• Neonatal Medicine
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• v.17 no.2
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• pp.155-160
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• 2010

Metabolic acidosis is commonly encountered issues in the management of critically ill neonates and especially of preterm infants during early neonatal days. In extremely premature infants, low glomerular filtration rate and immaturity of renal tubules to produce new bicarbonate causes renal bicarbonate loss. Higher intake of amino acids, relatively greater contribution of protein to the energy metabolism and mineralization process in growing bones are also responsible for higher acid load in premature infant than in adult. Despite widespread use of sodium bicarbonate in the management of severe metabolic acidosis, use of sodium bicarbonate in premature infants should be restricted to a reasonable but unproven exception such as ongoing renal loss. Despite concern about the low pH value (<7.2) which can compromise cellular metabolic function, no treatment guideline has been established regarding the management of metabolic acidosis in premature infants. Appropriately powered randomized controlled trials of base therapy to treat metabolic acidosis in critically ill newborn infants are demanding.

• Journal of Chest Surgery
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• v.17 no.1
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• pp.101-109
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• 1984

The influences of acute respiratory and metabolic acid-base disturbances on the carotid, renal and coronary blood flow were measured in dogs. Respiratory acidosis was induced by artificial respiration with 8% CO2 -02 gas mixture and respiratory alkalosis was induced by hyperventilation under the control of respirator. Metabolic acidosis and metabolic alkalosis were induced by intravenous infusion of 0.3N hydrochloric acid and 0.6M sodium bicarbonate solution. To observe the effect of hyperkalemia, isotonic potassium chloride solution was infused. CVI electromagnetic flowmeter probes were placed on the left common carotid artery, left renal artery and left circumflex coronary artery. Each flow was recorded on polygraph. 1. The carotid blood flow showed rapid showed rapid and marked increase in acute respiratory acidosis. Even in the cases when arterial blood pressure was lowered during the state of respiratory acidosis, carotid blood flow increased. By the infusion of hydrochloric acid, carotid blood flow increased slowly and returned to the previous label after discontinuation of the infusion. Carotid blood flow also increased by the infusion of large amount of sodium bicarbonate, but it might be the combined effect of expansion of extracellular fluid and compensatory elevation of carbon dioxide tension. 2.The renal blood flow remained unchanged during the acute acid-base disturbances, suggesting effective autoregulation. Renal blood flow, however, increased very slowly when the infusion of potassium chloride continued for a long period. 3.Although less marked than the carotid blood flow, the coronary blood flow increased in the acute respiratory and metabolic acidosis. In asphyxiated condition, coronary blood flow increased most markedly and this might be the combined effect of hypoxia, hypercapnea, and lowering of pH. In summary, the carotid blowflow showed more marked change in the acute respiratory and metabolic acidosis than the renal and coronary blood flow. Respiratory and metabolic components of acid-base disturbances may influence the local blood flow concomitantly, there being more differences in the individual responses, but respiratory component manifested more rapid and marked effect than metabolic component.

• Journal of Trauma and Injury
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• v.32 no.4
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• pp.238-242
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• 2019

Extreme acidosis is a life-threatening physiological state that causes disturbances in the cardiovascular, pulmonary, immune, and hematological systems. Trauma patients commonly present to the operating room (OR) in hypovolemic shock, leading to tissue hypoperfusion and the development of acute metabolic acidosis with or without a respiratory component. It is often believed that trauma patients presenting to the OR in severe metabolic acidosis (pH <7.0) will have a nearly universal mortality rate despite aggressive resuscitation and damage control. The current literature does not include reports of successful resuscitations from a lower pH, which may lead providers to assume that a good outcome is not possible. However, here we describe a case of successful resuscitation from an initial pH of 6.5 with survival to discharge home 95 days after admission with almost full recovery. We describe the effects of acute acidosis on the respiratory and cardiovascular systems and hemostasis. Finally, we discuss the pillars of management in patients with extreme acute acidosis due to hemorrhage: transfusion, treatment of hyperkalemia, and consideration of buffering acidosis with bicarbonate and hyperventilation.

• The korean journal of orthodontics
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• v.20 no.1
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• pp.47-59
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• 1990

Respiration is one of the most important functions which are carried out in stomatognathic system. When nasal orifice is obstructed or the resistance of upper airway is increased mouth breathing is initiated. Mouth breathing is regarded as an important etiologic factor of dentofacial anomalies. This experiment was performed to observe the influences of metabolic acidosis, tracheal resistance and vagotomy on mouth breathing. After rabbits were anesthetized with sodium pentobarbital, a pair of wire electrode was inserted into mylohyoid muscle, anterior belly of digastric muscle and dilator naris muscle to record EMG activity. Femoral vein and artery were cannulated for infusion of 0.3N HCl and collection of blood sample to determine the blood pH, and tracheal intubation was done to control airway resistance. Mouth breathing was induced by metabolic acidosis. Increase of the airway resistance through tracheal cannula intensified the activity of dilator naris, mylohyoid and digastric muscle. The higher the resistance, the larger the EMG amplitude. After bilateral vagotomy, respiratory volume and inspiatory time were increased and the activities of dilator naris, mylohyoid and digastric muscle were strengthened. It was concluded that the muscle activity related to mouth breathing was induced by metabolic acidosis and increase of tracheal tube resistance.

• Journal of Korean Neurosurgical Society
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• v.56 no.2
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• pp.135-140
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• 2014

Objective : Propofol and volatile anesthesia have been associated with metabolic acidosis induced by increased lactate. This study was designed to evaluate changes in pH, base excess (BE), and lactate in response to different anesthetic agents and to characterize propofol infusion-associated lactic acidosis. Methods : The medical records of patients undergoing neurosurgical anesthesia between January 2005 and September 2012 were examined. Patients were divided into 2 groups : those who received propofol (total intravenous anesthesia, TIVA) and those who received sevoflurane (balanced inhalation anesthesia, BIA) anesthesia. Propensity analysis was performed (1 : 1 match, n=47), and the characteristics of the patients who developed severe acidosis were recorded. Results : In the matched TIVA and BIA groups, the incidence of metabolic acidosis (11% vs. 13%, p=1) and base excess (p>0.05) were similar. All patients in the TIVA group who developed severe acidosis did so within 4 hours of the initiation of propofol infusion, and these patients improved when propofol was discontinued. Conclusions : The incidence of metabolic acidosis was similar during neurosurgical anesthesia with propofol or sevoflurane. In addition, severe acidosis associated with propofol infusion appears to be reversible when propofol is discontinued.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.107-107
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• 2002

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.107-107
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• 2002

It has been reported that antinatriuresis is induced by acute cadmium intoxication. However, the mechanisms related to the increase in renal sodium reabsorption by cadmium exposure is not clear yet although it has been suggested that the elevated aldosterone might involve in this process.(omitted)

• 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 the Korean Applied Science and Technology
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• v.35 no.4
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• pp.1433-1441
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• 2018

The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid which causes the release of a proton and the formation of the acid salt sodium lactate. Through this explanation, when the rate of lactate production is high enough to exceed cellular proton buffering capacity, cellular pH is decreased. This biochemical process has been termed lactic acidosis. This belief has been an interpretation that lactate production causes acidosis and fatigue during intense exercise. However, this review provides clear evidence that there is no biochemical support for lactate production causing acidosis and fatigue. Metabolic acidosis is caused by an increased reliance on nonmitochondrial ATP turnover. Lactate production is essential for muscle to produce cytosolic $NAD^+$ to support continued ATP regeneration from glycolysis. In addition, Lactate production consumes protons. Although lactate accumulation can be a good indirect indicator for decreased cellular and blood pH, that is not direct causing acidosis.

• Journal of Chest Surgery
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• v.12 no.4
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• pp.395-402
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• 1979

Intracellular pH was determined by distribution of 5.5-dimethyl-2,4-oxazolidlnedione [DMO]in the skeletal muscle of dogs before and after lactic acidosis induced by intravenous infusion of lactic acid solution. After infusion of lactic acid solution arterial pH decreased from 7.40 to around 7.12 [P<0.001]and metabolic acidosis was induced. However, dose-pH change response was not proportional as in the case of hydrochloric acid infusion. During lactic acidosis, intracellular pH changed very little except when venous blood $pCO_2$ increased significantly. The decrease of intracellular pH in lactic acidosis might be due primarily to the increase of intracellular $pCO_2$. And during lactic acidosis, change of extracellular pH was larger than that of intracellular pH, and this was also the case of change In hydrogen Ion concentration in extracellular and intracellular fluid. The fact was estimated that exogenous lactic acid transported into the cell does not contribute to pH change by the participation in the metabolism. Change in plasma potassium Ion concentration was not eminent as metabolic acid-base disturbances by other origin, and changing pattern of Hi/He ratio was not same as Ki/Ke ratio. In spite of no changes in extracellular potassium ion concentration after exogenous lactic acidosis total amount of potassium ion in extracellular fluid increased from 12.62mEg to 18.26mEg [P< 0.05].