ライフサイエンスコーパス: metabolic acidosis

1 pH 6.8, followed by 2 h at pH 7.4 (in vitro metabolic acidosis).

2 ponatremia, but in large volumes may lead to metabolic acidosis.

3 s led to new ways of managing hyperchloremic metabolic acidosis.

4 terone, with salt wasting, hyperkalemia, and metabolic acidosis.

5 sis in the whole cohort and in patients with metabolic acidosis.

6 al Lowe syndrome, none of these patients had metabolic acidosis.

7 ren deficient in enzyme activity have severe metabolic acidosis.

8 rbonate load, but there was no effect during metabolic acidosis.

9 ertension, hyperkalemia, hyperchloremia, and metabolic acidosis.

10 w-grade, pathogenically significant systemic metabolic acidosis.

11 y impaired renal acid secretion resulting in metabolic acidosis.

12 potension, decreased urine output (UOP), and metabolic acidosis.

13 higher than that of controls, indicative of metabolic acidosis.

14 adaptation helps maintain homeostasis during metabolic acidosis.

15 evented IC subtype alterations and magnified metabolic acidosis.

16 I)--features hypertension, hyperkalemia, and metabolic acidosis.

17 ith weight loss, hypertonic dehydration, and metabolic acidosis.

18 luding hyperkalemia, hyperaldosteronism, and metabolic acidosis.

19 unmeasured anions were the leading cause of metabolic acidosis.

20 n in the papilla, and chronic hyperchloremic metabolic acidosis.

21 ociated with hyperkalemia and hyperchloremic metabolic acidosis.

22 ogical tissue damage despite more pronounced metabolic acidosis.

23 ssium channel activation and respiratory and metabolic acidosis.

24 nd increased urinary acid elimination during metabolic acidosis.

25 c4a7) in rat brain is upregulated by chronic metabolic acidosis.

26 d plexus epithelia was unaffected by chronic metabolic acidosis.

27 ule reabsorption of bicarbonate resulting in metabolic acidosis.

28 tion of breathing elicited by hypercapnia or metabolic acidosis.

29 bicarbonate therapy for patients with severe metabolic acidosis.

30 used in resuscitation can themselves produce metabolic acidosis.

31 e mixed acid-base disorders in patients with metabolic acidosis.

32 a further decrease of PMo2 by 68% and worse metabolic acidosis.

33 and hippocampal neurones was in response to metabolic acidosis (22 mm--> 14 mm HCO(3)(-)), which cau

34 l manifestations: cardiac (3.8 [2.88-4.91]), metabolic acidosis (3.7 [2.7-5.0]), renal failure (1.9 [

35 ackground ventilatory drive, increasing with metabolic acidosis (-6.7 mm Hg) and nonhypoxic periphera

36 Patients who have metabolic acidosis, a bicarbonate or inotrope/vasopresso

37 have alkaline urine but do not exhibit overt metabolic acidosis, a renal phenotype similar to that of

38 on disease, metabolism abnormalities such as metabolic acidosis, abnormal fatty acid metabolism, hype

39 ular acidoses (dRTA), whose features include metabolic acidosis accompanied by disturbances of potass

40 cytokines and did not exhibit hypothermia or metabolic acidosis after CLP.

41 at administration of AM/AMBP-1 would prevent metabolic acidosis after uncontrolled hemorrhage via dow

42 Metabolic acidosis alone induces neovascularization simi

43 lood pressure, core temperature, and greater metabolic acidosis (analysis of variance, P < 0.0001).

44 out the study period; 1,609 met criteria for metabolic acidosis and 145 had normal acid-base values.

45 tal renal tubular acidosis, as manifested by metabolic acidosis and alkaline urine pH.

46 nal, bone and mineral metabolism, correcting metabolic acidosis and anemia, achieving excellent blood

47 ised by more severe inflammation, shock, and metabolic acidosis and by worse clinical outcomes.

48 on was then compared between rats in chronic metabolic acidosis and control rats.

49 ts in energy supply and demand can result in metabolic acidosis and diminished delivery and/or availa

50 cause high-protein (HP) Western diets induce metabolic acidosis and hypercalciuria.

51 ensue from a mitochondrial dysfunction (e.g. metabolic acidosis and hyperthermia) and that MH-suscept

52 The findings suggest that diet-induced metabolic acidosis and its sequelae in humans eating con

53 Metabolic acidosis and lactatemia resolved significantly

54 H(3)), an environmental pollutant leading to metabolic acidosis and liver and kidney toxicity; dimeth

55 tation with Hextend was associated with less metabolic acidosis and longer survival in this experimen

56 dded benefits but alleviated the severity of metabolic acidosis and mortality after LNA.

57 rongly associated with mortality were severe metabolic acidosis and need for endotracheal intubation.

58 ciated with mortality, whereas patients with metabolic acidosis and noncardiac structural or chromoso

59 Ethylene glycol poisoning causes metabolic acidosis and renal failure and may cause death

60 Mild hyperchloremia, metabolic acidosis and suppressed plasma renin activity

61 HF patients experienced faster correction of metabolic acidosis and tended to be more rapidly weaned

62 oplasty in childhood can lead to significant metabolic acidosis and that compensation with bone buffe

63 ive anions responsible for the main types of metabolic acidosis and the outcome.

64 rinary citrate excretion fourfold in chronic metabolic acidosis and threefold in K+-depletion.

65 olloids are associated with a hyperchloremic metabolic acidosis, and a hypocoagulable state although

66 lloids) are associated with a hyperchloremic metabolic acidosis, and a hypocoagulable state, although

67 The patient developed cardiac arrhythmia, metabolic acidosis, and cardiac failure, which resulted

68 decreased mean arterial pressure, increased metabolic acidosis, and decreased urine output.

69 ominal tenderness, severe hepatic cytolysis, metabolic acidosis, and hemodynamic dysfunction.

70 n, increased blood oxygen content, prevented metabolic acidosis, and improved 6-hour survival (42% in

71 d hyponatremia, hyperkalemia, hypercalcemia, metabolic acidosis, and increased serum lithium concentr

72 issive hypercapnia in the presence of shock, metabolic acidosis, and multi-organ system dysfunction m

73 membrane oxygenation, development of severe metabolic acidosis, and number of early extubations in t

74 increased expression in response to chronic metabolic acidosis, and originally was cloned as a tumor

75 ed by processes other than the post-exercise metabolic acidosis, and that changes in peripheral chemo

76 scle protein breakdown include inflammation, metabolic acidosis, angiotensin II, and neural and hormo

77 id excretion and bicarbonate reabsorption in metabolic acidosis are closely similar to those operativ

78 Although the protein catabolic effects of metabolic acidosis are well established, it is unclear w

79 provement in hemodynamics, urine output, and metabolic acidosis, as well as a perceived increase in s

80 The mice developed metabolic acidosis, as well as profound acidemia and hyp

81 The models predict that the graded metabolic acidosis associated with mild renal failure af

82 erely injured trauma patients, the degree of metabolic acidosis at the time of admission identified t

83 n two study groups: children presenting with metabolic acidosis (base deficit >8) and children withou

84 Patient diagnosis, absence of severe metabolic acidosis before ECMO support, and uncomplicate

85 n with hyperkalemia/potassium level and with metabolic acidosis/bicarbonate level.

86 Methanol poisoning may result in metabolic acidosis, blindness, and death.

87 provide control data with a varying level of metabolic acidosis, but with no prior exercise.

88 Chronic metabolic acidosis caused hypocitraturia in rats and inc

89 Metabolic acidosis causes a reversal of polarity of HCO(

90 d acidotic rats is mediated by NHE3 and that metabolic acidosis causes increased expression of renal

91 ral markers of cardiovascular compromise and metabolic acidosis correlate with mortality.

92 l metabolism, in addition to roles played by metabolic acidosis, cytokines, and degradation of parath

93 cluding urinary tract infections, hematuria, metabolic acidosis, dehydration, and reflux pancreatitis

94 Evaluation II score, mechanical ventilation, metabolic acidosis, delirium on the prior day, and coma

95 acidosis with blood pH </= 7.15, persistent metabolic acidosis despite adequate supportive measures

96 dehydration, hypotension, hyperkalaemia and metabolic acidosis, despite elevated aldosterone levels.

97 nd shock refractory to inotropic agents, and metabolic acidosis developed in the patient within 2 hou

98 er of pathophysiologic conditions, including metabolic acidosis, diabetes, sepsis, and high angiotens

99 Acute metabolic acidosis did not affect the PTH-iCa curve.

100 ated by liver failure, renal failure, severe metabolic acidosis, disseminated intravascular coagulopa

101 y as capable as control livers in correcting metabolic acidosis during the first 24 hr posttransplant

102 weaning grew to adulthood; however, they had metabolic acidosis, elevated blood concentrations of Na(

103 nate synthesis from glutamine during chronic metabolic acidosis facilitate the excretion of acids and

104 gh energy phosphate stores and correction of metabolic acidosis following brief periods of global isc

105 rough feedback inhibition, likely to prevent metabolic acidosis from occurring.

106 NBC1-/- mice exhibited severe metabolic acidosis, growth retardation, reduced plasma N

107 y massive urinary excretion of 5-oxoproline, metabolic acidosis, haemolytic anaemia and central nervo

108 ll alkali supplementation trials, correcting metabolic acidosis has a strikingly broad array of poten

109 known to decrease bone mineral density, and metabolic acidosis has been shown to increase glucocorti

110 In vitro, metabolic acidosis has been shown to initially induce ph

111 me featuring hypertension, hyperkalaemia and metabolic acidosis, has revealed previously unrecognized

112 Children with severe malaria and metabolic acidosis have evidence of hypovolemia and evid

113 and proinflammatory mediators and correcting metabolic acidosis, high-volume hemofiltration (HVHF) mi

114 renal insufficiency, high plasma potassium, metabolic acidosis, hydronephrosis of varying severity,

115 erventions specifically targeting hypoxemia, metabolic acidosis, hyperglycemia, and cardiovascular in

116 ning, Atp6v0a4(-/-) mice demonstrated severe metabolic acidosis, hypokalemia, and early nephrocalcino

117 These results suggest that during acute metabolic acidosis, IMCD 11 beta-HSD2 is inhibited and m

118 Uremic metabolic acidosis impairs insulin signaling, which norm

119 definitive trial testing whether correcting metabolic acidosis improves clinical outcomes has not be

120 only transiently for 1 hr, and caused severe metabolic acidosis in all animals.

121 E-subunit; however, the greater severity of metabolic acidosis in Atp6v1b1(-/-) mice after oral acid

122 abrogation of weight loss, dehydration, and metabolic acidosis in inoculated pigs, and LT complement

123 symptoms, secondary hyperparathyroidism, and metabolic acidosis in patients with chronic renal failur

124 a demonstrating the benefits of azotemia and metabolic acidosis in survival of patients with metastat

125 tion (H+ secretion) in OMCD is stimulated by metabolic acidosis in vivo and in vitro by an increase i

126 that the osteopenia observed in response to metabolic acidosis in vivo is not due to an increase in

127 n after hemorrhagic shock is associated with metabolic acidosis, in which the up-regulated endothelin

128 In conclusion, metabolic acidosis increases ET-1 expression, which incr

129 Chronic metabolic acidosis increases proximal tubular citrate up

130 Metabolic acidosis increases urine calcium excretion wit

131 etion by the kidney and resulted in a nongap metabolic acidosis, indicating that GPR4 is required to

132 NH4Cl gavage in the neonatal rat produces a metabolic acidosis-induced retinopathy which serves as a

133 In summary, the hypocitraturia of chronic metabolic acidosis is associated with an increase in ATP

134 Metabolic acidosis is associated with increased urinary

135 Metabolic acidosis is associated with poor outcomes in C

136 entifying these individuals with subclinical metabolic acidosis is challenging, but recent results su

137 Metabolic acidosis is common in septic shock, yet few da

138 sed brush border Na+-H+ exchange observed in metabolic acidosis is due to increased expression of NHE

139 The intraoperative development of metabolic acidosis is frequently attributed to hypovolem

140 f the rat renal glutaminase (GA) mRNA during metabolic acidosis is mediated by a pH-response element

141 Urine pH is more alkaline and metabolic acidosis is more severe in Atp6v1b1(-/-) mice

142 Metabolic acidosis is not uncommon in CKD and is linked

143 Metabolic acidosis is partially compensated by a pronoun

144 hloride levels should be assessed whenever a metabolic acidosis is seen perioperatively.

145 ock, as measured by systemic hypotension and metabolic acidosis, is significantly associated with a h

146 Our data also support the idea that metabolic acidosis itself can lead to impaired intrapulm

147 tomy and urinary diversion may cause chronic metabolic acidosis, leading to long-term bone loss in pa

148 intractable myocardial failure preceded by a metabolic acidosis, lipaemic plasma, fatty infiltration

149 During metabolic acidosis (MAc), AE3 speeds initial acidificati

150 ular acidification during the early phase of metabolic acidosis (MAc), not just in neurons but, surpr

151 Dietary patterns that promote mild metabolic acidosis may have a negative effect on bone de

152 paired acid excretion in CKD, with potential metabolic acidosis, may contribute to the progression of

153 opics and the prevalence and risk factors of metabolic acidosis, mechanisms of acid-mediated organ in

154 cate that AM/AMBP-1 administration prevented metabolic acidosis, mitigated organ injury, down-regulat

155 mal babies, and those with mixed respiratory/metabolic acidosis (more profound and prolonged hypoxia)

156 the shock-related lactic acidosis but caused metabolic acidosis, most likely resulting from reduced c

157 y urine, variable hyperchloremic hypokalemic metabolic acidosis, nephrocalcinosis, and nephrolithiasi

158 e of a normal salt intake led to a degree of metabolic acidosis not significantly different from that

159 Although metabolic acidosis occurs in both hypovolaemia and malar

160 Atp6v1b1vxt/vtx mice do not recapitulate the metabolic acidosis of dRTA patients, they provide a new

161 resent study addressed the effect of chronic metabolic acidosis on a cytosolic enzyme of citrate meta

162 Therefore, the effect of pure metabolic acidosis on the developing retinal vasculature

163 s shifted from secretion to absorption after metabolic acidosis or acid incubation of the CCD.

164 ECLS, patients who develop renal failure or metabolic acidosis or undergo venoarterial ECLS should b

165 tions include volume overload, hyperkalemia, metabolic acidosis, overt uremia, and even progressive a

166 s of dehydration, electrolyte imbalance, and metabolic acidosis (P < 0.05).

167 Mice infected with P. berghei exhibit (i) metabolic acidosis (pH < 7.3) associated with elevated p

168 icipated events were categorized as isolated metabolic acidosis (pH <7.20), hypercapnia (P(CO2), >70

169 petitive substrate methylaminoisobutyrate or metabolic acidosis (pH 7.1) depleted intracellular L-Gln

170 asma urea nitrogen (6.7 +/- 2.53 mmol/L), or metabolic acidosis (pH: 7.36 +/- 0.05).

171 of a trauma patient with severe unexplained metabolic acidosis, possibly attributable to the vasocon

172 creased urinary calcium excretion induced by metabolic acidosis predominantly results from increased

173 Paco2 and Pao2 remained stable, but metabolic acidosis progressed, as expected, throughout t

174 Metabolic acidosis promotes muscle wasting, and the net

175 3 days included hyperglycemia with resultant metabolic acidosis, pulmonary dysfunction, nausea, vomit

176 owing criteria was met: severe hyperkalemia, metabolic acidosis, pulmonary edema, blood urea nitrogen

177 onate administration to patients with severe metabolic acidosis remains controversial.

178 rdiac symptoms, rhabdomyolosis, hypotension, metabolic acidosis, renal failure, and age each affected

179 Profound hypotension, leukopenia, metabolic acidosis, renal impairment, thrombocytopenia,

180 per 1 mg/dl increase in total bilirubin) and metabolic acidosis (RR, 0.95; 95% CI, 0.90 to 0.99 per 1

181 In rats and humans, metabolic acidosis stimulates protein degradation and gl

182 Chronic metabolic acidosis stimulates the catabolism of bone and

183 One complication of uremia, metabolic acidosis, stimulates the degradation of branch

184 A metabolic acidosis study was performed in rats with 1, 4

185 ation of trauma patients, may exacerbate the metabolic acidosis that occurs with injury, and this aci

186 The disease manifests as metabolic acidosis that significantly slows the growth r

187 ervation of visual acuity, the resolution of metabolic acidosis, the inhibition of formic acid produc

188 During the response to metabolic acidosis, the intercalated cell of the collect

189 urones indicates that, except in response to metabolic acidosis, the neurones from the chemosensitive

190 In patients with metabolic acidosis, the results were similar.

191 eating Western diets have chronic, low-grade metabolic acidosis, the severity of which is determined

192 rates, but it is not clear if it responds to metabolic acidosis to increase H+ secretion.

193 arterial hypertension with hyperkalemia and metabolic acidosis, unmasked a complex multiprotein syst

194 The effects of low (metabolic acidosis) versus normal bicarbonate dialysis w

195 Acetazolamide induces a metabolic acidosis via an alternative biochemical mechan

196 In treated animals, urine output was higher, metabolic acidosis was attenuated, and renal tubular arc

197 Metabolic acidosis was common at presentation (mean base

198 lated from rats with 5 days of NH4Cl-induced metabolic acidosis was increased 1.5-fold compared with

199 Metabolic acidosis was one of the earliest complications

200 Metabolic acidosis was prevented in the 4-aminopyridine

201 antibody-treated animals, UOP was decreased, metabolic acidosis was worsened, and median survival tim

202 on, as reflected by a hyperosmolar anion gap metabolic acidosis, was observed in critically ill adult

203 base deficit (as a reflection of severity of metabolic acidosis) were recorded immediately before the

204 Mild metabolic acidosis, which can be caused by diet, may res

205 locking muscle wasting include correction of metabolic acidosis, which can suppress muscle protein lo

206 He developed a significant metabolic acidosis with a lactic acid level of 10.9 mmol

207 osis in humans, a condition characterized by metabolic acidosis with an inappropriately alkaline urin

208 thanol: coma, seizures, new vision deficits, metabolic acidosis with blood pH </= 7.15, persistent me

209 denced by a high anion gap (> or =15 mmol/L) metabolic acidosis with elevated osmol gap (> or =10 mOs

210 s of autosomal recessive dRTA include severe metabolic acidosis with inappropriately alkaline urine,

211 spiratory alkalosis developed, followed by a metabolic acidosis with increased levels of blood lactat

212 phalopathy, failure to thrive, and recurrent metabolic acidosis with intercurrent infections.

213 oad, whereas Rhcg(-/-) mice developed severe metabolic acidosis with reduced ammonuria and high morta

214 actic, unmeasured anions, and hyperchloremic metabolic acidosis with that of patients without acid-ba