ライフサイエンスコーパス: contractile dysfunction

1 ide riboside reduced cardiomyocyte death and contractile dysfunction.

2 c maladaptation precedes the onset of severe contractile dysfunction.

3 entilation promote diaphragmatic atrophy and contractile dysfunction.

4 ventilator-induced diaphragmatic atrophy and contractile dysfunction.

5 entilation-induced diaphragmatic atrophy and contractile dysfunction.

6 h mechanical ventilation-induced atrophy and contractile dysfunction.

7 c weakness attributable to fiber atrophy and contractile dysfunction.

8 cal ventilation-induced myofiber atrophy and contractile dysfunction.

9 ess resulting from both myofiber atrophy and contractile dysfunction.

10 lation can promote diaphragmatic atrophy and contractile dysfunction.

11 ve cardiomyocyte and cardiac hypertrophy and contractile dysfunction.

12 cyte hypertrophy, interstitial fibrosis, and contractile dysfunction.

13 y transitioned to ventricular dilatation and contractile dysfunction.

14 lation is also associated with diaphragmatic contractile dysfunction.

15 rsing maladaptive hypertrophy, fibrosis, and contractile dysfunction.

16 and substrate utilization may contribute to contractile dysfunction.

17 cerol (TAG) metabolism in the development of contractile dysfunction.

18 xibility and render the heart susceptible to contractile dysfunction.

19 of p38 mitogen-activated protein kinase, and contractile dysfunction.

20 Its overexpression results in contractile dysfunction.

21 and calsequestrin but resulted in no obvious contractile dysfunction.

22 t (CA) and reperfusion and may contribute to contractile dysfunction.

23 otilin mutations promote aggregate-dependent contractile dysfunction.

24 atinib-treated mice develop left ventricular contractile dysfunction.

25 ipitates into cardiac insulin resistance and contractile dysfunction.

26 endotoxin-induced cardiac mitochondrial and contractile dysfunction.

27 ac activity, ischemic myocardial damage, and contractile dysfunction.

28 the change in its expression contributes to contractile dysfunction.

29 reatic beta-cell dysfunction, and myocardial contractile dysfunction.

30 loading of Na+/Ca2+, and produced myocardial contractile dysfunction.

31 de (BNP) are sensitive biomarkers of cardiac contractile dysfunction.

32 in gene expression that are associated with contractile dysfunction.

33 mice were protected against S aureus-induced contractile dysfunction.

34 des within cardiomyocytes is associated with contractile dysfunction.

35 ust induction of the fetal gene program, and contractile dysfunction.

36 lation-induced diaphragmatic proteolysis and contractile dysfunction.

37 omplex phenomenon not simply attributable to contractile dysfunction.

38 lum calcium pump (SERCA), contribute to this contractile dysfunction.

39 egy protecting the heart from arrhythmia and contractile dysfunction.

40 dative stress and subsequent proteolysis and contractile dysfunction.

41 tial to limit the extent of resultant MI and contractile dysfunction.

42 but appear unlikely to contribute to chronic contractile dysfunction.

43 uced injury together with the development of contractile dysfunction.

44 ne cell infiltration, myocardial injury, and contractile dysfunction.

45 oved ischemia/reperfusion-induced myocardial contractile dysfunction.

46 was first ascribed to papillary muscle (PM) contractile dysfunction.

47 resulted in a reduction of ischemia-induced contractile dysfunction.

48 tic impairment during AF could contribute to contractile dysfunction.

49 dimer formation and attenuated H2O2-induced contractile dysfunction.

50 ne model of hypovascular nonnecrotic cardiac contractile dysfunction.

51 play a role in the subsequent development of contractile dysfunction.

52 , resulting in abnormal calcium handling and contractile dysfunction.

53 isolated from these hearts did not manifest contractile dysfunction.

54 a response associated with profound cardiac contractile dysfunction.

55 denced by reduced hypertrophy, fibrosis, and contractile dysfunction.

56 impaired systolic strain indicating a subtle contractile dysfunction.

57 ular and lipid metabolic changes, as well as contractile dysfunction.

58 yocardial hypertrophy, cardiac fibrosis, and contractile dysfunction.

59 tial strain (Ecc) at 12 months, a measure of contractile dysfunction.

60 al ventilation-induced diaphragm atrophy and contractile dysfunction.

61 otective intervention to limit post-ischemic contractile dysfunction.

62 nt attenuation of both diaphragm atrophy and contractile dysfunction.

63 lease across the myocyte and contributing to contractile dysfunction.

64 a significant factor contributing to cardiac contractile dysfunction.

65 cularity, does not prevent mitochondrial and contractile dysfunction.

66 preserve mitochondrial function and prevent contractile dysfunction.

67 ilure suggests a novel mechanism of cellular contractile dysfunction.

68 target for the treatment of arrhythmias and contractile dysfunction.

69 plicing defects, enlarged hearts, and severe contractile dysfunction.

70 Postischemic dopamine treatment of contractile dysfunction activates pro-apoptotic signal c

71 CSQ mice developed contractile dysfunction after 60 days of age, with only

72 tes of AF may be sufficient to induce atrial contractile dysfunction after cardioversion.

73 etreatment of ascorbic acid would reduce the contractile dysfunction after electrical shock.

74 protected isolated hearts against injury and contractile dysfunction after ischemia-reperfusion.

75 n of angiogenesis, larger infarct areas, and contractile dysfunction after MI.

76 on and reduced myocardial injury and cardiac contractile dysfunction after regional ischemia/reperfus

77 ggravated cardiac hypertrophy, fibrosis, and contractile dysfunction after transverse aortic constric

78 t may in addition to contributing to myocyte contractile dysfunction also contribute to the induction

79 ure, ischemia, hypertrophy, etc.) leading to contractile dysfunction and adverse remodeling.

80 mine whether chronic CGP treatment mitigates contractile dysfunction and arrhythmias in an animal mod

81 r Ca(2)(+) homeostasis is a central cause of contractile dysfunction and arrhythmias in failing myoca

82 cium release, a major determinant of cardiac contractile dysfunction and arrhythmias.

83 nregulated integrin activation leads to both contractile dysfunction and arrhythmias.

84 d metabolic mechanism that may contribute to contractile dysfunction and arrhythmias.

85 ryanodine receptor (RyR2) may contribute to contractile dysfunction and arrhythmogenesis in heart fa

86 lation appears to be a critical link between contractile dysfunction and arrhythmogenesis.

87 echanical ventilation leads to diaphragmatic contractile dysfunction and atrophy.

88 ventricular failure associated with myocyte contractile dysfunction and calcium dysregulation.

89 (ROS/RNS) in cardiomyocytes, which leads to contractile dysfunction and cardiac abnormalities.

90 aky channels, altered calcium signaling, and contractile dysfunction and cardiac arrhythmias.

91 mmon human disorder that is characterized by contractile dysfunction and cardiac remodeling.

92 es prevent the progression of HF in terms of contractile dysfunction and cardiomyocyte survival.

93 1 activity in the adult heart may ameliorate contractile dysfunction and cellular injury in the face

94 n the hearts of ZDF rats was associated with contractile dysfunction and changes in gene expression s

95 rylation in the failing heart contributes to contractile dysfunction and decreased adrenergic reserve

96 F mice with CIMP significantly abrogated the contractile dysfunction and decreased the oxidative stre

97 iographic findings suggestive of subclinical contractile dysfunction and diastolic filling abnormalit

98 -myosin heavy chain promoter) did not induce contractile dysfunction and did not affect mitochondrial

99 r myocytes that, when disrupted, can lead to contractile dysfunction and dilated cardiomyopathy.

100 e had unaltered NDPK-C expression but showed contractile dysfunction and exacerbated cardiac remodeli

101 tic potential of beta subunits to ameliorate contractile dysfunction and excitability in heart failur

102 nt of diaphragm weakness as a result of both contractile dysfunction and fiber atrophy.

103 he balanced growth and angiogenesis leads to contractile dysfunction and heart failure.

104 Ischemic heart disease is characterized by contractile dysfunction and increased cardiomyocyte deat

105 Contractile dysfunction and increased deposition of O-li

106 se pathway in interleukin 6-mediated cardiac contractile dysfunction and inotrope insensitivity.

107 (GoF) subunits results in profound lymphatic contractile dysfunction and LSM hyperpolarization that i

108 ion in hypertrophied hearts protects against contractile dysfunction and LV dilation after chronic pr

109 DT exacerbated both ischemia-induced cardiac contractile dysfunction and necrosis.

110 n of MEK-ERK signaling prevented TAC-induced contractile dysfunction and pathological remodeling.

111 Here we report that the contractile dysfunction and pathological structural chan

112 fibrillation (AF) is associated with severe contractile dysfunction and structural and electrophysio

113 S contributes importantly to post-infarction contractile dysfunction and subsequent LV remodeling, su

114 ibrillar energetics may contribute to atrial contractile dysfunction and that protein nitration may b

115 ay explain the observed disparity between LV contractile dysfunction and the extent of myocardial inj

116 sclerosis, cardiac hypertrophy, arrhythmias, contractile dysfunction and the underlying alterations i

117 Contractile dysfunction and ventricular arrhythmias asso

118 rdiac gp130 signaling in the pathogenesis of contractile dysfunction and ventricular arrhythmias.

119 a(2+) ATPase pump (SERCA2a) may improve both contractile dysfunction and ventricular arrhythmias.

120 mice die as juveniles with hearts displaying contractile dysfunction and ventricular chamber enlargem

121 cytes by AdPLB-dn gene transfer reversed the contractile dysfunction (and restored positive FFR) by i

122 ice develop spontaneous cardiac hypertrophy, contractile dysfunction, and "fetal" gene induction.

123 lude altered metabolism and calcium cycling, contractile dysfunction, and cell death.

124 e heart predisposes the heart to arrhythmia, contractile dysfunction, and clinical heart failure.

125 in association with myocardial inflammation, contractile dysfunction, and death of cardiomyocytes by

126 tabolism (protein loss, insulin resistance), contractile dysfunction, and disruption of myogenesis.

127 viduals developed left ventricular dilation, contractile dysfunction, and episodic ventricular arrhyt

128 uced remodeling includes chamber dilatation, contractile dysfunction, and fibrosis.

129 itions but caused left ventricle dilatation, contractile dysfunction, and heart failure with intersti

130 te phase led to decreased capillary density, contractile dysfunction, and impaired cardiac growth.

131 including border zone myocardial perfusion, contractile dysfunction, and LV wall stress.

132 microinfarcts with an inflammatory response, contractile dysfunction, and reduced coronary reserve.

133 sociated with cytoskeletal protein disarray, contractile dysfunction, and reduced energy production.

134 ith the development of diaphragm atrophy and contractile dysfunction, and respiratory muscle weakness

135 s for pathological stress-induced growth and contractile dysfunction, and the therapeutic potential o

136 reduction in total myocyte number per heart, contractile dysfunction, and ventricular dilatation in z

137 diotoxic PAHs, and the mechanisms underlying contractile dysfunction are not known.

138 ired mitochondrial function and dynamics and contractile dysfunction are observed in diabetic patient

139 Ventricular arrhythmias and contractile dysfunction are the main causes of death in

140 at total loss of Ryr2 leads to cardiomyocyte contractile dysfunction, arrhythmia, and reduced heart r

141 mic insult has been shown to protect against contractile dysfunction, arrhythmias, and infarction.

142 KO mice developed cardiac hypertrophy and contractile dysfunction as well as sarcomere disruption

143 important contributor to the electrical and contractile dysfunction associated with ageing.

144 eneficial therapeutic strategy to ameliorate contractile dysfunction associated with sepsis.

145 Ca loss that mediate altered Ca handling and contractile dysfunction associated with sepsis.

146 t protein kinase II has a causal role in the contractile dysfunction associated with sepsis.

147 d attenuated left ventricular remodeling and contractile dysfunction at 28 days.

148 ights significantly improve understanding of contractile dysfunction at a level of noninvasive interr

149 Sepsis is associated with cardiac contractile dysfunction attributed to alterations in Ca

150 ed mechanical ventilation worsened diaphragm contractile dysfunction, augmented diaphragm interleukin

151 Lymphatic contractile dysfunction, barrier dysfunction and valve d

152 activation of apoptotic pathways may lead to contractile dysfunction before cell death.

153 ver, knockdown of SERCA2a resulted in severe contractile dysfunction both in vitro and in vivo, which

154 d protect against endotoxin-mediated cardiac contractile dysfunction by attenuating NO production and

155 tethering, suggesting the hypothesis that PM contractile dysfunction can actually diminish MR due to

156 ed chronic MI, the TEI approaches 50% before contractile dysfunction can be systematically identified

157 e, a reduction in Ca transient amplitude and contractile dysfunction can by caused by Ca leak through

158 PM contractile dysfunction can paradoxically decrease MR fr

159 onded to chronic catecholamine toxicity with contractile dysfunction, cardiomyocyte hypertrophy, card

160 I reduced myocardial infarction and improved contractile dysfunction caused by ischemia/reperfusion i

161 CMV-induced diaphragm atrophy and contractile dysfunction coincided with marked increases

162 volved in maladaptive cardiac remodeling and contractile dysfunction [corrected].

163 ES volume index following MV repair indicate contractile dysfunction, despite pre-surgical LVEF >60%.

164 Contractile dysfunction develops in the chronically inst

165 fused mouse hearts and diminished injury and contractile dysfunction during ischemia/reperfusion.

166 y underlie the progression of sarcopenia and contractile dysfunction during muscle aging.

167 dial necrosis and fibrosis, left ventricular contractile dysfunction, electrocardiographic abnormalit

168 demonstrate that chronic hypoxia can induce contractile dysfunction even before substantial ventricu

169 artment into RAG2KO mice before TAC enhanced contractile dysfunction, fibrosis, collagen accumulation

170 We hypothesized that in a model of contractile dysfunction following ischemia, a commonly u

171 ompensated, is associated with cardiomyocyte contractile dysfunction from depressed sarcoplasmic reti

172 a(+)/H(+) exchanger (NHE) would alter atrial contractile dysfunction from rapid rates.

173 Myocardial contractile dysfunction has been proposed to be a major

174 ether viable myocardial regions with chronic contractile dysfunction have true reduction in rest myoc

175 aracterized by exercise intolerance, cardiac contractile dysfunction, hepatopulmonary congestion and

176 but Nox4-null animals developed exaggerated contractile dysfunction, hypertrophy, and cardiac dilata

177 Functional studies show that contractile dysfunction, i.e. a reduction in specific fo

178 ablished betaAR abnormalities and ameliorate contractile dysfunction in a large animal model of heart

179 n the endothelium would reduce the extent of contractile dysfunction in a murine model of infarct-ind

180 ilation results in diaphragmatic atrophy and contractile dysfunction in animals.

181 emission protects against fibre atrophy and contractile dysfunction in both cardiac and skeletal mus

182 ttenuated cardiac hypertrophy, fibrosis, and contractile dysfunction in both models.

183 tion of recombinant rat C5a induced dramatic contractile dysfunction in both sham and CLP cardiomyocy

184 sm in the mechanisms of arrhythmogenesis and contractile dysfunction in cardiac muscle.

185 d ASK1 activation, cTnT phosphorylation, and contractile dysfunction in cardiomyocytes showed similar

186 vide a final common pathway for dilation and contractile dysfunction in dilated cardiomyopathy.

187 the development of cardiac mitochondrial and contractile dysfunction in endotoxin-induced sepsis.

188 and functional disruption of JMCs underlies contractile dysfunction in failing hearts.

189 Contractile dysfunction in G6PD(def) hearts was associat

190 hin might provide a final common pathway for contractile dysfunction in heart failure and these chang

191 nscriptional mechanism may contribute to the contractile dysfunction in heart failure patients with d

192 tes cardiac contractility and contributes to contractile dysfunction in heart failure, although the p

193 onship between reduced ATP-CK metabolism and contractile dysfunction in HF has never been demonstrate

194 , and may thus contribute to arrhythmias and contractile dysfunction in HF.

195 tribute to lower cAMP levels and the related contractile dysfunction in HF.

196 Cardiac remodeling and contractile dysfunction in hypertrophied hearts were ass

197 (2+) release associated with arrhythmias and contractile dysfunction in inherited and acquired cardia

198 ns in the heart and induces acute myocardial contractile dysfunction in ischemia-reperfusion injury.

199 d no evidence of structural abnormalities or contractile dysfunction in Kv4.2W362FxKv1.4(-/-) mouse h

200 lic stress driven by AMPK activation induces contractile dysfunction in mice lacking SRC-2.

201 ading to increased mortality, dilatation and contractile dysfunction in mice.

202 and lipofuscin accumulation resulting in LV contractile dysfunction in MR.

203 e, reperfused MI, revealing the existence of contractile dysfunction in noninfarcted regions of the h

204 timate the degree of detrusor remodeling and contractile dysfunction in PBOO.

205 DG precedes and triggers the onset of severe contractile dysfunction in pressure-overload left ventri

206 tenuate or prevent ventricular expansion and contractile dysfunction in response to hypertension, inf

207 Contractile dysfunction in single myocytes manifested or

208 ered hypertrophic remodeling and exacerbated contractile dysfunction in surviving LUMKO 1-10w post-AB

209 chronic hibernating myocardium with regional contractile dysfunction in the absence of heart failure.

210 c arrhythmia that arises from electrical and contractile dysfunction in the atria.

211 An important contributor to contractile dysfunction in the diabetic state is an impa

212 ated circulating levels of TNF-alpha provoke contractile dysfunction in the diaphragm through an endo

213 ation-induced oxidative stress, atrophy, and contractile dysfunction in the diaphragm.

214 We tested the hypothesis that myocyte contractile dysfunction in the Galphaq mouse heart is me

215 epsis produces significant mitochondrial and contractile dysfunction in the heart, but the role of su

216 contributes to cell death and electrical and contractile dysfunction in the post-ischemic heart.

217 tors may be more important in the genesis of contractile dysfunction in the remodeled rat heart up to

218 contribute to reduced cardiac efficiency and contractile dysfunction in the type 1 diabetic Akita mou

219 y of PLN ablation to correct hypertrophy and contractile dysfunction in two well-characterized and hi

220 yBP-C(C10mut) protein is sufficient to cause contractile dysfunction in vitro.

221 how haploinsufficiency of MLCK may result in contractile dysfunction in vivo, leading to dissections

222 Post-ischemic contractile dysfunction is a contributor to morbidity an

223 myocardium confirm studies in rodents where contractile dysfunction is associated with activation of

224 AF-induced contractile dysfunction is attenuated by verapamil and m

225 Acute cardiac contractile dysfunction is common after cardiopulmonary

226 In Galphaq-induced cardiomyopathy, myocyte contractile dysfunction is mediated, at least in part, b

227 levels and activity are decreased and severe contractile dysfunction is present, overexpression of SE

228 The most clearly defined mediator of contractile dysfunction is tumour necrosis factor (TNF).

229 Contractile dysfunction is underdiagnosed in early stage

230 phragmatic weakness, due to both atrophy and contractile dysfunction, is a well-documented response f

231 overloading (gradient, 152+/-16 mm Hg) with contractile dysfunction, LV function was measured at bas

232 These data suggest that progressive contractile dysfunction may contribute to the pathophysi

233 otection against endotoxemia-induced cardiac contractile dysfunction, most probably by preserving myo

234 motional stress can produce left ventricular contractile dysfunction, myocardial ischemia, or disturb

235 showed increased left ventricular (LV) mass, contractile dysfunction, myofibrillar disarray, and fibr

236 Isolated perfused Mif-/- hearts had greater contractile dysfunction, necrosis, and JNK activation th

237 thogenic or nonpathogenic SIV caused neither contractile dysfunction nor cardiac pathology.

238 een shown to contribute significantly to the contractile dysfunction observed in heart failure.

239 d [Na(+)](i) may be critical in limiting the contractile dysfunction observed in HF.

240 the reduction of its phosphorylation and the contractile dysfunction observed in human heart failure.

241 tion of MV-induced diaphragmatic atrophy and contractile dysfunction occurred in conjunction with a r

242 Contractile dysfunction occurs after a brief period of m

243 24) with ischemic heart disease that chronic contractile dysfunction occurs in myocardial regions wit

244 Myocyte contractile dysfunction occurs in pathological remodelin

245 ply does not match myocardial demand cardiac contractile dysfunction occurs, and prolongation of this

246 When atrial contractile dysfunction occurs, there is recovery of AF

247 arction rat heart failure model and reversed contractile dysfunction of failing myocardium in vivo an

248 t reduced energy delivery contributes to the contractile dysfunction of heart failure (HF).

249 ellular Ca2+ is likely to play a role in the contractile dysfunction of HF because the amplitude and

250 tion of the sarcomere's thin filament to the contractile dysfunction of human cardiomyopathy is not w

251 um, which represents "prolonged postischemic contractile dysfunction of myocardium salvaged by reperf

252 2.5 versus 55.3+/-2.2, P:<0.01) and regional contractile dysfunction of noninfarcted myocardium (% sy

253 of S100A1 protein critically contributes to contractile dysfunction of the diseased heart, which is

254 abolic maladaptation plays a pivotal role in contractile dysfunction of the heart, the understanding

255 may contribute to concentric remodeling and contractile dysfunction of the LV in diabetes.

256 Heart failure is characterized by contractile dysfunction of the myocardium and elevated s

257 ty is associated with lipid accumulation and contractile dysfunction of the obese Zucker rat.

258 ularly for cardiotoxicities characterized by contractile dysfunction or structural injury.

259 ring the -10% trial females experienced less contractile dysfunction (P = 0.011).

260 CA2a can protect diabetic hearts from severe contractile dysfunction, presumably by improving the cal

261 they relate to the excessive hypertrophy and contractile dysfunction regularly observed in patients w

262 C expression and HCM development, especially contractile dysfunction, remain unclear.

263 lationship between HIV infection and cardiac contractile dysfunction remains obscure.

264 Although the mechanism of rapid rate-related contractile dysfunction remains unknown, ischemia, pH ch

265 resence of antibody to erbB2 may explain the contractile dysfunction seen in patients receiving concu

266 ng physiologic mechanisms underlying chronic contractile dysfunction should consider the role played

267 d protein kinase (AMPK), partially prevented contractile dysfunction, suggesting that cardiac deleter

268 of the UPR(mt) ameliorates mitochondrial and contractile dysfunction, suggesting that it may serve an

269 Ddtfl/fl mice exhibited more necrosis and LV contractile dysfunction than control hearts after corona

270 re determinative role in producing postshock contractile dysfunction than does energy.

271 e severe energetic abnormalities and greater contractile dysfunction than R-92L hearts.

272 sensitizer EMD57033 produced an even greater contractile dysfunction than the I79N mutation at fast p

273 s an important mechanism for the ventricular contractile dysfunction that develops in large mammals w

274 tomyosin cross-bridges may contribute to the contractile dysfunction that is apparent after low-flow

275 scous loading of active myofilaments, causes contractile dysfunction that is normalized by microtubul

276 etal abnormality is important in the in vivo contractile dysfunction that occurs in experimental aort

277 lls bearing the p.S358L mutation also showed contractile dysfunction that was partially restored afte

278 ents the development of cardiac dilation and contractile dysfunction, the hallmarks of heart failure.

279 ls and subsequently results in cardiomyocyte contractile dysfunction through dysregulation of calcium

280 ress-induced fructose metabolism, growth and contractile dysfunction, thus defining signalling compon

281 ffective against myocardial inflammation and contractile dysfunction, thus representing a promising c

282 olated TTNtv cardiomyocytes showed sustained contractile dysfunction unlike wild-type ( P=0.0004 and

283 Sacubitril/valsartan for 1-week limited LV contractile dysfunction vs. vehicle and both sacubitril/

284 d 35%, respectively (P<0.01), and myocardial contractile dysfunction was also improved.

285 Contractile dysfunction was also observed in isolated ad

286 Contractile dysfunction was associated with an increased

287 pressure overload or doxorubicin treatment, contractile dysfunction was attenuated in both cases.

288 l histone doses (30 mg/kg), left ventricular contractile dysfunction was the prominent abnormality wi

289 In addition to the contractile dysfunction, we found various ventricular ar

290 interleukin-1 in myocardial inflammation and contractile dysfunction, we treated a patient with fulmi

291 ecrosis, apoptosis, interstitial fibrosis or contractile dysfunction, were not observed in either of

292 nd insulin resistance (IR), as well as major contractile dysfunction, which was associated with alter

293 s with respect to ET-1 signaling and myocyte contractile dysfunction with cardioplegic arrest and rep

294 provide a framework to study development of contractile dysfunction with disease and evaluate the ma

295 ine which PKC isoforms contribute to myocyte contractile dysfunction with ET-1 and CA.

296 obesity was associated with less pronounced contractile dysfunction without any significant perturba

297 Segmental ischemic LV contractile dysfunction without dilation, even in the PM

298 stimulate muscle wasting and also can induce contractile dysfunction without overt catabolism.

299 led mechanical ventilation-induced diaphragm contractile dysfunction without preventing atrophy.

300 Ischemia-reperfusion alone caused contractile dysfunction without significant myocardial n