +/- 3 v

67 machine-assisted slow controlled oxygenated rewarming (COR) for 90 minutes before engrafting.

68 ance) for capillary morphologic features and rewarming curve characteristics.

69 kin temperature, and for the areas under the rewarming curves (0.684).

70 atures were measured and baseline images and rewarming curves were analyzed.

71 Area measurements and rewarming distinguished true temperature sensitivity fro

72 Hypothermia for 48 h with slow rewarming does not reduce mortality of improve global fu

73 We examined brain cooling and rewarming during pH-stat and alpha-stat cardiopulmonary

74 age due to prolonged cold ischemia times and rewarming during the long benching procedure.

75 Rewarming eliminated open canalicular system dilation an

76 g hypothermia (FPR 3; 95% CI, 1-7) and after rewarming (FPR 0; 95% CI, 0-18) were reliable predictors

77 Complement activation occurs during rewarming from mild therapeutic hypothermia after cardia

78 commenced (hypotensive, hypothermic), after rewarming (hypotensive, normothermic) just before discon

79 3.5 degrees C for 72 hours, followed by slow rewarming (hypothermia group).

80 (3) preconditioning/cardioplegic arrest and rewarming, hypoxia (20 minutes) and reoxygenation (20 mi

81 herapeutic hypothermia for 48-72 h with slow rewarming improved mortality in children after brain inj

82 cultures followed by cardioplegic arrest and rewarming improved myocyte function compared with cardio

83 ive temperature 36.0 degrees C, using active rewarming in 92% and 1-hour presurgical antibiotic admin

84 inuous venovenous hemofiltration circuit for rewarming in a juvenile goat model after induction of mo

85 rain histology were evaluated 60 hours after rewarming in all dogs.

86 y blood flow was similar and unchanged after rewarming in the three experimental groups.

87 hours; (2) simulated cardioplegic arrest and rewarming, incubated in crystalloid cardioplegic solutio

88 ion of 2-MAC and DFO significantly inhibited rewarming-induced apoptotic cell death (plus 2-MAC: 3+/-

89 ers protection against both cold storage and rewarming-induced necrosis and apoptosis.

90 However, rewarming is associated with significant apoptosis in th

91 The optimal rate of rewarming is unknown.

92 At most sites examined in PPCr, rewarming M1 resulted in a reestablishment of the baseli

93 sodes is unknown, but one suggestion is that rewarming may be related to replacement of gene products

94 uced by short-term hypothermic perfusion and rewarming, may protect hearts against ischaemic/reperfus

95 Optimal duration of, and rewarming methods from, resuscitative hypothermia need c

96 The present study has used the chilling-rewarming model, together with microtubule stabilizing (

97 rees C x 2 hours followed by reperfusion and rewarming (n = 62); and (3) PCO/cardioplegia: 5 minutes

98 ees C x 2 hours) followed by reperfusion and rewarming (n = 8); and (2) PCO/cardioplegia: institution

99 ) or 24 hours (n = 179), followed by gradual rewarming of 0.5 degrees C per hour until reaching 37 de

100 restoration after submaximal stimulation or rewarming of chilled platelets.

101 ep hypothermic circulatory arrest (DHCA) and rewarming on CPB.

102 effects during cooling and the effects after rewarming on drug metabolism and response.

103 cooling to 32-33 degrees C followed by slow rewarming or controlled normothermia.

104 ular cells whether apoptosis is specific for rewarming or it also occurs during cold storage and whet

105 ing different periods of cold ischemia (CI), rewarming, or reperfusion, and (ii) effects of inhibitio

106 ": during induction, maintenance of cooling, rewarming, or within 15 hrs after normothermia in 57% (2

107 mic) rats at the end of both hypothermia and rewarming (p <.05), demonstrating that hypothermia reduc

108 ersity of Wisconsin solution after four-hour rewarming (P<0.05).

109 Activity also increased within 30 min of rewarming, peaking at 120 min.

110 sion volume, those animals undergoing a slow rewarming period (120 mins) demonstrated significantly (

111 al membrane was inhibited during the initial rewarming period after cold exposure.

112 ary hypoxia and stress the importance of the rewarming period in this therapeutic intervention.

113 In addition, the importance of the rewarming period on histopathologic outcome was investig

114 During the rewarming period, however, reductions in SjvO2 to < 50%

115 01) and with lower average rSO(2) during the rewarming phase (72+/-12% versus 83+/-9%, P=.003) and du

116 mpared with group C and group HTS during the rewarming phase (P < .05).

117 netics of dopamine are maintained during the rewarming phase at moderate hypothermia.

118 seven received initiation of LLV during the rewarming phase of CPB (treatment).

119 The rewarming phase was passive.

120 xclusively fuels deep torpor and most of the rewarming process.

121 y artery catheter were randomized to a rapid rewarming protocol using continuous arteriovenous rewarm

122 et temperature, duration of hypothermia, and rewarming protocols were extracted.

123 studies are needed to determine the optimal rewarming rate and strategy.

124 solution was used during the paired RCCs and rewarming, RCC2/RCC1 x 100 was increased to 96 and 95% i

125 During rewarming, regional brain temperatures and neocortical t

126 econditioning during cardioplegic arrest and rewarming remain unclear.

127 Although active rewarming remains an accepted and valid process measure,

128 Passive rewarming resulted in a temperature of 37.8 +/- 0.5 degr

129 Rewarming resulted in restoration of disc shape, pseudop

130 Increased durations of CI preceding rewarming resulted in significantly higher activity (P <

131 pothermia during torpor followed by periodic rewarming (REW) during interbout arousal (IBA), proapopt

132 iod of cardioplegia-ischemia was followed by rewarming, separation from CPB, and 2 hours of post-CPB

133 After rewarming, significant cytoprotection was also observed

134 eriovenous rewarming (CAVR) or to a standard rewarming (SR) control group.

135 ing induced hypothermia (T1), directly after rewarming (T2), and another 24 hrs later (T3).

136 , and five were assigned to the experimental rewarming technique of a modified continuous venovenous

137 Rewarming the cells caused even greater bleb formation a

138 ation toward baseline although at the end of rewarming the metabolic recovery was complete in both gr

139 Rewarming the protoplasts to 29 degrees C reestablished

140 3.5 degrees C for 72 hours, followed by slow rewarming (the hypothermia group).

141 During the first 10 minutes of rewarming, the cerebral microvascular diameter was signi

142 Upon rewarming, the jugular bulb oxygenation remained constan

143 Upon rewarming, the mean flow velocity in the middle cerebral

144 ime was 223.8 and 175.7 min (P=0.07) and the rewarming time was 60.3 and 30.3 min (P=0.03) in the LKT

145 Mean console, warm ischemia, and rewarming times were 130.8 minutes, 2.3 minutes and 42.9

146 bules (MTs) by cold treatment and subsequent rewarming to 29 degrees C.

147 After rewarming to 36.5 degrees C, neurologic examination show

148 ere hypothermia at T(b)= 25 degrees C and on rewarming to 37 degrees C.

149 l cooling, the importance of slow controlled rewarming to avoid rebound brain edema, and the high ris

150 hypothermia for 24 hours followed by passive rewarming to normothermia.

151 Rewarming took a median of 21.5 hours (16-35 hr) and was

152 r 45 mins of reperfusion after which passive rewarming was allowed.

153 A significant increase after rewarming was demonstrated on high-mobility group box-1

154 SjvO2 during rewarming was dependent on mean arterial pressure, with

155 oup (p=0.051) to a median of 2.2 mg/L during rewarming was observed and was not explained by dosing d

156 When the rewarming was performed either in Na(+)- and Ca(2+)-free

157 The whole body lactate during early rewarming was significantly less with the pH stat strate

158 ere <20%, a repeat short exercise test after rewarming was useful in patients with myotonia congenita

159 ctile processes with cardioplegic arrest and rewarming were examined in a final series of experiments

160 ehydrogenase [LDH] release) before and after rewarming were studied.

161 the cytoplasm after hypothermia followed by rewarming, whereas Na-K-ATPase retained its basolateral

162 urs increased endothelial permeability after rewarming, which appears to depend on the duration of co

163 the survivors were directly extubated after rewarming while two were once more sedated due to pneumo

164 latory arrest at 15 degrees C, and 40-minute rewarming with alpha-stat (group alpha) or pH-stat (grou

165 How to achieve optimized hypothermia and rewarming without delayed brain herniation remains a cha