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1 , respectively, autosomal recessive forms of metabolic alkalosis.
2 is are closely similar to those operative in metabolic alkalosis.
3 ulation with secretin and often present with metabolic alkalosis.
4 ses numerous mechanisms that help to prevent metabolic alkalosis.
5 ia, hypophosphatemia, metabolic acidosis, or metabolic alkalosis.
6    Non-type A ICs excrete bicarbonate during metabolic alkalosis.
7 at SCTR is necessary for acute correction of metabolic alkalosis.
8 ential for renal base excretion during acute metabolic alkalosis.
9  by renal salt loss, marked hypokalemia, and metabolic alkalosis.
10 h respiratory alkalosis (5%--> 3% CO(2)) and metabolic alkalosis (22 mm--> 35 mm HCO(3)(-)), DeltapH(
11  (almitrine; -5.9 mm Hg) and decreasing with metabolic alkalosis (-3.7 mm Hg).
12  kidney caused hypotension, hypokalemia, and metabolic alkalosis, an exact mirror image of PHA-II.
13  was diagnosed with CF after presenting with metabolic alkalosis and hypokalemia.
14 steronism with hypokalemic and hypochloremic metabolic alkalosis and low to normal blood pressure.
15 toring, or emergencies such as hypoglycemia, metabolic alkalosis, and even COVID-19 patient care, a p
16 ion, and electrolyte imbalance (hypokalemia, metabolic alkalosis, and hypomagnesemia).
17 ines but had more frequent hypophosphatemia, metabolic alkalosis, and thrombocytopenia.
18 phatemia (aOR, 2.83; 95% CI, 1.82-4.40), and metabolic alkalosis (aOR, 2.60; 95% CI, 1.63-4.15).
19 consisting of a hypokalemic, hypomagnesemic, metabolic alkalosis associated with seizures, sensorineu
20 0.5 mEq/L; P < .001) and number of days with metabolic alkalosis (between-group difference, -1; 95% C
21 plasma secretin level increases during acute metabolic alkalosis, but its role in systemic acid-base
22 nic obstructive pulmonary disease (COPD) and metabolic alkalosis, but no large randomized placebo-con
23 ort in B-type of intercalated cells, whereas metabolic alkalosis caused the opposite changes in inter
24 e data indicate that in the setting of acute metabolic alkalosis, CBF is regulated by PaCO2 rather th
25 acidosis was never detected, although a mild metabolic alkalosis developed on day 30 of HDTBR by a me
26    In addition, PCO2 higher than 30 mm Hg or metabolic alkalosis did not have an effect on this proce
27 , oral base loading induced a dose-dependent metabolic alkalosis, fast urinary removal of base, and a
28                               Maintenance of metabolic alkalosis for any length of time means that re
29                               Maintenance of metabolic alkalosis generated by chloride depletion is o
30 ectrolyte homeostasis including hypokalaemic metabolic alkalosis; Gitelman's syndrome represents the
31                          Previous studies in metabolic alkalosis have demonstrated that two factors a
32   These data suggest that hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption.
33 epithelial Na(+) channel, caused hypokalemic metabolic alkalosis in ClC-K2(fl/fl) B1 ATPase mice.
34 n arterial pH per se in the setting of acute metabolic alkalosis in humans.
35 nduced urinary HCO(3) (-) excretion, explain metabolic alkalosis in patients with CF, and suggest fea
36 an extracellular alkali sensor that controls metabolic alkalosis in the regulation of the acid-base b
37 ered intravenously in cases of pure or mixed metabolic alkalosis, initiated within 48 hours of ICU ad
38                                     Although metabolic alkalosis is frequently not dangerous, in cert
39                                              Metabolic alkalosis is maintained by the excessive sweat
40              Surprisingly, NaHCO(3) -induced metabolic alkalosis (MAlk) and high-salt diet (HSD) also
41 requently not dangerous, in certain settings metabolic alkalosis may contribute to mortality and shou
42                                       In CF, metabolic alkalosis may contribute to the commonly reduc
43                                          The metabolic alkalosis of congenital chloride-losing diarrh
44  PaCO2 ) with and without acute experimental metabolic alkalosis on neurovascular coupling (NVC).
45 ined the effects of alkalosis (hypocapnic or metabolic alkalosis) on alveolar fluid reabsorption in t
46  amount of HCO(3)(-) into the urine leads to metabolic alkalosis [P.
47  microdose (15 microg/kg) pretreatment or by metabolic alkalosis (pH 7.60).
48 n of acid in KO mouse urine, leading to mild metabolic alkalosis ("renal tubular alkalosis").
49  process is greatly upregulated in models of metabolic alkalosis, such as following aldosterone admin
50 t diet, they developed hyponatremia and mild metabolic alkalosis, symptoms characteristic of human Ba
51  specifically volume overload, hyponatremia, metabolic alkalosis, uremia, and hyperglycemia, than tho
52  these findings, KO mice developed prolonged metabolic alkalosis when exposed to acute oral or intrap
53 r filtration rate, urinary NaCl wasting, and metabolic alkalosis with hypokalemia, thereby recapitula
54 ders manifested by hypokalemic hypochloremic metabolic alkalosis with normotensive hyperreninemic hyp
55 rofound volume depletion, renal failure, and metabolic alkalosis without hypokalemia, which were all