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1 to mild metabolic alkalosis ("renal tubular alkalosis").
2 ly-induced acid-base scenarios (acidosis and alkalosis).
3 this response was unaffected by respiratory alkalosis.
4 us mechanisms that help to prevent metabolic alkalosis.
5 ion gap changes of HCl acidosis and diuretic alkalosis.
6 ) acidosis and increased in diuretic-induced alkalosis.
7 tion, but elicits hypocapnia and respiratory alkalosis.
8 osphatemia, metabolic acidosis, or metabolic alkalosis.
9 in hyperthermia with and without respiratory alkalosis.
10 e A ICs excrete bicarbonate during metabolic alkalosis.
11 ing released from the small intestine during alkalosis.
12 necessary for acute correction of metabolic alkalosis.
13 sion primarily from heat-induced respiratory alkalosis.
14 ace environment, causing systemic hypocapnic alkalosis.
15 renal base excretion during acute metabolic alkalosis.
16 lation, ineffective efforts, and respiratory alkalosis.
17 salt loss, marked hypokalemia, and metabolic alkalosis.
18 isplay profound hypertension and hypokalemic alkalosis.
19 characterized by polyuria, hypokalemia, and alkalosis.
20 sis should replace the notion of contraction alkalosis.
21 toplasmic pH as cells underwent drug-induced alkalosis.
22 /L), consistent with compensated respiratory alkalosis.
23 vely, autosomal recessive forms of metabolic alkalosis.
24 constriction was suppressed by endotoxin and alkalosis.
25 sely similar to those operative in metabolic alkalosis.
26 ddition of 500 microM-5 mM Ba2+ restored the alkalosis.
27 on, hyponatremia, uremia, hyperglycemia, and alkalosis.
28 th secretin and often present with metabolic alkalosis.
29 ory alkalosis (5%--> 3% CO(2)) and metabolic alkalosis (22 mm--> 35 mm HCO(3)(-)), DeltapH(i)/DeltapH
32 G by human MIPP1 is sensitive to physiologic alkalosis; activity decreases 50% when pH rises from 7.0
35 changes in NVC; and (2) stepwise respiratory alkalosis and acidosis would each progressively reduce t
40 hniques resulted in intermittent respiratory alkalosis and hypoxia resulting in profoundly increased
42 ift of the VE-PET,CO2 relationship is due to alkalosis and not to hyperventilation; (ii) the increase
44 venously; it was associated with hypokalemic alkalosis and Pitressin-resistant impairment of urinary
45 n non-type A ICs function protecting against alkalosis and reveal a hitherto unrecognized need of bas
47 es C, this was not influenced by respiratory alkalosis, and (2) although biomarkers of pro-oxidation
48 emergencies such as hypoglycemia, metabolic alkalosis, and even COVID-19 patient care, a potential f
50 tion of patients with inherited hypokalaemic alkalosis, and suggest potential phenotypes in heterozyg
51 Plasma secretin levels increase during acute alkalosis, and the secretin receptor (SCTR) is functiona
53 a combined influence of Q10 and respiratory alkalosis; and (2) the net cerebral release of pro-oxida
54 p is due to the hyperventilation and not the alkalosis; and (iii) ventilatory sensitivity to hypoxia
57 sturbances, such as metabolic or respiratory alkalosis, are relatively common in critically ill patie
58 rized by renal salt wasting with hypokalemic alkalosis associated with epilepsy, ataxia, and sensorin
59 of a hypokalemic, hypomagnesemic, metabolic alkalosis associated with seizures, sensorineural deafne
60 P < .001) and number of days with metabolic alkalosis (between-group difference, -1; 95% CI, -2 to -
61 retin level increases during acute metabolic alkalosis, but its role in systemic acid-base homeostasi
62 ctive pulmonary disease (COPD) and metabolic alkalosis, but no large randomized placebo-controlled tr
64 itionally, chronic hypoxia, hypokalemia, and alkalosis can increase the block of hERG current by fent
66 ype of intercalated cells, whereas metabolic alkalosis caused the opposite changes in intercalated ce
67 icate that in the setting of acute metabolic alkalosis, CBF is regulated by PaCO2 rather than arteria
69 CO(3)(-) ] during acute respiratory acidosis/alkalosis contribute to cerebrovascular acid-base regula
71 as never detected, although a mild metabolic alkalosis developed on day 30 of HDTBR by a mean (95% co
73 d renal dysfunction, including hypochloremic alkalosis, diabetes insipidus, and salt-sensitive hypote
75 cal for the renal response to defend against alkalosis during an alkali load or chronic furosemide tr
76 or hypercapnic conditions; under respiratory alkalosis (e.g. hypoxia) RTN neurons are silent and the
77 n of diuretics in the setting of contraction alkalosis (eg, addition of acetazolamide), second agent
78 time in this model; and c) determine whether alkalosis enhanced vascular reactivity to subsequent pre
79 e loading induced a dose-dependent metabolic alkalosis, fast urinary removal of base, and a moderate
82 homeostasis including hypokalaemic metabolic alkalosis; Gitelman's syndrome represents the predominan
85 ter's syndrome, characterized by hypokalemic alkalosis, hypercalciuria, increased serum aldosterone,
91 anic disorder demonstrate reduced or blunted alkalosis, implicating increased lactate as overly compe
98 de resulted in a more pronounced hypokalemic alkalosis in male ATP6v1b1-/- versus Atp6v1b1+/+ mice th
99 nary HCO(3) (-) excretion, explain metabolic alkalosis in patients with CF, and suggest feasibility o
100 iochemical insights into the effect of acute alkalosis in preserving contracting muscle function duri
101 umulating bicarbonate but exhibited a slight alkalosis in response to copper either alone or with OA.
102 llular alkali sensor that controls metabolic alkalosis in the regulation of the acid-base balance.
104 ctor for determining neuronal activity, with alkalosis increasing and acidosis reducing excitability.
105 in isolated lamb lungs; b) determine whether alkalosis-induced pulmonary vasodilation decreases over
106 study sought to a) identify the mediator of alkalosis-induced pulmonary vasodilation in isolated lam
108 venously in cases of pure or mixed metabolic alkalosis, initiated within 48 hours of ICU admission an
111 the hypothesis that the respiratory-induced alkalosis is associated with lower circulating microvesi
113 ring is diminished by inhibition of ECA, the alkalosis is enhanced and NMDA receptor (NMDAR)-mediated
116 stimulation of [15N]urea synthesis in acute alkalosis is mediated via increased flux through PDG and
117 poreninemia, hypoaldosteronemia, hypokalemic alkalosis, low birth weight, failure to thrive, poor gro
118 Surprisingly, NaHCO(3) -induced metabolic alkalosis (MAlk) and high-salt diet (HSD) also increase
119 After an initial vasodilator response to alkalosis, many children with pulmonary hypertension exh
121 not dangerous, in certain settings metabolic alkalosis may contribute to mortality and should be trea
123 e temperature + 2 degrees C with respiratory alkalosis, microvesicles derived from endothelial cells,
124 hypoperfusion, it is possible that the mild alkalosis might help to attenuate cerebral inflammation.
128 ffects of alkalosis (hypocapnic or metabolic alkalosis) on alveolar fluid reabsorption in the isolate
129 compared after 20 and 100 mins of hypocarbic alkalosis or normocarbia in control and cyclooxygenase-i
130 s appropriate for patients with head injury, alkalosis, or hyponatremia, but in large volumes may lea
134 test showed partially compensated pulmonary alkalosis (pH, 7.43; normal range, 7.35-7.42; PCO(2), 26
136 ysis of patients with inherited hypokalaemic alkalosis resulting from salt-wasting has proved fertile
138 s greatly upregulated in models of metabolic alkalosis, such as following aldosterone administration
140 ey developed hyponatremia and mild metabolic alkalosis, symptoms characteristic of human Bartter synd
141 ure response to aldosterone and enhances the alkalosis that follows the administration of this steroi
142 or SDA), gastric pH, the postprandial blood alkalosis (the "alkaline tide") and growth in juvenile r
144 ects with panic disorder demonstrate greater alkalosis to hyperventilation, implicating increased lac
145 lly volume overload, hyponatremia, metabolic alkalosis, uremia, and hyperglycemia, than those patient
147 dings, KO mice developed prolonged metabolic alkalosis when exposed to acute oral or intraperitoneal
148 conditions, such as hypoxia, hypokalemia, or alkalosis, which may increase the risk of fentanyl-induc
149 may perturb the kidney's ability to correct alkalosis will lead to improved clinical approaches to d
150 on rate, urinary NaCl wasting, and metabolic alkalosis with hypokalemia, thereby recapitulating the p
153 ested by hypokalemic hypochloremic metabolic alkalosis with normotensive hyperreninemic hyperaldoster
154 mutations are characterized by hypokalaemic alkalosis with salt-wasting, low blood pressure, normal
155 lume depletion, renal failure, and metabolic alkalosis without hypokalemia, which were all corrected