ライフサイエンスコーパス: myocardial dysfunction

1 PL) on plasma lipoproteins may contribute to myocardial dysfunction.

2 nflammation and atherosclerosis in incipient myocardial dysfunction.

3 s and endothelial cells that leads to severe myocardial dysfunction.

4 sordered Na+ and Ca2+ homeostasis leading to myocardial dysfunction.

5 ergic drugs for supporting endotoxin-induced myocardial dysfunction.

6 linked to inflammation and sepsis-associated myocardial dysfunction.

7 OSA) is associated with oxidative stress and myocardial dysfunction.

8 rrhythmias and intensifies postresuscitation myocardial dysfunction.

9 l transition from compensatory remodeling to myocardial dysfunction.

10 ic agent for management of postresuscitation myocardial dysfunction.

11 rate imaging permit recognition of regional myocardial dysfunction.

12 CIH leads to oxidative stress and LV myocardial dysfunction.

13 elaxation is a cardinal feature of senescent myocardial dysfunction.

14 c features, pathogenesis, family history, or myocardial dysfunction.

15 aureus sepsis is associated with significant myocardial dysfunction.

16 iod and may play a role in postresuscitation myocardial dysfunction.

17 increases the severity of postresuscitation myocardial dysfunction.

18 ids with cardiac lipotoxicity and subsequent myocardial dysfunction.

19 athophysiology of cardiovascular disease and myocardial dysfunction.

20 recurrent VF, and lessened postresuscitation myocardial dysfunction.

21 vered and thereby minimize postresuscitation myocardial dysfunction.

22 d increase the severity of postresuscitation myocardial dysfunction.

23 jective, quantitative assessment of regional myocardial dysfunction.

24 failure is thought to exacerbate underlying myocardial dysfunction.

25 -1beta and thereby prevents ischemia-induced myocardial dysfunction.

26 noninsulin-dependent diabetes mellitus, and myocardial dysfunction.

27 d increase the severity of postresuscitation myocardial dysfunction.

28 urate identification and grading of regional myocardial dysfunction.

29 hypertrophy and contributes to postischemic myocardial dysfunction.

30 rdiomyocyte structure and function can cause myocardial dysfunction.

31 se interact to accelerate the progression of myocardial dysfunction.

32 ibition could not reverse, endotoxin-induced myocardial dysfunction.

33 may be useful to treat inflammatory-induced myocardial dysfunction.

34 ificantly less severity of postresuscitation myocardial dysfunction.

35 s rates and (2) persistent post-countershock myocardial dysfunction.

36 ptor densities can potentially contribute to myocardial dysfunction.

37 characterization of various types of altered myocardial dysfunction.

38 e not associated with less postresuscitation myocardial dysfunction.

39 arization of ischemic myocardium accentuates myocardial dysfunction.

40 ression and other conditions of inflammatory myocardial dysfunction.

41 mia and consequently accentuate postischemic myocardial dysfunction.

42 ne MRI for identifying regions of reversible myocardial dysfunction.

43 ha, an autocrine contributor to postischemic myocardial dysfunction.

44 n, or calsequestrin participate in senescent myocardial dysfunction.

45 lity, localized neutrophil accumulation, and myocardial dysfunction.

46 for peroxynitrite in inflammation-associated myocardial dysfunction.

47 iomyopathy and may contribute to progressive myocardial dysfunction.

48 pathways in the heart that may contribute to myocardial dysfunction.

49 d graft-derived vasculature, and ameliorated myocardial dysfunction.

50 s as possible contributors to HIV-associated myocardial dysfunction.

51 etween endothelial dysfunction and intrinsic myocardial dysfunction.

52 esponse to CVB3 infection and contributes to myocardial dysfunction.

53 ent proinflammatory mediator that may induce myocardial dysfunction.

54 DA5 mice were protected against EMCV-induced myocardial dysfunction.

55 cting the heart from direct viral injury and myocardial dysfunction.

56 tibility of certain T2DM patients to develop myocardial dysfunction.

57 ments in functional recovery and ameliorated myocardial dysfunction.

58 imaging surrogates for diffuse fibrosis and myocardial dysfunction.

59 er insights into the primary pathogenesis of myocardial dysfunction.

60 and increased severity of postresuscitation myocardial dysfunction.

61 -grade arteriovenous block in the absence of myocardial dysfunction (2D) if not already tried; 5) in

62 f could, at least in obesity, pose a risk of myocardial dysfunction above and beyond known cardiovasc

63 ns unclear if HSP70 can also protect against myocardial dysfunction after brief ischemia.

64 Previous studies demonstrated myocardial dysfunction after electrical shock and indica

65 Polymicrobial sepsis in mice causes myocardial dysfunction after generation of the complemen

66 n4 reduces adverse myocardial remodeling and myocardial dysfunction after MI.

67 cess of defibrillation and postresuscitation myocardial dysfunction after prolonged ventricular fibri

68 Although myocardial dysfunction after resuscitation from ventricu

69 y, can reliably predict recovery of regional myocardial dysfunction after revascularization in these

70 with oxidative stress and mitochondrial and myocardial dysfunction, although interaction among which

71 g-term AAS use appears to be associated with myocardial dysfunction and accelerated coronary atherosc

72 FAO disorders often present in infancy with myocardial dysfunction and arrhythmias after exposure to

73 a (TNF-alpha) is an autocrine contributor to myocardial dysfunction and cardiomyocyte death in ischem

74 -dependent protein kinase II (CaMKII) favors myocardial dysfunction and cell membrane electrical inst

75 3 overexpression (NOS3TG) are protected from myocardial dysfunction and death associated with endotox

76 increases the severity of postresuscitation myocardial dysfunction and decreases the duration of sur

77 Severe myocardial dysfunction and dysrhythmias may accompany re

78 novel insights into potential mechanisms of myocardial dysfunction and early mortality in obesity.

79 esis of HF, elucidating distinct patterns of myocardial dysfunction and events that are associated wi

80 pressure or volume over-load hypertrophy to myocardial dysfunction and failure.

81 Lethality correlated with severe myocardial dysfunction and fulminant heart failure.

82 AF is uncommon and occurs in the setting of myocardial dysfunction and graft rejection.

83 y recognized phenomenon of postresuscitation myocardial dysfunction and hamper efforts to reestablish

84 sed systemic inflammation has been linked to myocardial dysfunction and heart failure in patients wit

85 ility regions and novel biomarkers linked to myocardial dysfunction and heart failure, we performed t

86 cardiac arrest, mitigated postresuscitation myocardial dysfunction and improved survival.

87 minimized the severity of postresuscitation myocardial dysfunction and increased the duration of pos

88 TNF contributes to postischemic myocardial dysfunction and induces proinflammatory signa

89 nd local inflammatory cytokine production to myocardial dysfunction and injury occurring during ische

90 Sepsis can be complicated by severe myocardial dysfunction and is associated with increased

91 We hypothesized that MIF-induced myocardial dysfunction and mitochondrial respiration def

92 ment sensitivity to Ca(2+), thereby reducing myocardial dysfunction and mortality in murine models of

93 n in the rescue mode, normalized LPS-induced myocardial dysfunction and partially restored abnormal c

94 elate with the severity of postresuscitation myocardial dysfunction and postresuscitation survival.

95 sonance imaging (CMR) can predict reversible myocardial dysfunction and remodeling in heart failure p

96 n patients with more extensive CAD and worse myocardial dysfunction and remodeling.

97 f interleukin 6 strongly predicted degree of myocardial dysfunction and severity of disease in childr

98 id U-74389G would minimize postresuscitation myocardial dysfunction and thereby improve neurologicall

99 g CPR, they may ameliorate postresuscitation myocardial dysfunction and thereby improve postresuscita

100 cations contribute to the pathophysiology of myocardial dysfunction and thus may provide a target for

101 Interstitial fibrosis can lead to myocardial dysfunction and ultimately heart failure.

102 eculation of the left ventricle, progressive myocardial dysfunction, and early mortality.

103 ation, whether patients with AD present with myocardial dysfunction, and if the 2 conditions bear a c

104 ld hypothermia, attenuated postresuscitation myocardial dysfunction, and improved neurologic outcome

105 c resuscitation, minimized postresuscitation myocardial dysfunction, and increased the duration of po

106 characterized the biology of the associated myocardial dysfunction, and tested novel therapeutic str

107 ntial cardiac donors show various degrees of myocardial dysfunction, and the most severely affected h

108 atrol on cecal ligation and puncture-induced myocardial dysfunction are associated with increased per

109 astolic characteristics of postresuscitation myocardial dysfunction are not well defined.

110 ssion of HSP70 protects against postischemic myocardial dysfunction as shown by better preserved myoc

111 r added to vasopressor in the presence of a) myocardial dysfunction as suggested by elevated cardiac

112 urrent ventricular fibrillation or transient myocardial dysfunction as with epinephrine alone.

113 All exhibited severe myocardial dysfunction at extracorporeal membrane oxygen

114 Myocardial NOS3 prevented postcardiac arrest myocardial dysfunction, attenuated end-organ damage, and

115 Strain echocardiography reveals myocardial dysfunction before significant changes in eje

116 ssue Doppler and could detect early regional myocardial dysfunction before the onset of congestive he

117 gnized to cause cardiomyocyte (CM) death and myocardial dysfunction, but the role of cell-matrix inte

118 dden cardiac arrest is limited by postarrest myocardial dysfunction, but understanding of this phenom

119 hypothesized that detailed investigation of myocardial dysfunction by echocardiography can provide i

120 evidence that refutes the notion that acute myocardial dysfunction by high-dose TAT-HKII peptide adm

121 counteracted cecal ligation puncture-induced myocardial dysfunction by improving left ventricular pre

122 ts of repetitive shocks on postresuscitation myocardial dysfunction by using an isolated rat heart mo

123 if the molecular signals responsible for the myocardial dysfunction can be identified and blocked.

124 Reversible myocardial dysfunction can be identified by contrast-enh

125 rst time that impairment of angiogenesis and myocardial dysfunction can be regulated by Ad.Trx1 gene

126 As these patients reach adulthood, myocardial dysfunction can occur, leading to cardiac tra

127 Improved postresuscitation myocardial dysfunction (cardiac index, dP/dt40, -dP/dt)

128 Remarkably, CBD attenuated myocardial dysfunction, cardiac fibrosis, oxidative/nitr

129 rogressively, particularly with the onset of myocardial dysfunction (caspase-3 7.92 +/- 1.19 vs. 1.00

130 energy phosphate metabolism may underlie the myocardial dysfunction caused by hypobaric hypoxia.

131 sudden death (5 of 7 families), progressive myocardial dysfunction causing death or heart transplant

132 t (or myocarditis) is the proximate cause of myocardial dysfunction, causing injury that can range fr

133 treatment for fatal arrhythmia, it produces myocardial dysfunction closely related to the intensity

134 ar voltage mapping can identify irreversible myocardial dysfunction consistent with fibrosis, even in

135 As myocardial dysfunction contributes to poor outcome in cr

136 Myocardial dysfunction contributes to the high mortality

137 as well as support and even reverse existing myocardial dysfunction, deferring the need for heart tra

138 FA pretreatment blunts myocardial dysfunction during ischemia and ameliorates p

139 chemic period may be the main determinant of myocardial dysfunction during reperfusion.

140 c hypertrophy, interstitial fibrosis, severe myocardial dysfunction, 'fetal' gene induction, apoptosi

141 Indeed, postresuscitation myocardial dysfunction has been implicated as a potentia

142 urrent levels to minimize post-resuscitation myocardial dysfunction has been largely unexplored.

143 Postresuscitation myocardial dysfunction has been recognized as a leading

144 Postresuscitation myocardial dysfunction has been recognized as a leading

145 Postresuscitation myocardial dysfunction has more recently emerged as a po

146 Treatment of such postresuscitation myocardial dysfunction has not been examined previously.

147 prolonged primary MR leads to LV remodeling, myocardial dysfunction, heart failure, and death.

148 lood and organ nitrite depletion, reversible myocardial dysfunction, impaired alveolar gas exchange,

149 The post cardiac arrest syndrome subsumes myocardial dysfunction, impaired microcirculation, syste

150 en subclinical atherosclerosis and incipient myocardial dysfunction in a population free of clinical

151 retention was an independent determinant of myocardial dysfunction in cardiac amyloidosis.

152 onsible for the vicious cycle of progressive myocardial dysfunction in chronic heart failure.

153 atients, are postulated to contribute to the myocardial dysfunction in diabetes.

154 Myocardial dysfunction in endotoxemia correlates mainly

155 have been implicated in the pathogenesis of myocardial dysfunction in ischemia-reperfusion injury, s

156 death may have a role in the pathogenesis of myocardial dysfunction in meningococcal septicemia.

157 useful in the identification of subclinical myocardial dysfunction in patients with DM.

158 ortant target for novel therapies to reverse myocardial dysfunction in patients with meningococcal se

159 e responsiveness is associated with advanced myocardial dysfunction in patients with RA.

160 ng of either TNF-alpha or IL-1beta may limit myocardial dysfunction in sepsis.

161 The aim of our study was to explore myocardial dysfunction in severe sepsis.

162 The present study demonstrates myocardial dysfunction in severe sepsis.

163 lower and minimized early postresuscitation myocardial dysfunction in the rectilinear biphasic, dual

164 Postresuscitation myocardial dysfunction in this animal model was characte

165 volved in the mechanism of postresuscitation myocardial dysfunction in this setting.

166 tigate the role of NOS2 in endotoxin-induced myocardial dysfunction in vivo, we studied wild-type and

167 investigated the role of CD14 in LPS-induced myocardial dysfunction in vivo.

168 ced reactive oxygen species accumulation and myocardial dysfunction in wild-type mice.

169 peptido-agonist conferred protection against myocardial dysfunction in wild-type, but not Fpr2/3(-/-)

170 Hyper-aldosteronism is associated with myocardial dysfunction including induction of cardiac fi

171 As our knowledge and understanding of myocardial dysfunction increases, particularly in the ne

172 sion (autoradiography and binding assay) and myocardial dysfunction, indicated by increases in corona

173 ors of myocardial damage, including regional myocardial dysfunction, infarct distribution, infarct si

174 , we explored the role of CB(1) receptors in myocardial dysfunction, inflammation, oxidative/nitrativ

175 stigated the effects of cannabidiol (CBD) on myocardial dysfunction, inflammation, oxidative/nitrativ

176 -induced nitroxidative stress, inflammation, myocardial dysfunction, injury, and adverse remodeling.

177 Myocardial dysfunction is a characteristic component of

178 Myocardial dysfunction is a common and important problem

179 Myocardial dysfunction is a frequent complication in pat

180 Myocardial dysfunction is a major consequence of septic

181 of severe LV pressure overload hypertrophy, myocardial dysfunction is associated with increased micr

182 Complete recovery from myocardial dysfunction is expected after dual coronary r

183 These results indicate that myocardial dysfunction is largely caused by the removal

184 Whether myocardial dysfunction is mediated directly by nitric ox

185 ardial infarction (MI) exacerbates long-term myocardial dysfunction is not known.

186 ata indicate that lipopolysaccharide-induced myocardial dysfunction is not solely caused by elevated

187 Postresuscitation myocardial dysfunction is one of the leading causes of e

188 mental doses of high-dose insulin therapy if myocardial dysfunction is present (2D), IV lipid-emulsio

189 The severity of postresuscitation myocardial dysfunction is related, at least in part, to

190 tion (ECMO) is used in the setting of severe myocardial dysfunction, left ventricular end-diastolic a

191 onversely, rather than being a root cause of myocardial dysfunction, left ventricular noncompaction m

192 rioration, requiring mechanical ventilation; myocardial dysfunction may accompany respiratory decompe

193 Anthracycline-induced cardiotoxicity and myocardial dysfunction may be associated with apoptosis.

194 ion per se, a better understanding of septic myocardial dysfunction may be usefully extended to other

195 for both) and correlated with the degree of myocardial dysfunction measured by strain parameters.

196 Myocardial dysfunction occurred early after return of sp

197 inflammatory mediators either contribute to myocardial dysfunction or are elaborated systemically by

198 uccessful resuscitation achieved, reversible myocardial dysfunction, or "stunning," may occur.

199 /- 1.4, p < .005) and less postresuscitation myocardial dysfunction (p < .05).

200 in adenosine-AR signaling were secondary to myocardial dysfunction rather than to TNF overexpression

201 tion of functional recovery in patients with myocardial dysfunction referred for revascularization.

202 ng disordered cell membrane excitability and myocardial dysfunction remain uncertain.

203 ar mechanisms responsible for sepsis-induced myocardial dysfunction remain undefined.

204 ide (NO) in lipopolysaccharide (LPS)-induced myocardial dysfunction remains controversial as some inv

205 e contributes to both systolic and diastolic myocardial dysfunction, respectively.

206 Estrogen protects against endothelial and myocardial dysfunction resulting from brief ischemia/rep

207 In the face of pre-existing myocardial dysfunction resulting from preoperative press

208 f subclinical left ventricular (LV) regional myocardial dysfunction (RMD) measured by magnetic resona

209 establishing energy depletion as a cause of myocardial dysfunction, should be relevant to the acquir

210 Despite the absence of myocardial dysfunction, steady-state NCX1 transcript and

211 al defibrillation had less postresuscitation myocardial dysfunction than rectilinear biphasic and dua

212 s a complex clinical syndrome resulting from myocardial dysfunction that impairs the cardiovascular s

213 ve important implications for explaining the myocardial dysfunction that is associated with increased

214 ovides evidence of dyssynchrony and regional myocardial dysfunction that occurs early with compensato

215 trast, banded animals treated with T4 had no myocardial dysfunction; these hearts had increased contr

216 R-92a in mice attenuated the infarct-related myocardial dysfunction to a larger extent than cardiomyo

217 s in understanding of the molecular basis of myocardial dysfunction, together with the development of

218 nces in understanding the molecular basis of myocardial dysfunction, together with the evolution of i

219 s in understanding of the molecular basis of myocardial dysfunction, together with the evolution of i

220 s in understanding of the molecular basis of myocardial dysfunction, together with the evolution of i

221 in the myocardium and serum from donors with myocardial dysfunction (unused donors) and compared them

222 eveloped rodent models of in vivo postarrest myocardial dysfunction using extracorporeal membrane oxy

223 ative settings: agents for the management of myocardial dysfunction, vasomotor dysfunction, pulmonary

224 Endotoxin-induced myocardial dysfunction was associated with increased ven

225 rated that the severity of postresuscitation myocardial dysfunction was closely related to the magnit

226 Regional myocardial dysfunction was defined as the presence of im

227 perimental observation that the magnitude of myocardial dysfunction was in part related to the energy

228 tion left ventricular systolic and diastolic myocardial dysfunction was reversible after 72 hrs in th

229 To investigate determinants of incipient myocardial dysfunction, we examined the association betw

230 ne levels in 13 patients with stress-related myocardial dysfunction were compared with those in 7 pat

231 Maximum survival and minimum myocardial dysfunction were observed with the low-capaci

232 scitation, and severity of postresuscitation myocardial dysfunction were observed.

233 b may attenuate or prevent postresuscitation myocardial dysfunction when administered immediately aft

234 inotropic drug for supporting sepsis-induced myocardial dysfunction when cardiac output index remains

235 involves a downward spiral: Ischemia causes myocardial dysfunction, which, in turn, worsens ischemia

236 dyssynchrony may mediate the association of myocardial dysfunction with age and LV hypertrophy.

237 SC) is a syndrome characterized by transient myocardial dysfunction with unknown etiology.

238 zebrafish (Danio rerio) embryos resulted in myocardial dysfunctions with disintegration of the sarco

239 Brief ischemic periods lead to myocardial dysfunction without myocardial infarction.