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1 n diets, and none of the uremic animals were acidotic.
2 blood analysis revealed that they are mildly acidotic.
3                                 In muscle of acidotic adrenalectomized rats receiving dexamethasone,
4  renal cortex of rats that were made acutely acidotic also exhibit a similar increase in binding to t
5 iation (LTP) and mediates neuroprotection in acidotic and ischemic conditions.
6 arbonate reabsorption capacity was higher in acidotic and NHE3 null animals.
7                                In OMCDs from acidotic animals, and in OMCDs incubated in acid in vitr
8 ad an unusually mild clinical course without acidotic attacks.
9  turnover with intense exercise overcame the acidotic attenuation of carbohydrate-linked oxidative ph
10 crease UT-A protein in liver, rats were made acidotic, but not uremic, by feeding them HCl.
11 dosis would explain the predominance of this acidotic change; however, no increase in plasma volume o
12 I3-K/Akt pathway was evaluated in muscles of acidotic, CKD and pair-fed control rats under physiologi
13 n was greater in brush border membranes from acidotic compared with control rats.
14 urrent (INa) amplitude compared to WT; under acidotic conditions (pH 7.0) typically found with hypoxi
15 sine concentrations, in particular under the acidotic conditions associated with ischemia.
16 e of the IP(3) receptor or under nonspecific acidotic conditions.
17                                  For the non-acidotic days (day 1-8), diet contained 50:50 forage to
18 roximately half of the inhibition was due to acidotic effects of NMDA-mediated currents, as demonstra
19                        To distinguish direct acidotic effects on tracer pharmacokinetics from acidosi
20                                        These acidotic effects were largely retained following a singl
21 lu-co-Lys), to effect this transformation in acidotic environments.
22 ral corticosteroids to all patients with non-acidotic exacerbations of COPD requiring hospital admiss
23               We recruited patients with non-acidotic exacerbations of COPD who were randomly assigne
24 bioenergetically more active, hypoxemic, and acidotic femoral circulation (P<0.05 versus cerebral).
25 = 0 hr), and at death (7.0 +/- 0.3 hrs) were acidotic, hypocapnic, and hypothermic (rectal temperatur
26                                              Acidotic hypoxia stimulated lysosomal activity and autop
27               HIF-1alpha stabilization under acidotic hypoxia was transient, declining over 48 h.
28 ial anemia and can also benefit comatose and acidotic malaria patients.
29 cosal hypoperfusion does not account for the acidotic mucosal tonometric pH in endotoxic shock.
30 he inner stripes of kidneys from control and acidotic (NH4Cl-fed for 3 d) rabbits.
31 bicarbonate reabsorption but are only mildly acidotic owing to reduced glomerular filtration rate and
32 ignificantly more hypercarbic (p < 0.01) and acidotic (p < 0.01) than those undergoing conventional l
33 sed heterogeneity of calcium distribution in acidotic participants.
34                                              Acidotic patients had worse hemodynamic indicators, with
35                                              Acidotic patients received fluid resuscitation with eith
36 ption will provide insight into bone loss in acidotic patients with chronic kidney disease.
37 e early use of NIV for mildly and moderately acidotic patients with COPD in the general ward setting
38                    The initial protection by acidotic pH and glycine during simulated reperfusion was
39                     During chemical hypoxia, acidotic pH prevented cell death.
40                                  Glycine and acidotic pH prevented cell killing after reperfusion but
41 7.4) and during 45 minutes of perfusion with acidotic (pH 6.0) Tyrode's solution with (n=8) and witho
42 ere was a 61% higher H flux in segments from acidotic rabbits (11.3+/-0.2 vs. 7.0+/-0.2 pmol/min per
43                                 Tubules from acidotic rabbits showed higher rates of HCO3- absorption
44 larized to total retinal area was smaller in acidotic rats (94%+/-4% versus 96%+/-2%, P < 0.001).
45 ocampus showed a slight increase in NDCBE in acidotic rats (p=0.05).
46      BCKAD E1alpha subunit mRNA in muscle of acidotic rats given dexamethasone was increased 1.89-fol
47 y in brush border membranes from control and acidotic rats is mediated by NHE3 and that metabolic aci
48                                              Acidotic rats showed growth retardation (final weight 16
49 etinal neovascularization occurred in 36% of acidotic rats versus 5% of controls (P < 0.001).
50 nal cytosolic extracts prepared from acutely acidotic rats.
51 ntly increased by 50% in livers from uremic, acidotic rats; bicarbonate administration prevented the
52                                 At baseline, acidotic subjects had higher markers of bone turnover, l
53 until acid-challenged, when they became more acidotic than +/+ animals.
54 infarct (P < 0.0001), which in turn was more acidotic than hypoperfused tissue that survived (P < 0.0
55 on channel 1 which, when activated under the acidotic tissue conditions found in inflammatory lesions
56 culation but transforms spontaneously in the acidotic tumor microenvironment to a cell-penetrating pa
57 u][Cu(ATSM)] despite no evidence of it being acidotic when characterised by (31)P NMR.
58 later be withdrawn, but -/- animals remained acidotic with alkaline urine.