ライフサイエンスコーパス: ischemia

1 rt failure and death during acute myocardial ischemia.

2 32.8+/-14% before to 53.6+/-12% 1 day after ischemia.

3 vessels causing ischemia versus not causing ischemia.

4 enal nucleotide and nucleoside levels during ischemia.

5 effectively resolves the renal damage after ischemia.

6 t in the initiation of vascular repair after ischemia.

7 were identified in the blood during cerebral ischemia.

8 supply, thereby attenuating exercise-induced ischemia.

9 ts for diagnosis and treatment of myocardial ischemia.

10 ngiography to evaluate symptoms and signs of ischemia.

11 ion injury (IRI) in various models of tissue ischemia.

12 terine hemodynamics with consequential fetal ischemia.

13 se of marginal livers, while minimizing cold ischemia.

14 e to injury during periods of hypoxia and/or ischemia.

15 rge renal transcriptome drift observed after ischemia.

16 rvival and muscle function in the setting of ischemia.

17 lytic degradation of the BBB during cerebral ischemia.

18 ng the surgical induction of mouse hind-limb ischemia.

19 ctive hyperemia occurs following a period of ischemia.

20 , or urgent peripheral revascularization for ischemia.

21 ted miR487b, which is also upregulated after ischemia.

22 neovascularization due to extensive retinal ischemia.

23 % before to 11.7+/-1.6% (P=0.02) 1 day after ischemia.

24 s and a massive BBB leakage at 4.5-hour post-ischemia.

25 ophosphate, but not adenosine levels, during ischemia.

26 phy was used as reference standard to define ischemia.

27 myocardial injury is not caused by coronary ischemia.

28 vity may prevent injury of organs exposed to ischemia.

29 mation, cellular damage, and sustained local ischemia.

30 cularization in an animal model of hind limb ischemia.

31 highest accuracy for diagnosis of myocardial ischemia.

32 llmark of many diseases including cancer and ischemia.

33 s-induced neuronal damage following cerebral ischemia.

34 pling in instances of anticipated myocardial ischemia.

35 pathway in delayed neuronal death induced by ischemia.

36 se of death in patients suffering myocardial ischemia.

37 ated to characterize metabolite responses to ischemia.

38 roidism, or even symptoms of left upper limb ischemia.

39 is a novel, noninvasive test for myocardial ischemia.

40 all, however, BP poorly predicted downstream ischemia.

41 K and upstream liver kinase B1 (LKB1) during ischemia.

42 r delayed cell death from hypoxia or hypoxia-ischemia.

43 ew cancer therapy-induced cardiomyopathy and ischemia.

44 red after 10 min of reperfusion after global ischemia.

45 to sustain the cardiomyocyte during extended ischemia.

46 in determining transcriptional responses to ischemia.

47 r Ile81, and subjected the mice to hind-limb ischemia.

48 etal muscle mass and function after cerebral ischemia.

49 e transcriptome remodeling during myocardial ischemia.

50 ografts were subjected to 30 minutes of warm ischemia, 3.5 hours of cold ischemia, and then perfused

51 % of hemodialysis sessions featured cerebral ischemia; 31.9% of these events were symptomatic.

52 plasma miRNAs 4 h after transient myocardial ischemia (45 min) or sham procedure.

53 Myocardial ischemia (50 minutes followed by reperfusion) was induce

54 rrhage patients at risk for delayed cerebral ischemia across a wide range of hemoglobin values and su

55 Tissue ischemia adversely affects the function of mitochondria,

56 We have analyzed the pathway networks of ischemia-affected and remote myocardial areas after repe

57 and transcriptomic profiling of the distal (ischemia-affected) and proximal (non-affected) anterior

58 ty-two patients at risk for delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage with h

59 T: We are presenting a case of critical hand ischemia after coronary angiography performed through ra

60 (-) under normoxic conditions or exposure to ischemia alone results in minimal S-nitrosation of prote

61 abetes using a novel in vivo murine hindlimb ischemia-amputation model.

62 development and aging and in models of brain ischemia and Alzheimer's disease.

63 ve limbs (of 89 patients) with critical limb ischemia and ankle brachial index >/=1.4 who underwent l

64 ead to hypoxia-dependent pathologies such as ischemia and cancer.

65 eniles but not adults shortly after onset of ischemia and during blood reperfusion.

66 estimated intradialytic exposure to cerebral ischemia and hypotension for each patient, and entered t

67 vation and auto-transplantation, reperfusion ischemia and hypoxia have been reported as major obstacl

68 Following traumatic brain injury (TBI), ischemia and hypoxia play a major role in further worsen

69 the mobilization of LSK cells in response to ischemia and impaired the recovery of blood flow, both o

70 n patients with myocardial and critical limb ischemia and in animal models.

71 he cvrPhone can be used to detect myocardial ischemia and periods of respiratory apnea using a readil

72 y of patient populations, appropriate use of ischemia and QT-interval monitoring among select populat

73 significantly impaired in aged hearts during ischemia and reperfusion (P < 0.05 vs. young hearts).

74 Ischemia and reperfusion injury (IRI) is an inevitable e

75 Sestrin2 prevents age-related intolerance to ischemia and reperfusion injury by modulating substrate

76 alpha C119S/C162S and subjected to simulated ischemia and reperfusion.

77 al cysts in Itf88 knockout mice subjected to ischemia and Six2cre;Pkd1(Fl/Fl) mice, other renal cysto

78 he delayed degeneration of CA1 neurons after ischemia and support a hypothesis that mitochondrial Zn(

79 rotocol provides a model to study myocardial ischemia and the actions of novel and established antian

80 subpopulations according to local levels of ischemia and their position relative to the vasculature.

81 VA was assessed for 60 min after ischemia and then LSG tissues were collected for molecul

82 ctive actions in animal models of myocardial ischemia and ventricular dysfunction through incompletel

83 al stresses such as those caused by hypoxia, ischemia, and diabetes.

84 e"), and an application to assess underlying ischemia, and estimate the respiration rate (RR) and tid

85 ey and liver donor risk indices, kidney cold ischemia, and inferior overall survival.

86 Inflammation-mediated leukostasis, retinal ischemia, and neovascularization and their contribution

87 on, sectoral retinal hemorrhages in areas of ischemia, and predilection for venules and peripheral in

88 te=early positive treadmill or single-vessel ischemia, and severe=large ischemic region abnormality).

89 minutes of warm ischemia, 3.5 hours of cold ischemia, and then perfused with a humanized anti-CD47 m

90 ic AMPK activation and higher sensitivity to ischemia- and reperfusion- induced injury).

91 nesis and its major complication, myocardial ischemia; and summarizes LOX-1 modulation by some natura

92 viability and contractile function following ischemia are limited in their efficacy, we developed a u

93 han the fully automatic method at predicting ischemia (areas under the receiver-operating characteris

94 improved body weight recovery after cerebral ischemia, as well as muscle strength and motor function.

95 e OCTA parameters reveal subclinical macular ischemia at both the superficial and deep retinal capill

96 Report of myocardial ischemia before or after onset of ocular condition was 5

97 end point was absolute change in myocardial ischemia by SPECT.

98 reconditioning, and how long the duration of ischemia can be so that adjunct cardioprotection by post

99 One of them is upper limb ischemia caused by radial artery thrombosis.

100 Brain ischemia causes oxygen and glucose deprivation (OGD) in

101 italized for the management of critical limb ischemia (CLI), but limited data are available on the in

102 are promising therapeutics for critical limb ischemia (CLI).

103 d stem cells in PIRI including critical limb ischemia (CLI).

104 ore likely to have stress-induced myocardial ischemia compared with those with normal or hypotensive

105 The extent to which ischemia contributes to ischemia/reperfusion injury has

106 Increased Rac1 activity caused by OGD/ischemia contributes to neuronal death in hippocampal ne

107 rent I/R protocols: 40-minute I/R (prolonged ischemia, controls), 20-minute I/R (short-duration ische

108 d tetrapolar bioimpedance sensors for tissue ischemia detection.

109 s despite several risk factors of upper limb ischemia - diabetes, end-stage renal failure, hyperparat

110 Presence of macular ischemia did not affect BCVA outcome or treatment freque

111 ac embolic source, TIA/stroke and myocardial ischemia differ among various ocular arterial occlusive

112 all-cause mortality, myocardial infarction, ischemia-driven revascularization, or stent thrombosis a

113 all-cause mortality, myocardial infarction, ischemia-driven revascularization, or stent thrombosis a

114 ary end point (death, myocardial infarction, ischemia-driven revascularization, or stent thrombosis)

115 oint (all-cause mortality, reinfarction, and ischemia-driven revascularization; hazard ratio [HR], 0.

116 rget vessel myocardial infarction [TVMI], or ischemia-driven target lesion revascularization) at 1 ye

117 % confidence interval, 1.69-3.23; P<0.0001), ischemia-driven target vessel revascularization (adjuste

118 asonably sized encapsulation devices promote ischemia due to high beta cell densities creating prohib

119 ype, occluded vessel, quantification method, ischemia duration and follow-up duration.

120 To study the effect of ischemia duration and protective interventions on the te

121 he impact of cardioprotective strategies and ischemia duration on postischemia/reperfusion (I/R) myoc

122 g of events associated with cerebral hypoxia-ischemia during cardiopulmonary bypass (CPB) remains lim

123 The relationship between BP and downstream ischemia during hemodialysis has not been characterized.

124 8 plasma miRNAs that were elevated following ischemia, eight were tested for their ability to induce

125 cts of GM-CSF in PAD, since exercise-induced ischemia enhances progenitor cell release and may promot

126 In the pathophysiologic setting of cerebral ischemia, excitotoxic levels of glutamate contribute to

127 ia preceded by preconditioning, or prolonged ischemia followed by postconditioning.

128 ubjecting them to 90 minutes of warm hepatic ischemia followed by reperfusion for 6 or 24 hours.

129 Intestinal ischemia followed by reperfusion leads to local and remo

130 ood flow is the hallmark of delayed cerebral ischemia following subarachnoid hemorrhage.

131 n with reduced OIR severity, suggesting that ischemia from UPI could yield protective angiogenic effe

132 significantly associated with the extent of ischemia (hazard ratio for small ischemic defects: 2.2,

133 have previously shown that cerebral Hypoxia-ischemia (HI) results in activation of Src kinase in the

134 Following global cerebral ischemia, hippocampal CA1 pyramidal neurons are more vul

135 9, 95% CI 1.08-1.55, P=0.005) and acute limb ischemia (HR 4.23, 95% CI 2.86-6.25, P<0.001) when compa

136 e femoral head (ONFH) primarily results from ischemia/hypoxia to the femoral head, and one of the cel

137 There were 72 of 286 (25%) vessels causing ischemia in 52 of 115 (45%) patients.

138 This allowed induction of ischemia in a specific cortical region of conscious mice

139 adenosine levels were lower before and after ischemia in CD73-deficient mice.

140 To assess the spectrum of perivenular ischemia in eyes with retinal vascular obstruction (typi

141 These events can reverse hindlimb ischemia in mice for >24 hours and increase muscle blood

142 lysis of neurogenesis in a model of cortical ischemia in mice.

143 ricytes (APCs) improves recovery from tissue ischemia in preclinical animal models by still unknown m

144 ated by hypoxia in vitro and global cerebral ischemia in rats in vivo We show that pharmacologic or g

145 ed intravenously 24 and 48 hours after renal ischemia in rats.

146 rapy, >/=1 myocardial segment with inducible ischemia in Tc-99m SPECT who underwent bone marrow biops

147 ed by Dapk1 deficiency in vitro or following ischemia in vivo.

148 Cerebral ischemia induced a time-dependent increase of blood occl

149 slets to develop a detailed profile of early ischemia induced changes and targets for intervention.

150 We recently reported that ischemia induced rapid degradation of tight junction pro

151 Moreover, the severity of ischemia induced VA was decreased in A-803467 groups.

152 We previously reported that ischemia-induced angiogenesis is compromised in type 2 d

153 rmacologically or genetically aggravates the ischemia-induced brain damage, motor deficits and mortal

154 1 as a promising target for the treatment of ischemia-induced myocardial damage.

155 hy and ICA has poor discriminatory power for ischemia-inducing lesions.

156 Brain ischemia inhibits immune function systemically, with res

157 Ischemia involving >/=2 quadrants is a risk factor for n

158 Ischemia involving >/=2 quadrants was associated with in

159 Prolonged ischemia is a known risk factor for delayed graft functi

160 issue ischemia, such as transient myocardial ischemia, leads to release of cellular RNA including mic

161 ever, exposure to NO2(-) in conjunction with ischemia led to extensive S-nitrosation of protein thiol

162 c anemia, severe thrombocytopenia, and organ ischemia linked to disseminated microvascular platelet r

163 profibrotic cardiac repair and healing after ischemia, little is known about whether T cells directly

164 or adverse limb events defined as acute limb ischemia, major amputation, or urgent peripheral revascu

165 at control vascular changes before and after ischemia may result in novel approaches to slow the prog

166 Upon cardiac pathological conditions such as ischemia, microenvironmental changes instruct a series o

167 cts of increased CD39 in an in vivo cerebral ischemia model, we developed a transgenic mouse expressi

168 ssel perfusion function in a murine hindlimb ischemia model.

169 AND In different murine models of myocardial ischemia, myeloperoxidase deficiency profoundly decrease

170 ndings were both compatible with small bowel ischemia-necrosis and perforation.

171 udy demonstrates that intradialytic cerebral ischemia occurs frequently, is not easily predicted from

172 a on the number of low-risk patients (no new ischemia on ECG and hs-cTnT measurements <0.005 microg/L

173 ludin with a sharp increase at 4.5-hour post-ischemia onset, which concurrently occurred with the los

174 basal level within the first 24 hours after ischemia onset.

175 tection (ie, those undergoing short-duration ischemia or preconditioning).

176 ed 24 and 72 hours after 30 minutes of renal ischemia or sham operation.

177 aneurysm formation (>/=6 cm), organ or limb ischemia, or new uncontrollable hypertension or pain.

178 tream LKB1 is impaired in aged hearts during ischemia (P < 0.05 vs. young hearts).

179 iple disorders (hepatitis, brain and cardiac ischemia, pancreatitis, viral infection and inflammatory

180 ute I/R (short-duration ischemia), prolonged ischemia preceded by preconditioning, or prolonged ische

181 Median duration of ischemia pretreatment was 2.4 hours.

182 significant intestinal injury occurs during ischemia prior to reperfusion and that this is due to ac

183 rogenesis and thrombosis-mediated myocardial ischemia, processes that are accelerated in diabetes.

184 the ongoing ischemic event during peripheral ischemia produces superoxide and diminishes the NO bioav

185 ia, controls), 20-minute I/R (short-duration ischemia), prolonged ischemia preceded by preconditionin

186 cular ejection fraction, myocardial scar and ischemia, rate-pressure product, type of radiotracer or

187 ned the relationship between BP and cerebral ischemia (relative drop in cerebral saturation >15%) and

188 brain, their impact on BBB integrity during ischemia remains unclear.

189 rine models of acute liver damage induced by ischemia reperfusion and N-acetyl-p-aminophenol (acetami

190 s were assessed in hepatic lymphocytes after ischemia reperfusion injury (IRI) in high-fat diet (HFD)

191 impaired oxygen supply to the periphery and ischemia reperfusion injury, inflammation, oxidative str

192 ry circulation, and has a protective role in ischemia reperfusion.

193 ing MerTK in cardiac repair after myocardial ischemia reperfusion.

194 nt and recruited phagocytes after myocardial ischemia reperfusion.

195 eotide exerts a protective effect in hepatic ischemia-reperfusion (HIR) injury.

196 oad-spectrum antibiotics and performed renal ischemia-reperfusion (I/R) injury in mice.

197 RK2 ablation-each initiated after myocardial ischemia-reperfusion (I/R) injury-was investigated to ev

198 Retinal ischemia-reperfusion (IR) injury causes irreversible los

199 tive effects in a murine model of myocardial ischemia-reperfusion (MI/R) injury with a bell shape the

200 ith spinal cord injury after thoracic aortic ischemia-reperfusion (TAR) in mice.

201 nd alanine aminotransferase (ALT) (marker of ischemia-reperfusion [I/R] injury) were measured in perf

202 es 12-week-old Wistar rats were subjected to ischemia-reperfusion and assigned to four groups: amniot

203 In vivo, more severe renal ischemia-reperfusion injury (IRI) associated with increa

204 t regulators CD55 and CD59 exacerbates renal ischemia-reperfusion injury (IRI) in mouse models, but t

205 e of CD47 signaling has been shown to reduce ischemia-reperfusion injury (IRI) in various models of t

206 However, its role in renal ischemia-reperfusion injury (IRI) is controversial.

207 Ischemia-reperfusion injury (IRI) leading to delayed gra

208 Renal ischemia-reperfusion injury (IRI) leads to acute kidney

209 e of the CD47 signaling pathway could reduce ischemia-reperfusion injury (IRI) of renal allografts do

210 C1) stimulation (10 min) protected mice from ischemia-reperfusion injury (IRI).

211 Ischemia-reperfusion injury also promoted DC-dependent c

212 at the early phase of kidney transplant when ischemia-reperfusion injury and cyclosporin A toxicity m

213 reveals an important regulation of cerebral ischemia-reperfusion injury by O-GlcNAcylation and also

214 Ischemia-reperfusion injury induced influx of monocytes,

215 circulating proinflammatory cytokines during ischemia-reperfusion injury is not well understood.

216 fect of amniotic fluid stem cells in a renal ischemia-reperfusion injury model.

217 Mechanisms of renal ischemia-reperfusion injury remain unresolved, and effec

218 Mesenteric ischemia-reperfusion injury was induced in male Wistar r

219 tor-amniotic fluid stem cells can worsen the ischemia-reperfusion injury when delivered in a high dos

220 cerebral hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and kidney degeneration in

221 amniotic fluid stem cells in rats with renal ischemia-reperfusion injury, mainly by mitogenic, angiog

222 plasma samples from rats subjected to renal ischemia-reperfusion injury, pigs subjected to renal tra

223 Compared with controls, mouse models of ischemia-reperfusion injury, urinary obstruction, and hy

224 sis induced by folic acid (FA) or unilateral ischemia-reperfusion injury.

225 ell (CPC)-derived exosomes in a rat model of ischemia-reperfusion injury.

226 on (tMCAO) model was used to establish brain ischemia-reperfusion injury.

227 d higher presence of regulatory T cell after ischemia-reperfusion injury.

228 inflammatory response after sublethal renal ischemia-reperfusion injury.

229 s) treatment with necrostatin-1 during renal ischemia-reperfusion injury.

230 quently apoptosis in epithelial cells during ischemia-reperfusion injury.

231 ed media and delivered to athymic rats after ischemia-reperfusion injury.

232 Tissue damage associated with ischemia-reperfusion, vascular injury, and/or rejection

233 pecific deletion of Drp1 prevented the renal ischemia-reperfusion-induced kidney injury, inflammation

234 s of hypusinated eIF5A and protected against ischemia-reperfusion-induced renal injury.

235 patocellular oxidant production during liver ischemia-reperfusion.

236 mimetic, plays a protective role in cardiac ischemia/reperfusion (I/R) but the molecular mechanism r

237 tective effects were examined in mouse focal ischemia/reperfusion (I/R) model.

238 report the early molecular changes following ischemia/reperfusion (I/R).

239 and remote myocardial areas after repetitive ischemia/reperfusion (r-I/R) injury without ensuing myoc

240 Because prolonged ischemia/reperfusion also damages electron transport com

241 duced by T cells to cardiac remodeling after ischemia/reperfusion and define its mechanism of action.

242 erimental study, 20 pigs underwent 40-minute ischemia/reperfusion followed by serial CMR examinations

243 ed gene response within microglia exposed to ischemia/reperfusion in both in vitro and in vivo experi

244 pair of damaged mucosa induced by mesenteric ischemia/reperfusion in the small intestine and by dextr

245 , the pathogenic mechanisms underlying renal ischemia/reperfusion injury (IRI) are not fully defined.

246 b ischemia/reperfusion may reduce myocardial ischemia/reperfusion injury and improve patients' progno

247 The extent to which ischemia contributes to ischemia/reperfusion injury has not been thoroughly stud

248 ice fully protected the liver against lethal ischemia/reperfusion injury, allowing 100% survival rate

249 variety of pathological disorders including ischemia/reperfusion injury, cataract formation, and neu

250 by early insults to the allograft, including ischemia/reperfusion injury, infections, and rejection.

251 doxically, it preserves heart function after ischemia/reperfusion injury, potentially by decreasing p

252 limb ischemia/reperfusion reduces myocardial ischemia/reperfusion injury.

253 mma2-AMPK sensitizes the heart to myocardial ischemia/reperfusion injury.

254 AMPK activity is required to protect against ischemia/reperfusion injury.

255 Renal ischemia/reperfusion is a major cause of acute kidney in

256 ning (RIPC) by repeated brief cycles of limb ischemia/reperfusion may reduce myocardial ischemia/repe

257 dels of Bmal1(fx/fx);Tek-Cre mice, a retinal ischemia/reperfusion model and a neointimal hyperplasia

258 ning (RIPC) by repeated brief cycles of limb ischemia/reperfusion reduces myocardial ischemia/reperfu

259 ced by a 50% reduction of infarct size after ischemia/reperfusion versus wild type.

260 confirmed both in vitro H/H-N/N- and in vivo ischemia/reperfusion-induced microglial ISG responses by

261 ity favors the survival of the myocardium at ischemia/reperfusion.

262 ey cellular effectors in the CNS response to ischemia/reperfusion.

263 ic stress, isolated hearts were subjected to ischemia/reperfusion.

264 After 30 minutes of warm ischemia, right kidneys were removed from 30-kg Yorkshir

265 r, the prognostic relevance of remnant liver ischemia (RLI) after resection of colorectal liver metas

266 ial recanalization (Thrombolysis in Cerebral Ischemia scores 2B to 3; drip and ship, 84 [84.0%]; moth

267 r ischemia within 30 days, the daily risk of ischemia significantly exceeded the daily risk of bleedi

268 Tissue ischemia, such as transient myocardial ischemia, leads t

269 The WISE study (Women's Ischemia Syndrome Evaluation) was a prospective cohort s

270 red to the superficial retinal plexus due to ischemia that did not recover after intravitreal dexamet

271 For patients with critical limb ischemia, the goals of revascularization are to relieve

272 e U.S. study had a significantly longer cold ischemia time (the time elapsed between procurement of t

273 donor organ was subjected to 1 hour of warm ischemia time after circulatory cessation, then flushed

274 donors, and is associated with a longer cold ischemia time and a potentially higher rejection rate.

275 Mean kidney cold ischemia time was 10 +/- 3 and 50 +/- 15 hours, for grou

276 solation time was 185 (37) minutes, and warm ischemia time was 51 (62) minutes.

277 for planning surgery and also decreases cold ischemia time, potentially translating into a higher suc

278 occlusions decrease tissue perfusion causing ischemia to lower limbs in patients with peripheral arte

279 quence, infarction develops from the core of ischemia to the areas of less severe hypoperfusion.

280 inary efficacy of intravenously administered ischemia-tolerant MSCs (itMSCs) in patients with nonisch

281 CAT-II trial (Rule Out Myocardial Infarction/Ischemia Using Computer Assisted Tomography) comparing a

282 crimination between coronary vessels causing ischemia versus not causing ischemia.

283 cal studies showed that tissue damage during ischemia was associated with increased expression of C3/

284 Remnant liver ischemia was defined as reduced or absent contrast enhan

285 gic flux as an adaptive response to TAE-like ischemia was found by the authors.

286 Cerebral ischemia was induced by middle cerebral artery occlusion

287 Chronic ischemia was induced percutaneously (day 0) in the circu

288 Prevalence of obstructive CAD and myocardial ischemia was low (11.9% versus 12.7%, respectively), wit

289 Cells surviving ischemia were autophagy dependent.

290 his study, the acute effects of high-density ischemia were investigated in human islets to develop a

291 llitus (DM) have less angina and more silent ischemia when compared with those without DM.

292 pply, and incompleteness may lead to digital ischemia when the radial artery becomes obstructed after

293 e vasculature that promote hypoperfusion and ischemia, while also affecting the extent of injury and

294 Control of warm ischemia (WI) lesions that occur with donation after cir

295 op a consensus on the syndrome of myocardial ischemia with no obstructive coronary arteries.

296 patocellular carcinoma (HCC) cells surviving ischemia with respect to cell cycle kinetics, chemosensi

297 657 differentially expressed genes following ischemia, with many that are associated with increased i

298 ates of myocardial infarction and acute limb ischemia, with similar composite rates of cardiovascular

299 gh the rates for bleeding exceeded those for ischemia within 30 days, the daily risk of ischemia sign

300 mooth muscle NOX4, the common denominator of ischemia within all ischemic organs, played no apparent