ライフサイエンスコーパス: postresuscitation

1 , IL-6, and IL-10 were measured at 1.5 hours postresuscitation.

2 n with partial return to baseline by 30 mins postresuscitation.

3 output were measured at intervals for 60 min postresuscitation.

4 lating plasma may contribute to organ damage postresuscitation.

5 er limit of cerebral autoregulation at 6 hrs postresuscitation.

6 unction returned to baseline level at 72 hrs postresuscitation.

7 We demonstrate that the postresuscitation administration of cyclosporine attenua

8 Postresuscitation administration of cyclosporine causes

9 Postresuscitation administration of doxycycline attenuat

10 Blood samples were collected 4 hrs postresuscitation and assayed for levels of liver enzyme

11 n preceding intensive care unit arrival, and postresuscitation arterial blood gas obtained.

12 Postresuscitation arterial pressure and left ventricular

13 systolic and diastolic function (prearrest, postresuscitation at 30 mins and 6 hrs) and 24-hr surviv

14 icated previously reported resuscitation and postresuscitation benefits.

15 ha2-vasopressor effect, resulted in improved postresuscitation cardiac and neurological recovery.

16 ha with infliximab would prevent or minimize postresuscitation cardiac dysfunction.

17 Postresuscitation cardiac index, left ventricular end-di

18 Postresuscitation cardiac output, ejection fraction, and

19 At 1.5 hrs postresuscitation, cardiac output and blood flow were de

20 ble to improvement in acute resuscitation or postresuscitation care and examined trends in neurologic

21 roved survival during acute resuscitation or postresuscitation care and whether they occurred at the

22 pproach of maintaining otherwise recommended postresuscitation care during interfacility transfer is

23 irst defibrillation attempt and standardized postresuscitation care for 24 hours.

24 ical System; and a recently added aggressive postresuscitation care for resuscitated but comatose pat

25 eview findings from recent literature on the postresuscitation care of cardiac arrest patients using

26 Despite several advances in postresuscitation care over the past decade, population-

27 o make important and nuanced decisions about postresuscitation care that may determine the efficacy o

28 It is not known if aggressive postresuscitation care, including therapeutic hypothermi

29 ry resuscitation, emerging field treatments, postresuscitation care, prognostication tools, and trend

30 the mechanistic target; and heterogeneity in postresuscitation care, prognostication, and withdrawal

31 m are addressed, from preparation through to postresuscitation care.

32 spite the costs associated with high-quality postresuscitation care.

33 rly high risk and require a renewed focus on postresuscitation care.

34 ntrol resuscitation and limited capacity for postresuscitation care.

35 For postresuscitation comatose patients, early quantitative

36 duced hepatic hypoperfusion at 3 and 4 hours postresuscitation compared with HS/CR alone.

37 Postresuscitation contractile and left ventricular diast

38 CPR, they may have favorable effects on the postresuscitation course.

39 8 animals were successfully resuscitated and postresuscitation data obtained.

40 ameliorated ischemic contracture, prevented postresuscitation diastolic dysfunction, and favored ear

41 it of the dobutamine infusion for overcoming postresuscitation diastolic dysfunction.

42 ngiography (ICA) irrespective of their first postresuscitation ECG and to determine whether this ECG

43 ere retrospectively grouped according to the postresuscitation ECG blinded for ICA results: (1) ST el

44 /pVT OHCA with ST-segment elevation on their postresuscitation ECG, the prevalence of coronary artery

45 T OHCA without ST-segment elevation on their postresuscitation ECG, the prevalence of coronary artery

46 nary angiograms were reevaluated blinded for postresuscitation ECGs.

47 ive defibrillation attempts had more intense postresuscitation ectopic activity and worse survival.

48 al-path sequential defibrillation had higher postresuscitation ejection fraction than rectilinear bip

49 rest (OHCA) with ST-segment elevation on the postresuscitation electrocardiogram (ECG), this strategy

50 However, prehospital factors such as postresuscitation electrocardiogram pattern or clinical

51 igin but without ST-segment elevation on the postresuscitation electrocardiogram were eligible for in

52 ed after initial cardiac arrest, with normal postresuscitation electrocardiogram, sufficient hemodyna

53 s had no evidence of ST-segment elevation on postresuscitation electrocardiography.

54 ors that enabled determination of mortality: postresuscitation Glasgow coma scale (P-GCS) (adjusted o

55 One hundred forty-seven patients with a postresuscitation Glasgow Coma Scale score of < or = 12

56 th nonpenetrating traumatic brain injury and postresuscitation Glasgow Coma Scale score of 4-12 were

57 of patients were matched with regard to age, postresuscitation Glasgow Coma Scale scores, rates of ac

58 Postresuscitation hemodynamic and myocardial function qu

59 This association appears to be driven by postresuscitation hemodynamic dysfunction and oxygenatio

60 With comparable VF duration, postresuscitation hemodynamic dysfunction was ameliorate

61 rmful, and laboratory studies suggest that a postresuscitation hypertensive surge may be protective,

62 retrospective clinical studies suggest that postresuscitation hypotension may be harmful, and labora

63 us circulation were considered to have early postresuscitation hypotension.

64 wo hundred fourteen patients (56%) had early postresuscitation hypotension.

65 ive electroencephalography of 6-hr immediate postresuscitation hypothermia (at 33 degrees C), normoth

66 The preserved heart rate variability during postresuscitation hypothermia was associated with favora

67 toregulation after cardiac arrest and during postresuscitation hypothermia.

68 ave antiapoptotic properties and to decrease postresuscitation inflammation in rodent and porcine mod

69 The evidence for postresuscitation injury at the cellular level and its m

70 derstanding of how preconditioning may alter postresuscitation injury is important for two major reas

71 This postresuscitation injury may result in as many as 90% of

72 erfusion can significantly affect myocardial postresuscitation injury, in part by modifying mitochond

73 pressure (MAP) of 63 versus 77 mm Hg during postresuscitation intensive care.

74 e, however, remained elevated throughout the postresuscitation interval.

75 ently during the resuscitation effort or the postresuscitation interval.

76 Addition of postresuscitation lactate concentration to KCH criteria

77 Combined early and postresuscitation lactate concentrations had similar pre

78 t experimental study was designed to compare postresuscitation left ventricular (LV) function after c

79 We therefore investigated the postresuscitation left ventricular diastolic function fo

80 Animals receiving vasopressin had more postresuscitation left ventricular dysfunction than thos

81 est was increased to 8 mins, the severity of postresuscitation left ventricular dysfunction was magni

82 , an independent role for ionized calcium in postresuscitation left ventricular dysfunction was not d

83 ardiac arrest, play a role in development of postresuscitation left ventricular dysfunction.

84 Improvements in postresuscitation left ventricular ejection fraction and

85 rdiopulmonary resuscitation results in worse postresuscitation left ventricular function early but di

86 Postresuscitation left ventricular function was signific

87 ist produced vasodilation and improved early postresuscitation left ventricular systolic and diastoli

88 However, this postresuscitation left ventricular systolic and diastoli

89 sought to test the hypothesis that elevated postresuscitation mean arterial blood pressure is associ

90 Postresuscitation measurements, including cardiac output

91 toration of spontaneous circulation improved postresuscitation microcirculation, myocardial and cereb

92 However, postresuscitation microvascular flows and Pbo2 were grea

93 n reperfusion injury that leads to increased postresuscitation mortality and delayed neuronal death.

94 Most importantly, the postresuscitation mortality was dramatically higher in t

95 pontaneous circulation to reduce the risk of postresuscitation multiple organ injury.

96 ecurrent ventricular fibrillation and better postresuscitation myocardial and neurological function w

97 kade would improve initial resuscitation and postresuscitation myocardial and neurological functions.

98 Improved postresuscitation myocardial dysfunction (cardiac index,

99 al waveform (2.6 +/- 1.4, p < .005) and less postresuscitation myocardial dysfunction (p < .05).

100 veforms on the success of defibrillation and postresuscitation myocardial dysfunction after prolonged

101 ion, significantly increases the severity of postresuscitation myocardial dysfunction and decreases t

102 ute to the recently recognized phenomenon of postresuscitation myocardial dysfunction and hamper effo

103 dministered during cardiac arrest, mitigated postresuscitation myocardial dysfunction and improved su

104 a-opioid receptors minimized the severity of postresuscitation myocardial dysfunction and increased t

105 an important correlate with the severity of postresuscitation myocardial dysfunction and postresusci

106 ed that the lazaroid U-74389G would minimize postresuscitation myocardial dysfunction and thereby imp

107 administered during CPR, they may ameliorate postresuscitation myocardial dysfunction and thereby imp

108 However, the diastolic characteristics of postresuscitation myocardial dysfunction are not well de

109 stigated the effects of repetitive shocks on postresuscitation myocardial dysfunction by using an iso

110 Indeed, postresuscitation myocardial dysfunction has been implic

111 Postresuscitation myocardial dysfunction has been recogn

112 Postresuscitation myocardial dysfunction has been recogn

113 Postresuscitation myocardial dysfunction has more recent

114 Treatment of such postresuscitation myocardial dysfunction has not been ex

115 were significantly lower and minimized early postresuscitation myocardial dysfunction in the rectilin

116 Postresuscitation myocardial dysfunction in this animal

117 optosis was not involved in the mechanism of postresuscitation myocardial dysfunction in this setting

118 Postresuscitation myocardial dysfunction is one of the l

119 The severity of postresuscitation myocardial dysfunction is related, at

120 Dual-path sequential defibrillation had less postresuscitation myocardial dysfunction than rectilinea

121 e recently demonstrated that the severity of postresuscitation myocardial dysfunction was closely rel

122 rdiopulmonary resuscitation, and severity of postresuscitation myocardial dysfunction were observed.

123 rest and infliximab may attenuate or prevent postresuscitation myocardial dysfunction when administer

124 peptide induced mild hypothermia, attenuated postresuscitation myocardial dysfunction, and improved n

125 ved initial cardiac resuscitation, minimized postresuscitation myocardial dysfunction, and increased

126 sens reperfusion arrhythmias and intensifies postresuscitation myocardial dysfunction.

127 mine as an inotropic agent for management of postresuscitation myocardial dysfunction.

128 tresuscitation period and may play a role in postresuscitation myocardial dysfunction.

129 rine significantly increases the severity of postresuscitation myocardial dysfunction.

130 tivity preventing recurrent VF, and lessened postresuscitation myocardial dysfunction.

131 total energy delivered and thereby minimize postresuscitation myocardial dysfunction.

132 outcome of CPR and increase the severity of postresuscitation myocardial dysfunction.

133 ardial ischemia and increase the severity of postresuscitation myocardial dysfunction.

134 sociated with significantly less severity of postresuscitation myocardial dysfunction.

135 -energy shocks were not associated with less postresuscitation myocardial dysfunction.

136 mpromised outcomes and increased severity of postresuscitation myocardial dysfunction.

137 ms on the success of initial defibrillation, postresuscitation myocardial function and duration of su

138 Significantly better postresuscitation myocardial function and longer duratio

139 ft ventricular dysfunction was magnified and postresuscitation myocardial function and survival were

140 resuscitation but provided strikingly better postresuscitation myocardial function and survival.

141 ing CPR are evaluated as to their effects on postresuscitation myocardial function and survival.

142 ging from 3.7 to 25 kg without compromise of postresuscitation myocardial function or survival.

143 Postresuscitation myocardial function was measured by ec

144 Significantly better postresuscitation myocardial function was observed after

145 normothermic cardiopulmonary resuscitation, postresuscitation myocardial function was severely impai

146 However, postresuscitation myocardial function was significantly

147 sulted in significantly lesser impairment of postresuscitation myocardial function when compared with

148 ve cariporide could improve resuscitability, postresuscitation myocardial function, and short-term su

149 Postresuscitation myocardial function, as measured by th

150 In a rat model of cardiac arrest, better postresuscitation myocardial function, neurological defi

151 Postresuscitation myocardial function, neurological defi

152 Levosimendan has the potential of improving postresuscitation myocardial function.

153 secondary ischemic event and provided better postresuscitation myocardial function.

154 reduction in blood temperature and improved postresuscitation myocardial functions and survival afte

155 energy electrical shocks that contribute to postresuscitation myocardial injury.

156 ck algorithm did not have adverse effects on postresuscitation myocardial or neurologic function.

157 The postresuscitation myocardial protective effects provided

158 Full recovery of this postresuscitation myocardial stunning is seen by 48 h in

159 rhythmias, less ST-segment elevation, better postresuscitation neurologic deficit scores, and longer

160 Postresuscitation neurological function was also improve

161 ons resulted in significantly better 24-hour postresuscitation neurologically normal survival than di

162 ongly negatively correlated with 1- and 4-hr postresuscitation neuron-specific enolase (r = -.86, p <

163 were evaluated every 24 hrs during the 96-hr postresuscitation observation period.

164 ation of ET-1 during CPR can result in worse postresuscitation outcome.

165 s were used to assess whether differences in postresuscitation outcomes were modified by baseline pro

166 t patterns of association between gender and postresuscitation outcomes were observed in the secondar

167 cardiac arrest caused by pulmonary embolism, postresuscitation oxygenation and ventilation, prophylac

168 he temperature groups within the first 2 hrs postresuscitation (p < .01).

169 The median postresuscitation PaO(2) was 231 (interquartile range 14

170 In this large sample of postresuscitation patients, we found a dose-dependent as

171 en supranormal oxygen tension and outcome in postresuscitation patients.

172 Four hours postresuscitation, pediatric dosing resulted in fewer el

173 er 8 mins of cardiac arrest during the early postresuscitation period (3 hrs).

174 mins of cardiac arrest and during the early postresuscitation period (60-90 mins).

175 olic pressure increased significantly in the postresuscitation period (p < 0.05).

176 osis factor-alpha increases during the early postresuscitation period and may play a role in postresu

177 measured blood pressure over time during the postresuscitation period and tested its association with

178 effect with a specific V-1 antagonist in the postresuscitation period did not improve survival.

179 However, cooling during the postresuscitation period was slow, requiring 4 to 8 hour

180 During the immediate postresuscitation period, four of eight pigs in the epin

181 a vasopressin antagonist administered in the postresuscitation period.

182 uring CPR but had detrimental effects in the postresuscitation period.

183 fferences were sustained throughout the 3-hr postresuscitation period.

184 during both the immediate resuscitation and postresuscitation periods.

185 ng out-of-hospital cardiac arrest, the early postresuscitation phase is characterized by abnormalitie

186 oxidases-likely play important roles in the postresuscitation phase of cardiac arrest, and their mod

187 orm standard pupillary light reflex in early postresuscitation phase.

188 e diminishment of essential phospholipids in postresuscitation plasma and develop a novel therapeutic

189 IQ values of >0.523 at 60 mins postresuscitation predicted good neurologic outcome (72-

190 ables, pre-event factors, cardiac arrest and postresuscitation processes, and outcomes.

191 ecognition, patient variables, resuscitation/postresuscitation processes, and outcomes.

192 rophylactic antibiotics after resuscitation, postresuscitation seizure prophylaxis and treatment, and

193 in-hospital cardiac arrest patients and for postresuscitation shock did improve neurologic outcomes,

194 Patients in the VSE group with postresuscitation shock vs corresponding patients in the

195 during CPR and stress-dose hydrocortisone in postresuscitation shock, compared with epinephrine/salin

196 epinephrine followed by corticosteroids for postresuscitation shock.

197 rval of untreated VF, cariporide ameliorated postresuscitation shortening of the action potential dur

198 to cardiopulmonary resuscitation determined postresuscitation success rates, degree of neurologic in

199 unadjusted RR, 0.84 [95% CI, 0.81-0.88]) and postresuscitation survival (45.2% vs 55.5% for whites; u

200 01) and eliminated the racial differences in postresuscitation survival (adjusted RR, 0.99 [95% CI, 0

201 in association with significant increases in postresuscitation survival rate.

202 The duration of postresuscitation survival was significantly increased i

203 he hypothesis that initial resuscitation and postresuscitation survival would be improved.

204 e explained by acute resuscitation survival, postresuscitation survival, and/or greater temporal impr

205 neficial effects were associated with better postresuscitation survival.

206 l dysfunction, and increased the duration of postresuscitation survival.

207 tcomes were acute resuscitation survival and postresuscitation survival.

208 his was associated with significantly better postresuscitation survival.

209 postresuscitation myocardial dysfunction and postresuscitation survival.

210 n myocardial dysfunction and thereby improve postresuscitation survival.

211 ent in both acute resuscitation survival and postresuscitation survival.

212 ted with significantly increased duration of postresuscitation survival.

213 al dysfunction and increased the duration of postresuscitation survival.

214 Recipients were queried regarding use of postresuscitation therapeutic hypothermia.

215 However, significantly better postresuscitation tissue microcirculation, myocardial ej

216 At 1.5 hours postresuscitation, vascular responses to AM and AMBP-1,

217 This was associated with significantly fewer postresuscitation ventricular arrhythmias, less ST-segme

218 +/-29 versus 226+/-16 ms, P<0.05), minimized postresuscitation ventricular ectopic activity preventin

219 on but did not have a lasting effect on such postresuscitation ventricular function and decreased 24-

220 en content in hemorrhaged animals at 1.5 hrs postresuscitation were >50% lower as compared with sham-

221 Postresuscitation, zoniporide-treated pigs had higher le