ライフサイエンスコーパス: Krebs

1 Krebs cycle enzyme activity in Bacillus subtilis was exa

2 Krebs cycle flux was also stimulated by CGP37157 when gl

3 Krebs cycle intermediates such as succinate, citrate, an

4 Krebs cycle substrates (KCS) can stabilise the colour of

5 helate magnesium and to inhibit aconitase, a Krebs cycle enzyme.

6 such as the molecular chaperone Hsp60p and a Krebs cycle protein, Kgd2p.

7 required to allow the use of glutamine as a Krebs cycle substrate in T cells.

8 ranslation and RNA synthesis activities in a Krebs-2-derived in vitro system that supported complete,

9 al carcinoma, is caused by inactivation of a Krebs cycle enzyme due to mutation.

10 This work outlines the use of a Krebs cycle metabolon catalyst obtained through the in s

11 Succinate, a Krebs cycle intermediate, increases after dysregulated e

12 al. (2016) identify a mechanism that uses a Krebs cycle protein to control local activation of a ubi

13 v.) and nondiabetic rats and perfused with a Krebs-albumin-red cell solution (K2RBC, Hct 20%).

14 s a key component of the tricarboxylic acid (Krebs) cycle.

15 LECA later acquired the fully aerobic Krebs cycle-oxidative phosphorylation-mitochondrial meta

16 howed hypoglycemia, lactic acidosis, altered Krebs cycle function and dysregulated fatty acid oxidati

17 Interestingly, among Krebs cycle intermediates, only succinic acid monomethyl

18 32.2]), angiopoietin-2 (6.4 [1.3-30.4]), and Krebs von den Lungen-6 (5.1 [3.0-12.2]).

19 nt of electron transport chain complexes and Krebs cycle enzymes revealed that alpha-ketoglutarate de

20 ling to the glycolysis, gluconeogenesis, and Krebs cycle (n = 48) and an exploration by the next-gene

21 female mouse kidneys towards glycolysis and Krebs cycle activity.

22 dinated set of enzymes of the glycolytic and Krebs cycle pathways, which we propose may antagonize Tr

23 extensive catabolism via the glycolytic and Krebs cycle pathways.

24 articularly at the amino acid metabolism and Krebs cycle level.

25 s, ATP machinery, fatty acid metabolism, and Krebs cycle, which further decreased in expression durin

26 mulation is dependent on calcium release and Krebs cycle activity.

27 NaDC-1, couples the transport of sodium and Krebs cycle intermediates, such as succinate and citrate

28 of mitochondrial reactive oxygen species and Krebs' cycle intermediates, and increased resistance to

29 red rat hepatocytes were incubated in anoxic Krebs-Ringer-HEPES buffer at pH 6.2 for 4 hours and reox

30 reparation perfused in the descending aorta (Krebs-Henseleit bicarbonate, 5% albumin medium containin

31 In wheat germ and mouse ascites Krebs-2 in vitro translation systems, PCI6 inhibited tra

32 onsequently, the mitochondrial products ATP, Krebs cycle intermediates, glutamate, and acetoacetate w

33 utely alkaline loaded by replacing bilateral Krebs bicarbonate Ringer (KBR) with Hepes-buffered Ringe

34 guinea pigs and kept alive in oxygen bubbled Krebs' solution.

35 -) mice had diminished levels of circulating Krebs Von Den Lungen 6 (alveolar epithelial injury marke

36 trode in an airtight stirred bath containing Krebs solution buffered with HEPES at 37 degrees C (pH 7

37 its were suspended in organ baths containing Krebs solution; isometric tension was then measured.

38 ich persisted in TTX (0.5 microM)-containing Krebs solution, were reduced by 70% in a low-Na+ (26 mM)

39 perfused mouse liver model with deoxygenated Krebs-Henseleit buffer followed by oxygenated buffer.

40 sted even in perfusions of zero calcium-EGTA Krebs solution suggesting that the calcium oscillation i

41 Eight Krebs cycle enzyme components were isolated upon chemica

42 our drainage period, animals received either Krebs Ringer Henseleit (the bile-depleted group), or sod

43 ally before and after incubation with either Krebs solution alone or with the NO-inhibitor, NG-monome

44 zed arrest, hearts were arrested with either Krebs-Henseleit (KH) buffer (control), KH buffer contain

45 was compared in hearts protected with either Krebs-Henseleit solution (K-H), pinacidil (50 micromol/L

46 The nuclear-encoded Krebs cycle enzymes, fumarate hydratase (FH) and succina

47 e carbon into glucose via glutamine entering Krebs cycle at alpha-ketoglutarate or 2) through simple

48 ger than those elicited by other (equimolar) Krebs cycle intermediates.

49 [2-(13)C]pyruvate was also used to evaluate Krebs cycle metabolism and demonstrated a unique marker

50 In Ca2+-free Krebs-Ringer bicarbonate buffer containing 2.8 mmol/l gl

51 This current was inhibited in chloride-free Krebs solution or by inhibiting basolateral chloride upt

52 involved in basic metabolic processes (e.g. Krebs cycle), (iii) genes required to survive oxidative

53 of central carbon metabolic pathways (e.g., Krebs cycle enzymes), as well as transporters and enzyme

54 evidence of profoundly dampened glycolysis, Krebs cycle, fatty acid beta oxidation and amino acid me

55 y and inhibition by catalytic products, Hans Krebs first demonstrated the existence of multiple gluta

56 In Escherichia coli, the homodimeric Krebs cycle enzyme isocitrate dehydrogenase (EcIDH) is r

57 In Krebs extracts, dipyridamole specifically inhibited vira

58 on periods of 60 min each at 37 degrees C in Krebs Ringers Henseleit (KRH) solution in an atmosphere

59 The in vivo decrease in Krebs cycle activity in the 6-week post-MI heart may rep

60 ni were isolated by collagenase digestion in Krebs-Ringer bicarbonate (KRB) buffer at 37 degrees C.

61 longus muscles were preincubated for 4 h in Krebs-Henseleit solution containing glucose or glucose +

62 Dopamine was incubated in Krebs bicarbonate medium and its rate of chemical degrad

63 Vessels were incubated in Krebs buffer at 37 degrees C.O(2)(-) was measured by luc

64 s (human, rabbit, and rat) were incubated in Krebs solution containing [3H]-norepinephrine ([3H]NE) f

65 Intact porcine lenses were incubated in Krebs solution.

66 Sphincter muscle was incubated in Krebs-Ringer bicarbonate buffer in the absence and prese

67 After 10 minutes' incubation in Krebs bicarbonate medium, the dopamine concentration dec

68 re isolated, cultured, and then perifused in Krebs-Ringer bicarbonate buffer with 2 mmol/l glutamine

69 alterations after MI in which reductions in Krebs cycle activity precede a reduction in pyruvate deh

70 After storage, the cells were rewarmed in Krebs-Henseleit buffer with air at 37 degrees C for 1 hr

71 ce, they were presented with OS suspended in Krebs-Henseleit buffer in the presence or absence of car

72 teries without endothelium were suspended in Krebs-Ringer bicarbonate solution for isometric tension

73 everal previous studies, our method included Krebs cycle intermediates (m/z <200), which we found to

74 rmined to be significantly altered including Krebs cycle intermediates, amino acids that have not bee

75 ized energy production components, including Krebs cycle and electron transport genes, decreased by 4

76 to supply sufficient pyruvate for increased Krebs cycle flux when glucose is limiting.

77 ally improves glucose homeostasis, increases Krebs cycle activity, and reduces the levels of acylcarn

78 Using an isolated, Krebs solution-perfused rat heart we measured the change

79 tial shifted to -90 mV in a low-Na+, high-K+ Krebs solution.

80 cterial growth; depressed activities of many Krebs cycle enzymes, including pyruvate:ferredoxin oxido

81 In this study, we measured Krebs cycle flux in real time in perfused rat hearts usi

82 and AD patients included energy metabolism, Krebs cycle, mitochondrial function, neurotransmitter an

83 ative phosphorylation, glutamine metabolism, Krebs cycle, and fatty acid oxidation.

84 as glucose, amino acid and lipid metabolism, Krebs cycle, and immune responses and those hitherto unk

85 completely abolished by low Ca2+, high Mg2+ Krebs solution or Krebs solution containing Co2+ (2 mM)

86 Low Ca2+/high Mg2+ Krebs solution or TTX did not change the resting membran

87 either a high-K+ (7 mM) or Cd2+ (100 microM) Krebs solution.

88 eased substrate supply for the mitochondrial Krebs cycle compared with APAP alone.

89 d diminished production of the mitochondrial Krebs cycle substrate citrate, a precursor to cellular l

90 In addition, the mitochondrial Krebs cycle was modulated to increase synthesis of malic

91 the substrate flux through the mitochondrial Krebs cycle, it was observed that the reduced liver inju

92 a rate-limiting enzyme in the mitochondrial Krebs cycle.

93 At 6 weeks after MI, in vivo mitochondrial Krebs cycle activity was impaired, with decreased (13)C-

94 mol (5 x 10(5) cpm/ micromol) of HNE in 2 mL Krebs-Hansleit buffer for 1 hour at 37 degrees C.

95 on, were reduced by 70% in a low-Na+ (26 mM) Krebs solution, indicating the involvement of Na+ ions.

96 nstant flow of 10 mL/min by using a modified Krebs-Henseleit solution equilibrated with 95% oxygen an

97 tant flow rate of 10 mL/min using a modified Krebs-Henseleit solution equilibrated with 95% oxygen an

98 eys were isolated and perfused with modified Krebs-Henseleit buffer.

99 oved from the rat and perfused with modified Krebs-Henseleit buffers containing 7.5 or 2.5 g/dL bovin

100 trogenic, sodium-dependent transport of most Krebs cycle intermediates (Km = 20-60 microM), including

101 strate that in cell-free extracts from mouse Krebs-2 ascites, microRNA-mediated translational repress

102 - 2.3% with an IC50 of 19.9 microM in normal Krebs solution (2.5 mM Ca2+, 1.2 mM Mg2+) without effect

103 uscles were isolated and incubated in normal Krebs-Henseleit buffer (pH 7.4).

104 We report that glycolytic but not Krebs cycle metabolism of glucose is critically involved

105 ; Roe, 0.36 (P < 0.001); Collins, 0.82 (ns); Krebs, 0.14 (P < 0.01).

106 ollins usage occurred in the SE; and 100% of Krebs and 46% of Stanford usage occurred in the W.

107 of mitochondrial stress and accumulation of Krebs cycle intermediates in adipose tissue in diabetes

108 ly consumes O2, rendering standard assays of Krebs cycle turnover unusable.

109 radioactivity into and the concentrations of Krebs cycle intermediates was not of sufficient magnitud

110 er at constant flow; perfusates consisted of Krebs-Henseleit buffer or buffer plus washed RBCs at a H

111 Cardioplegia consisted of Krebs-Henseleit solution either alone (control) or with

112 ocytes results in a global downregulation of Krebs cycle and OXPHOS gene expression, defective mitoch

113 Therefore, CcpA controls expression of Krebs cycle genes directly by regulating transcription o

114 Langendorff method under a constant flow of Krebs-Henseleit buffer containing (18)F-FDG with a rate

115 and tandem mass spectrometry measurement of Krebs cycle intermediates revealed a negative impact of

116 molecule: malate dehydrogenase, a member of Krebs cycle, and adenosine triphosphate synthase.

117 The metabolism of Krebs cycle intermediates is of fundamental importance f

118 neoplasms, displays genetic modifications of Krebs cycle components as well as electron transport cha

119 horylation and Ca2+ -dependent regulation of Krebs cycle dehydrogenases, illustrating how the model c

120 ements and balances the bioenergetic role of Krebs cycle-derived electron donors.

121 Accordingly, Ca(2+)-induced stimulation of Krebs cycle dehydrogenases during beta-adrenergic stimul

122 t), involved in the transport and storage of Krebs cycle intermediates in tissues important in fly me

123 ting sequence appended restored viability on Krebs cycle substrates and ATP synthesis capabilities bu

124 We did not detect glycolysis or Krebs-cycle-related defects in the iar4 mutant, and a T-

125 hed by low Ca2+, high Mg2+ Krebs solution or Krebs solution containing Co2+ (2 mM) and Cd2+ (400 micr

126 secretion, blockers of pyruvate transport or Krebs cycle enzymes were without effect.

127 r effects on HIF-1 are not mimicked by other Krebs cycle intermediates, including succinate and fumar

128 the periphery and immersed in an oxygenated Krebs-Ringer buffer.

129 slices were first equilibrated in oxygenated Krebs buffer (KRB) (120 min) then superfused for 10 min

130 were harvested and maintained in oxygenated Krebs solution in an organ bath at 37 degrees C.

131 fused alternately with a modified oxygenated Krebs-Henseleit buffer and with buffer containing varied

132 minutes via the portal vein with oxygenated Krebs-Henseleit bicarbonate buffer solution at a pressur

133 owth inhibition was accompanied by perturbed Krebs cycle activity, inhibition of lipid and nucleotide

134 s, nicotinamides, tryptophan, phospholipids, Krebs and urea cycles, and revealed kidney dysfunction b

135 - 0.8 ml min-1 in hearts perfused with plain Krebs solution, by 3.8 +/- 0.8 ml min-1 in hearts to whi

136 re randomly assigned to perfusion with plain Krebs solution, or with Krebs solution to which L-NAME a

137 found to be primarily the result of reduced Krebs cycle gene transcription.

138 pyruvate concentrations coupled with reduced Krebs cycle intermediates and short-chain acylcarnitines

139 larographic chamber containing air-saturated Krebs-Henseleit buffer plus 20 mM glucose, PO2 being mon

140 These experiments use the sequential Krebs TCA cycle enzymes from yeast mitochondrial malate

141 orporation of [14C] bicarbonate into several Krebs cycle intermediates in 3T3-F442A adipocytes.

142 orrelated well with GSIS, in particular some Krebs cycle intermediates, malonyl-CoA, and lower ADP le

143 tilization and in the activities of specific Krebs cycle enzymes alpha-ketoglutarate dehydrogenase (K

144 amino acids, fumarate and malate, suggesting Krebs cycle up-regulation.

145 intermediate in the tricarboxylic acid (TCA, Krebs) cycle and a promising therapeutic agent in its ow

146 h that of other metabolites, indicating that Krebs cycle flux can be measured directly.

147 The Krebs cycle plays a fundamental role in cardiac energy p

148 The Krebs tricarboxylic acid cycle (TCA) is central to metab

149 se (PNPase), a DEAD-box RNA helicase and the Krebs cycle enzyme aconitase.

150 Lysine metabolism in plasma and the Krebs cycle in CSF were significantly affected in MCI vs

151 s by phosphoenolpyruvate carboxylase and the Krebs cycle were measured by 13C incorporation from [1-1

152 formation of acetyl CoA from glucose and the Krebs cycle.

153 production of 2-methylcitrate (2-MC) by the Krebs cycle enzyme citrate synthase (GltA).

154 of chemical modification of proteins by the Krebs cycle intermediate, fumarate, is significantly inc

155 previously been shown to be modulated by the Krebs cycle metabolite citrate in Escherichia coli.

156 ynthesis requires precursors supplied by the Krebs cycle, which in turn requires anaplerosis to reple

157 ntal occurrence of P3N, which shuts down the Krebs cycle by inactivating succinate dehydrogenase and

158 is generated internally in humans during the Krebs cycle, is an attractive alternative to these thera

159 Mutations in the gene encoding the Krebs cycle enzyme fumarate hydratase (FH) predispose to

160 tance not only for flux of fuel entering the Krebs cycle but for overall energy homeostasis.

161 at pyruvate, the precursor substrate for the Krebs cycle, regulates I(crac) to prolong Ca(2+) influx

162 n uptake for cellular function, e.g. for the Krebs cycle.

163 Removal of CaCl2 from the Krebs solution, disruption of the endothelium, and admin

164 )C enrichment in products of glycolysis, the Krebs cycle, the pentose phosphate pathway, nucleobases,

165 mplex (OGDHc), a rate-limiting enzyme in the Krebs (citric acid) cycle.

166 ural evidence of substrate channeling in the Krebs cycle metabolon.

167 s transported to mitochondria for use in the Krebs cycle to generate ATP.

168 erent as fuel procurement, catabolism in the Krebs cycle, and stepwise oxidation of reducing equivale

169 and fumarate, its immediate precursor in the Krebs cycle, in affected subjects' fibroblasts.

170 genase (IDH), a key regulatory enzyme in the Krebs cycle, is a multi-tetrameric enzyme.

171 esults in the inhibition of aconitase in the Krebs cycle, resulting in the accumulation of citrate an

172 -rehydration of citrate to isocitrate in the Krebs cycle.

173 genase (OGDH), a rate-limiting enzyme in the Krebs cycle.

174 eroxisomal citrate synthases involved in the Krebs tricarboxylic acid (TCA) cycle and glyoxylate path

175 trate synthase are sequential enzymes in the Krebs tricarboxylic acid cycle.

176 ve decarboxylation of alpha-ketoacids in the Krebs' cycle.

177 m normal rats were incubated for 1 hr in the Krebs-Henseleit buffer media containing normal rat sera,

178 m normal rats were incubated for 1 hr in the Krebs-Henseleit buffer media containing zymosan-activate

179 itive [4Fe-4S] (de)hydratases, including the Krebs cycle aconitase and the Entner-Doudoroff pathway 6

180 enzyme A (CoA) species incorporated into the Krebs cycle, whereas the myocardial concentration of ace

181 and decrease the entry of pyruvate into the Krebs cycle-without compromising the consumption of oxyg

182 ottlenecks of carbon substrate flux into the Krebs cycle.

183 mplex for enhanced flux of pyruvate into the Krebs cycle.

184 This process links the Krebs cycle to oxidative phosphorylation and ATP synthes

185 ubtilis encodes aconitase, the enzyme of the Krebs citric acid cycle, which is responsible for the in

186 ymes of the tricarboxylic acid branch of the Krebs citric acid cycle.

187 le in cellular energetics as a member of the Krebs cycle and as complex II of the aerobic respiratory

188 ydratase-1 resulted in the inhibition of the Krebs cycle and enhanced pyruvate shunting toward the gl

189 is the only membrane-bound component of the Krebs cycle and in addition functions as a member of the

190 drogenase (PDH) is the main regulator of the Krebs cycle and is located upstream of the electron tran

191 xidizes succinate to fumarate as part of the Krebs cycle and reduces ubiquinone in the electron trans

192 ct of H(2)S required a basal activity of the Krebs cycle and was most pronounced at intermediate conc

193 Supranormal stimulation of the Krebs cycle by methyl pyruvate can, however, overwhelm i

194 ible glutathionylation and inhibition of the Krebs cycle enzyme alpha-ketoglutarate dehydrogenase.

195 ts showed that the control and fluxes of the Krebs cycle in heart disease can be studied using hyperp

196 d isocitrate dehydrogenase activities of the Krebs cycle increased at 2, 3, 12, and/or 14 h, and thes

197 hortage and a reduction in the levels of the Krebs cycle intermediate alpha-ketoglutarate (alpha-KG).

198 )cysteine (2SC) is formed by reaction of the Krebs cycle intermediate fumarate with cysteine residues

199 formed by a Michael addition reaction of the Krebs cycle intermediate, fumarate, with cysteine residu

200 s apoptosis was preceded by depletion of the Krebs cycle intermediates, was prevented by two Krebs cy

201 Disruption of the Krebs cycle is a hallmark of cancer, and MDH2 has been r

202 zyme of the tricarboxylic acid branch of the Krebs cycle, exhibited reduced growth yield in broth med

203 zyme of the tricarboxylic acid branch of the Krebs cycle, had a greatly reduced ability to sporulate.

204 wo components of the oxidative branch of the Krebs cycle, IDH and citrate synthase.

205 fumA genes, encoding key constituents of the Krebs cycle, proved to be repressed by the loss of both

206 zyme of the tricarboxylic acid branch of the Krebs cycle, was shown to be required for de novo synthe

207 ymes of the tricarboxylic acid branch of the Krebs cycle.

208 rganic acids, including intermediates of the Krebs cycle.

209 ate as part of the proper functioning of the Krebs cycle.

210 er experimental work on the structure of the Krebs TCA cycle metabolon.

211 To understand the many roles of the Krebs tricarboxylic acid (TCA) cycle in cell function, w

212 The enzymes of the Krebs tricarboxylic acid cycle in mitochondria are propo

213 atase, one of the constituent enzymes of the Krebs tricarboxylic acid cycle.

214 ion of genes involved in beta-oxidation, the Krebs cycle, and the electron transport chain concomitan

215 y acid carbons substantially replenished the Krebs cycle, and were incorporated into aspartate (a nuc

216 nd showed reduced substrate flux through the Krebs cycle compared with GSH.

217 Besides being oxidized through the Krebs cycle, proline is used to make citrate via reducti

218 to which indomethacin had been added to the Krebs buffer.

219 tanoin, which provides key substrates to the Krebs cycle in the brain, we wished to assess its therap

220 DH and alpha-ketoglutarate (alpha-KG) to the Krebs cycle, hence increasing the beta-cell ATP-to-ADP r

221 carbon metabolism linking glycolysis to the Krebs cycle.

222 nitate, which is further catabolized via the Krebs cycle.

223 Aconitase activity associated with the Krebs cycle is also reduced in the striatum of PINK1(-/-

224 estigation of enzyme organization within the Krebs cycle metabolon was accomplished by in vivo cross-

225 These data suggest a common origin for these Krebs cycle enzymes in mitochondria and CFB group bacter

226 We show that this Krebs-cycle enzyme is essential for mtDNA maintenance in

227 mulation and (ii) energy deprivation through Krebs cycle disruption associated with branched-chain ke

228 d in the perfusate from rat liver exposed to Krebs-Ringer bicarbonate buffer only, 0-1mM [3,4-(13)C(2

229 odium-independent mechanism for transporting Krebs and citric acid cycle intermediates through the ep

230 ansporter-a membrane protein that transports Krebs cycle intermediates.

231 bs cycle intermediates, was prevented by two Krebs cycle substrates, but was unrelated to ATP synthes

232 Kidney proximal tubule cells take up Krebs cycle intermediates for metabolic purposes and for

233 ncentrations and decreased levels of urinary Krebs cycle metabolites when compared to controls, sugge

234 rations were inversely correlated with urine Krebs cycle metabolite concentrations.

235 (PV-HA) perfused rat liver (n = 6-10) using Krebs bicarbonate buffer at constant PV (12 ml min-1) an

236 Three groups were studied using Krebs-Henseleit buffer (KH): controls (12 mL/min, n = 6)

237 ntation and subsequent reperfusion with warm Krebs-Henseleit solution.

238 the at-risk population, when increased, were Krebs von den Lungen-6 (odds ratio [95% CI], 6.1 [3.0-12

239 = 77) later and placed in a tissue bath with Krebs-Henseleit buffer.

240 were initially perfused at 37 degrees C with Krebs-Ringer's (KR) solution (in mmol/L: Ca(2+) 2.5, K(+

241 were perfused (40 mL/min, 37 degrees C) with Krebs' solution in a recirculating system.

242 ere perfused as follows: seven controls with Krebs-Henseleit (KH) buffer (Group 1), five hearts with

243 t hearts were perfused at constant flow with Krebs-Henseleit buffer enriched with bovine red blood ce

244 The liver was removed and flushed with Krebs-Ringer buffer solution with 3% albumin, and the op

245 We perfused isolated working rat hearts with Krebs-Henseleit buffer containing [2-3H]glucose (5 mmol/

246 nutes of low-flow (0.5 mL/min) ischemia with Krebs-Henseleit buffer with or without 11 mmol/L glucose

247 rat hearts were reperfused for 30 mins with Krebs-Henseleit solution alone (control, n = 8), or with

248 Hearts were labeled for 40 minutes with Krebs-Henseleit buffer containing [35S]methionine, and t

249 e hearts were reperfused for 30 minutes with Krebs-Henseleit buffer.

250 fused initially by the Langendorff mode with Krebs-Henseleit buffer (KHB) for 15 minutes in the absen

251 used for 10 min in the Langendorff-mode with Krebs-Henseleit buffer in the absence or presence of bri

252 ts and perfused in the Langendorff mode with Krebs-Henseleit solution under the following conditions:

253 ant myocardial washout of (99m)TcN-NOET with Krebs-Henseleit buffer.

254 perfusion with plain Krebs solution, or with Krebs solution to which L-NAME and/or indomethacin had b

255 king Sprague-Dawley rat hearts perfused with Krebs buffer and glucose, or glucose plus insulin or bet

256 abbit hearts were isolated and perfused with Krebs buffer.

257 The cells were continuously perfused with Krebs equilibrated with 5% CO2/air or 5% CO2/argon at ro

258 In hearts perfused with Krebs solution alone, nitric oxide (NO) release into the

259 s with intact endothelium were perfused with Krebs solution containing phenylephrine.

260 ast in agarose gel threads and perfused with Krebs-Henseleit bicarbonate buffer.

261 Rat hindlimbs were perfused with Krebs-Henseleit bicarbonate containing 4% bovine serum a

262 abbit hearts were retrogradely perfused with Krebs-Henseleit buffer (KHB).

263 ir wild-type littermates, were perfused with Krebs-Henseleit buffer and subjected to 20 minutes of is

264 Hearts were perfused with Krebs-Henseleit buffer at 85 mm Hg.

265 olated working rat hearts were perfused with Krebs-Henseleit buffer containing only glucose 5 mmol/L

266 Rabbit hearts were perfused with Krebs-Henseleit buffer on a Langendorff apparatus.

267 Rat hearts were perfused with Krebs-Henseleit solution containing glucose and either n

268 lated canine atria (n=20) were perfused with Krebs-Henseleit solution.

269 d storage (SCS), livers were reperfused with Krebs-Henseleit buffer solution at 37 degree C for 30 mi

270 cally exposed and continuously suffused with Krebs Ringer bicarbonate warmed to 37 degrees C.

271 transducer and a motor arm, superfused with Krebs-Henseleit (K-H) solution (pH 7.4, room temperature

272 0.01 vs. control mesenteries superfused with Krebs-Henseleit buffer).

273 e measured in rat trabeculae superfused with Krebs-Henseleit solution, with or without propofol or is

274 ts was perfused at physiologic workload with Krebs-Henseleit buffer containing 10 mmol/L glucose; a s