• Journal of Veterinary Clinics
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• v.27 no.3
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• pp.257-261
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• 2010

The development of blood ionic changes could be precipitated in acid-base disorder and subsequent treatment. As technology for detecting circulating ionized $Mg^{2+}$ (the most interesting form with respect to physiological and biological properties) is now available in veterinary clinical medicine. This present study investigated the changes of whole blood ionized $Mg^{2+}$ correlated with acute metabolic and respiratory alkalosis in rodent model. Metabolic alkalosis was induced by intravenous infusion with $NaHCO_3$ and mechanical hyperventilation was applied for respiratory alkalosis. We founded that the blood ionized $Mg^{2+}$ could be reversibly decreased by the $NaHCO_3$-induced acute metabolic alkalosis but irreversibly increased by the mechanical hyperventilation-induced respiratory acidosis and respiratory acidosis. We suggested that the potential change in blood suggested that the potential change in blood ionized $Mg^{2+}$ should be counted in treatment of acid-base disorders.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.27 no.2
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• pp.88-94
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• 2024

Purpose: Infantile hypertrophic pyloric stenosis (IHPS) is a common gastrointestinal disease in neonates and hypochloremia metabolic alkalosis is a typical laboratory finding in affected patients. This study aimed to analyze the clinical characteristics of infants with IHPS and evaluate the association of clinical and laboratory parameters with ultrasonographic findings. Methods: Infants diagnosed with IHPS between January 2017 and July 2022 were retrospectively evaluated. Results: A total of 67 patients were included in the study. The mean age at diagnosis was 40.5±19.59 days, and the mean symptom duration was 11.97±9.91 days. The mean pyloric muscle thickness and pyloric canal length were 4.87±1.05 mm and 19.6±3.46 mm, respectively. Hyponatremia and metabolic alkalosis were observed in five (7.5%) and 36 (53.7%) patients, respectively. Serum sodium (p=0.011), potassium (p=0.023), and chloride levels (p=0.015) were significantly lower in patients with high bicarbonate levels (≥30 mmol/L). Furthermore, pyloric canal length was significantly higher in patients with high bicarbonate levels (p=0.015). To assess metabolic alkalosis in IHPS patients, the area under the receiver operating characteristic curve of pyloric canal length was 0.910 and the optimal cutoff value of the pyloric canal length was 23.5 mm. Conclusion: We found a close association between laboratory and ultrasonographic findings of IHPS. Clinicians should give special consideration to patients with pyloric lengths exceeding 23.5 mm and appropriate fluid rehydration should be given to these patients.

• Asian-Australasian Journal of Animal Sciences
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• v.31 no.2
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• pp.263-269
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• 2018

Objective: Heat stress (HS) triggers oxidative stress and respiratory alkalosis in pigs. The objective of this experiment was to study whether a short-term supranutritional amount of dietary vitamin E (VE) can mitigate oxidative stress and respiratory alkalosis in heat-stressed pigs. Methods: A total of 24 pigs were given either a control diet (17 IU/kg VE) or a high VE (200 IU/kg VE; HiVE) diet for 14 d, then exposed to thermoneutral (TN; $20^{\circ}C$, 45% humidity) or HS ($35^{\circ}C$, 35% to 45% humidity, 8 h daily) conditions for 7 d. Respiration rate and rectal temperature were measured three times daily during the thermal exposure. Blood gas variables and oxidative stress markers were studied in blood samples collected on d 7. Results: Although HiVE diet did not affect the elevated rectal temperature or respiration rate observed during HS, it alleviated (all p<0.05 for diet${\times}$temperature) the loss of blood $CO_2$ partial pressure and bicarbonate, as well as the increase in blood pH in the heat-stressed pigs. The HS reduced (p = 0.003) plasma biological antioxidant potential (BAP) and tended to increase (p = 0.067) advanced oxidized protein products (AOPP) in the heat-stressed pigs, suggesting HS triggers oxidative stress. The HiVE diet did not affect plasma BAP or AOPP. Only under TN conditions the HiVE diet reduced the plasma reactive oxygen metabolites (p<0.05 for diet${\times}$temperature). Conclusion: A short-term supplementation with 200 IU/kg VE partially alleviated respiratory alkalosis but did not reduce oxidative stress in heat-stressed pigs.

• Journal of Biomedical Engineering Research
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• v.14 no.4
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• pp.349-354
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• 1993

To investigate the relations between the physical constitutions, the acid-base balance, and the autonomic nervous function, the blood gas, the heart rate and the concentrations of Na, K of serum were measured pre-and poststimulation. As the result, it is shown that in the normal condition the macro-negative(strong liver- weak lung type) is the metabolic alkalosis, the macro-positive (strong lung-weak liver type) is the metabolic acidosis, the micro-negative(strong kidney-weak spleen type) is the alkalosis and the micro-positive (strong spleen-weak kidney type) is the acidosis. And the ntacro-positive and micro-positive are the sympathetic lead, the macro-negative and micro-negative are the parasympathetic lead. In the macro-positive and micro-positive subjects, the concentration of K in serum is relatively high. This si coincided with the acidosis. But in the macro-negative and micro-negative subjects, the concentration of K in serum is relatively low. This is coincided with the alkalosis.

• The Korean Journal of Physiology
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• v.5 no.2
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• pp.41-44
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• 1971

Thiocyanate space was determined in 23 bilaterally nephrectomized rabbits in acute metabolic acidosis and alkalosis. Acid-base disturbances were induced by the infusion of 0.3 N HCI or 0.3 N NaOH solution intravenously with the rate of 1 ml/min for 40 to 60 minutes. The blood pressure was monitored throughout the experiment and no changes in blood pressure was confirmed. The following results were obtained. 1. In the saline infused control rabbits, PH was 7.385 with negligible change in pH after the infusion, SCN space was 23.6% of body weight. 2. In the metabolic acidosis group, pH dropped from 7.417 to 7 130 and SCN space was 22.8% of body weight and suggested a negligible change in the extracellular space volume. 3. In the metabolic alkalosis group, pH increased from 7.393 to 7.478 and SCN space was 25.7% of body weight which confirmed a significant increase in the extracellular space volume.

• Journal of Yeungnam Medical Science
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• v.33 no.1
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• pp.48-51
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• 2016

Milk-alkali syndrome (MAS), a triad of hypercalcemia, metabolic alkalosis, and renal failure, is associated with ingestion of large amounts of calcium and absorbable alkali. MAS is the third most common cause of hypercalcemia in hospital, after primary hyperparathyroidism and malignant neoplasm. MAS is not often reported in the Korean literature. We describe MAS secondary to intake of calcium citrate for the treatment of osteoporosis with thoracic spine compression fracture. A 70-year-old man presented to our hospital with a 1-week history of general weakness and lethargy. He was found with acute kidney injury (serum creatinine, 4.6 mg/dL), hypercalcemia (total calcium, 14.8 mg/dL), and alkalosis. Laboratory evaluation excluded both hyperparathyroidism and malignancy. Mental status and serum calcium level was normalized within a week after proper hydration and intravenous administration of furosemide. However, he developed aspiration pneumonia, pseudomembranous colitis, and sepsis with multi-organ failure. Despite intensive treatment including inotropics, mechanical ventilation, and renal replacement therapy, he expired with no signs of renal recovery on the 28th hospital day.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.16 no.3
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• pp.195-199
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• 2013

Congenital chloride diarrhea (CLD) is a rare inherited autosomal recessive disorder. Mutations of the solute carrier family 26 member 3 gene cause profuse, chloride ion rich diarrhea, which results in hypochloremia, hyponatremia and metabolic alkalosis with dehydration. If a fetal ultrasound shows bowel dilatation suggestive of bowel obstruction, or if a neonate shows persistent diarrhea and metabolic alkalosis, CLD should be considered in the differential diagnosis. The severity of CLD varies, but early detection and early therapy can prevent complications including growth failure. We report a case of dizygotic twins affected by CLD who had been born to non-consanguineous parents. Both of them showed growth failure, but one of the twins experienced worse clinical course. He showed developmental delay, along with dehydration and severe electrolyte imbalance. He was diagnosed with CLD first at 6-month age, and then the other one was also diagnosed with CLD.

• Proceedings of the Korean Biophysical Society Conference
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• 2002.06b
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• pp.43-44
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• 2002

Basically all cells have the recovery mechanisms from the shift of intracellular pH (pHi). Many mechanisms were found and characterized. Generally the recovery mechanisms from acidosis are Na$\^$＋/-dependent, such as Na$\^$＋/-H$\^$＋/ exchange and Na$\^$＋/-HCO$_3$-symport. The recovery mechanism from alkalosis are Cl-dependent, such as Cl$\^$-/-HCO$_3$-exchange and Cal$\^$-/-OH$\^$-/ exchange.(omitted)

• Childhood Kidney Diseases
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• v.9 no.2
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• pp.255-262
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• 2005

Battler and Bartter-like syndromes, which include classic Bartter syndrome(type III), neonatat Bartter syndrome(type I, II or IV) and Gitelman syndrome, are autosomal - recessively inherited renal tubular disorders characterized b)r hypokalemic metabolic alkalosis, salt wasting and normal to low blood pressure. Neonatal Bartter syndrome is characterized by intrauterine polyhydramnios, premature delivery, life-threatening episodes of fever and dehydration, subsequent failure to thrive, and severe hypercalciuria with nephrocalcinosis and osteopenia. It is caused by mutations in NKCC2(type I), ROMK(type II) or BSND(type IV) genes. If diagnosed and treated early, the progression to renal failure can be prevented and catch-up growth and normal development are achieved. We report here a 6 month-old infant with neonatal Bartter syndrome who presented with hypokalemic metabolic alkalosis, polyhydramnios and premature delivery, persistent high fever and dehydration, failure to thrive, hypercalciuria, and nephrocalcinosis. He received indomethacin and potassium chloride per os and show ed catch-up growth and normal developmental profile at 19 months of age. (J Korean Soc Pediatr Nephrol 2005;9:255-262)

• Clinical and Experimental Pediatrics
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• v.46 no.3
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• pp.308-311
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• 2003

Congenital chloride diarrhea is a serious autosomal recessive disease, and defect of intestinal electrolyte absorption that involves, specifically, $Cl^-/{HCO_3}^-$ exchange in the distal part of the ileum and colon. The clinical feature is dominated by profuse, watery diarrhea containing high concentrations of chloride(>90 mmol/L) and sodium. The chloride loss results in severe dehydration with a hypochloremic alkalosis. The molecular pathology involves an epithelial $Cl^-/{HCO_3}^-$ exchanger protein. Mucosal ion transport is affected to differing degrees and the severity of the disease may thus vary. Recently, a gene defect on chromosome 7 has been identified. However, there was a deficit in replacement of fluid and electrolyte, abdominal distension remained and the character of stools was watery. We report a case of congenital chloride diarrhea in a premature female who presented with watery diarrhea containing high concentrations of chloride and abdominal distension.