ライフサイエンスコーパス: alkalosis

1 salt loss, marked hypokalemia, and metabolic alkalosis.

2 sis should replace the notion of contraction alkalosis.

3 isplay profound hypertension and hypokalemic alkalosis.

4 toplasmic pH as cells underwent drug-induced alkalosis.

5 /L), consistent with compensated respiratory alkalosis.

6 vely, autosomal recessive forms of metabolic alkalosis.

7 constriction was suppressed by endotoxin and alkalosis.

8 sely similar to those operative in metabolic alkalosis.

9 ddition of 500 microM-5 mM Ba2+ restored the alkalosis.

10 on, hyponatremia, uremia, hyperglycemia, and alkalosis.

11 characterized by polyuria, hypokalemia, and alkalosis.

12 us mechanisms that help to prevent metabolic alkalosis.

13 ion gap changes of HCl acidosis and diuretic alkalosis.

14 ) acidosis and increased in diuretic-induced alkalosis.

15 ory alkalosis (5%--> 3% CO(2)) and metabolic alkalosis (22 mm--> 35 mm HCO(3)(-)), DeltapH(i)/DeltapH

16 e; -5.9 mm Hg) and decreasing with metabolic alkalosis (-3.7 mm Hg).

17 For both respiratory alkalosis (5%--> 3% CO(2)) and metabolic alkalosis (22 m

18 G by human MIPP1 is sensitive to physiologic alkalosis; activity decreases 50% when pH rises from 7.0

19 Hypocarbic alkalosis acutely reduced hypoxic pulmonary vascular res

20 used hypotension, hypokalemia, and metabolic alkalosis, an exact mirror image of PHA-II.

21 yhydramnios, premature delivery, hypokalemic alkalosis and hypercalciuria.

22 osed with CF after presenting with metabolic alkalosis and hypokalemia.

23 hniques resulted in intermittent respiratory alkalosis and hypoxia resulting in profoundly increased

24 ift of the VE-PET,CO2 relationship is due to alkalosis and not to hyperventilation; (ii) the increase

25 venously; it was associated with hypokalemic alkalosis and Pitressin-resistant impairment of urinary

26 lectrolyte imbalance (hypokalemia, metabolic alkalosis, and hypomagnesemia).

27 tion of patients with inherited hypokalaemic alkalosis, and suggest potential phenotypes in heterozyg

28 ad more frequent hypophosphatemia, metabolic alkalosis, and thrombocytopenia.

29 p is due to the hyperventilation and not the alkalosis; and (iii) ventilatory sensitivity to hypoxia

30 Therefore, because acidosis and alkalosis are associated with altered PTH secretion in v

31 sturbances, such as metabolic or respiratory alkalosis, are relatively common in critically ill patie

32 of a hypokalemic, hypomagnesemic, metabolic alkalosis associated with seizures, sensorineural deafne

33 P < .001) and number of days with metabolic alkalosis (between-group difference, -1; 95% CI, -2 to -

34 ctive pulmonary disease (COPD) and metabolic alkalosis, but no large randomized placebo-controlled tr

35 ium and sodium depletion completely corrects alkalosis by a renal mechanism.

36 Alkalosis caused sustained vasodilation when pulmonary v

37 and estradiol contribute to the respiratory alkalosis common in cirrhotic patients.

38 n SBE: Acidosis deltaPaCO2 = 1.0 x deltaSBE, Alkalosis deltaPaCO2 = 0.6 x deltaSBE.

39 In this model an early respiratory alkalosis developed, followed by a metabolic acidosis wi

40 d renal dysfunction, including hypochloremic alkalosis, diabetes insipidus, and salt-sensitive hypote

41 tion, PCO2 higher than 30 mm Hg or metabolic alkalosis did not have an effect on this process.

42 or hypercapnic conditions; under respiratory alkalosis (e.g. hypoxia) RTN neurons are silent and the

43 time in this model; and c) determine whether alkalosis enhanced vascular reactivity to subsequent pre

44 Maintenance of metabolic alkalosis for any length of time means that renal homeos

45 Maintenance of metabolic alkalosis generated by chloride depletion is often attri

46 homeostasis including hypokalaemic metabolic alkalosis; Gitelman's syndrome represents the predominan

47 Previous studies in metabolic alkalosis have demonstrated that two factors are the pri

48 ndrome, featuring salt wasting, hypokalaemic alkalosis, hypercalciuria and low blood pressure.

49 ter's syndrome, characterized by hypokalemic alkalosis, hypercalciuria, increased serum aldosterone,

50 We examined the effects of alkalosis (hypocapnic or metabolic alkalosis) on alveola

51 Hypocarbic alkalosis, hypoxia, and infusion of the thromboxane mime

52 ta suggest that hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption.

53 Alkalosis impairs the natriuretic response to diuretics,

54 anic disorder demonstrate reduced or blunted alkalosis, implicating increased lactate as overly compe

55 ider CF when confronted with hypokalemia and alkalosis in a previously healthy patient.

56 Conceivably, correction of hypocapnic alkalosis in critically ill patients may contribute to t

57 Alkalosis in either compartment produced opposite effect

58 umulating bicarbonate but exhibited a slight alkalosis in response to copper either alone or with OA.

59 Reversal of the alkalosis increased the arterial and venous resistances,

60 in isolated lamb lungs; b) determine whether alkalosis-induced pulmonary vasodilation decreases over

61 study sought to a) identify the mediator of alkalosis-induced pulmonary vasodilation in isolated lam

62 Alkalosis inhibited the increase in arterial and venous

63 venously in cases of pure or mixed metabolic alkalosis, initiated within 48 hours of ICU admission an

64 Alkalosis is a clinical complication resulting from vari

65 othesized that therapy-induced alkalemia and alkalosis is associated with increased mortality.

66 for quantification of pHi regulation during alkalosis is discussed.

67 ring is diminished by inhibition of ECA, the alkalosis is enhanced and NMDA receptor (NMDAR)-mediated

68 Although metabolic alkalosis is frequently not dangerous, in certain settin

69 Metabolic alkalosis is maintained by the excessive sweat sodium ch

70 stimulation of [15N]urea synthesis in acute alkalosis is mediated via increased flux through PDG and

71 poreninemia, hypoaldosteronemia, hypokalemic alkalosis, low birth weight, failure to thrive, poor gro

72 After an initial vasodilator response to alkalosis, many children with pulmonary hypertension exh

73 Generation of alkalosis may be related to dysfunctional CFTR in the ki

74 not dangerous, in certain settings metabolic alkalosis may contribute to mortality and should be trea

75 Alkalemia and alkalosis occur frequently during CRRT, but they are not

76 The metabolic alkalosis of congenital chloride-losing diarrhea is caus

77 ffects of alkalosis (hypocapnic or metabolic alkalosis) on alveolar fluid reabsorption in the isolate

78 compared after 20 and 100 mins of hypocarbic alkalosis or normocarbia in control and cyclooxygenase-i

79 s appropriate for patients with head injury, alkalosis, or hyponatremia, but in large volumes may lea

80 (15 microg/kg) pretreatment or by metabolic alkalosis (pH 7.60).

81 ysis of patients with inherited hypokalaemic alkalosis resulting from salt-wasting has proved fertile

82 Chloride depletion alkalosis should replace the notion of contraction alkal

83 s greatly upregulated in models of metabolic alkalosis, such as following aldosterone administration

84 Acidosis enhances and alkalosis suppresses GABAA receptor neurotransmission wh

85 ure response to aldosterone and enhances the alkalosis that follows the administration of this steroi

86 monary vascular reactivity despite continued alkalosis therapy.

87 ects with panic disorder demonstrate greater alkalosis to hyperventilation, implicating increased lac

88 lly volume overload, hyponatremia, metabolic alkalosis, uremia, and hyperglycemia, than those patient

89 Brain alkalosis was associated with increased brain lactate/cr

90 may perturb the kidney's ability to correct alkalosis will lead to improved clinical approaches to d

91 itelman's syndrome, an inherited hypokalemic alkalosis with hypomagnesemia and hypocalciuria.

92 Inherited hypokalaemic alkalosis with low blood pressure can be divided into tw

93 ested by hypokalemic hypochloremic metabolic alkalosis with normotensive hyperreninemic hyperaldoster

94 mutations are characterized by hypokalaemic alkalosis with salt-wasting, low blood pressure, normal

95 lume depletion, renal failure, and metabolic alkalosis without hypokalemia, which were all corrected