• The Korean Journal of Physiology
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• 제26권1호
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• pp.89-97
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• 1992

In hypoxic tissue conditions, pyruvate can not enter the Krebs cycle and lactic acid, produced from pyruvate, accumulates to induce lactic acidosis. Pyruvate, However, can also be converted to alanine by glutamate pyruvate transaminase, that could be enhanced by glutamate. Therefore, it would be a fundamental measure to treat the lactic acidosis in tissue hypoxic conditions when one can convert the accumulated lactic acid, through pyruvate, to alanine. To test the above hypothesis, we induced a lactic acidosis in cats and the effect of glutamate on recovery of acid base state and removal of the lactic acid from blood were assessed and the results were compared with those of bicarbonate administration, which is one of the most frequently used conventional measure for correction of the acid base state during lactic acidosis. The results were that glutamate and combined glutamate bicarbonate solutions not only restored the acid base status completely from the lactic acidosis in an hour or two, but also restored the blood level of lactate partially. We concluded that administration of glutamate solution to convert pyruvate into alanine is effective in preventing lactic acid accumulation and treating lactic acidosis.

• Journal of Chest Surgery
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• 제12권4호
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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].

• Journal of Genetic Medicine
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• 제21권1호
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• pp.36-40
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• 2024

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episode (MELAS) syndrome is a maternally inherited mitochondrial disorder that usually affects the cerebral cortex and prevents high-energy demands from being met. Herein, we present the case of a male patient who rapidly developed multiple seizures, headaches, and altered mentality accompanied by severe metabolic acidosis and lactic acidosis. Initially, a brain imaging study confirmed stroke-like lesions (SLLs) only in the cerebellum. During follow-up, newly developed SLLs with lactic acidosis were observed in the basal ganglia (BG), cerebellum, and occipital lobe. The m.3243A>G variant had been found in the patient and MELAS was diagnosed, despite the BG and cerebellum being atypical locations for SLLs in MELAS. Since most cases of m.3243A>G variant MELAS show SLLs in the cerebral cortex, this case is unusual considering the location of the lesion. We emphasize that in the case of lactic acidosis accompanied by neurological symptoms, such as seizures, as in this case, MELAS should be included in the differential diagnosis, even if SLLs are observed in areas other than the cerebral cortex.

• 대한임상독성학회지
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• 제6권1호
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• pp.42-44
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• 2008

Metformin which is an oral hypoglycemic agents, acts by enhancing insulin sensitivity, decreasing hepatic glucose production and increasing peripheral utilization of glucose. Deliberate self poisoning with oral hypoglycemic agents is rare. The lactic acidosis associated with metformin toxicity is well described in the medical literature. Metformin overdose even in otherwise healthy patients may produce a profound and life threatening lactic acidosis. We report a case of massive metformin ingestion(75g) in a patient presenting with lactic acidosis and hypotension. She died 24h after presenting to our emergency department despite bicarbonate treatment and hemofiltration therapy.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제42권5호
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• pp.295-300
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• 2016

Submucosal infiltration and the topical application of epinephrine as a vasoconstrictor produce excellent hemostasis during surgery. The hemodynamic effects of epinephrine have been documented in numerous studies. However, its metabolic effects (especially during surgery) have been seldom recognized clinically. We report two cases of significant metabolic effects (including lactic acidosis and hyperglycemia) as well as hemodynamic effects in healthy patients undergoing orthognathic surgery with general anesthesia. Epinephrine can induce glycolysis and pyruvate generation, which result in lactic acidosis, via ${\beta}2$-adrenergic receptors. Therefore, careful perioperative observation for changes in plasma lactate and glucose levels along with intensive monitoring of vital signs should be carried out when epinephrine is excessively used as a vasoconstrictor during surgery.

• 대한임상독성학회지
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• 제5권2호
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• pp.126-130
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• 2007

Metformin is antihyperglycemic, not hypoglycemic. It causes neither insulin release from the pancreas nor hypo glycemia, even when taken in large doses. But, there are several reports of metformin-associated lactic acidosis (MALT). We present a case report of severe lactic acidosis most probably resulting from high doses of metformin in a patient with no known contraindications for metformin. A 43-year-old female was admitted to the emergency department due to a metformin overdose. She had diabetes for 6 years, well-controlled with metformin and novolet. One hour before admission, she impulsively took 50g metformin (100 mg or 100 tablets). Physical examination for symptoms revealed only irritability, and laboratory evaluation revealed only mild leukocytosis. After one hour the patient was drowsy, and arterial blood gas analysis showed severe lactic acidemia Seven hours after ED arrival, she commenced hemofiltration treatment and was admitted to the intensive care unit. Continuous venovenous hemodiafiltration was initiated. Forty-eight hours later, full clinical recovery was observed, with return to a normal serum lactate level. The patient was discharged from the intensive care unit on the third day. A progressive recovery was observed and she was discharged from the general word on the thirteenth day.

• Investigative Magnetic Resonance Imaging
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• 제22권2호
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• pp.119-122
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• 2018

Neurogenic weakness, ataxia and retinitis pigmentosa (NARP) syndrome is a rare maternally inherited mitochondrial disorder. Radiologic findings in NARP syndrome are varied; they include cerebral and cerebellar atrophy, basal ganglia abnormalities, and on rare occasions, leukoencephalopathy. This article describes an extremely rare case of NARP syndrome mimicking mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS).

• 한국응용과학기술학회지
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• 제35권4호
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• pp.1433-1441
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• 2018

고강도 운동 시 산성화의 과정은 수소이온의 방출과 젖산 나트륨염을 형성하는 젖산의 생산 증가에 따른 것이라 설명되어져 왔다. 이 설명에 의하면, 젖산의 생산 비율이 세포내의 수소이온 완충능력을 초과하였을 때 세포의 수소이온 농도는 증가한다고 한다. 이러한 생화학적 과정을 젖산의 산성화라 한다. 이 이론에 따라 고강도 운동 시 젖산의 생산이 대사적 산성화와 피로의 원인이 되는 것으로 해석되어져 왔다. 그러나, 본 고찰에서는 젖산의 생산이 산성화와 피로의 원인이라는 어떠한 생화학적 근거가 없음을 명확히 제시하고 있다. 오히려 젖산의 생산은 해당과정에서 필요한 $NAD^+$의 지속적인 공급을 위해 필수적이며 수소이온을 소비하는 대사과정이다. 젖산의 축적은 세포와 혈중의 수소이온 농도의 증가를 알려주는 좋은 지표가 될 수는 있지만 그것이 산성화의 직접적인 원인은 아니다.

• 한국임상수의학회지
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• 제31권3호
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• pp.199-205
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• 2014

쉽게 발효되는 탄수화물의 과도한 양의 섭취에 따른 급성 또는 만성의 산증은 방글라데시에서 염소의 생산성 문제로 나타나고 있다. 본 연구는 유산증의 분포와 다른 치료제간의 반응을 조사하였다. 본 연구를 위해, 야외 지역 동물 병원, Faridpur, Bangladseh에서 조사 한 1,128마리의 염소가 검사 되었으며, 그 중 40마리의 염소(3.55%의 분포율)가 유산증에 대해 양성으로 확인되었다. 토종 염소 (2.7%)에서는 3 년 이상된 연령(4.64%)의 암컷 (4.64%)에서 가장 높은 발병을 보였다. 40마리 염소의 치료 평가를 위해서 염소는 그룹당 10마리씩 4개의 그룹 A, B, C와 D로 분류 하였다. 그룹A는 경구, 8% 수산화 마그네슘(v/w)을 체중 1 g/kg으로 경구 투여 하였다. 그룹 B에서는 그룹 A와 같은 량의 8% 수산화 마그네슘에 더하여 체중 0.9 ml/kg 비율로 7.5%의 중탄산 나트륨을 정맥 내 투여 하였다. 그룹 D에서 염소는 생강, nuxvomica, 탄산나트륨, 황산 코발트, 분말 형태의 황산제1철 과 티아민 질산염의 혼합물을 1 g/kg 체중의 비율로 경구 투여하였다. 그룹 C의 염소는 그룹 A, B와 D의 조합 약물로 치료하였다. 각 그룹은 치료 전후에 직장 온도, 맥박수, 호흡 수를 검사하였다. 평균 $21{\pm}1.8$ 시간으로 그룹 C가 가장 높은 회복률을 보였다. 결론적으로 유산증은 염소에서 흔한 질병이며 치료효과는 약물의 조합을 통해서 효과적으로 증상을 감소 시킬 수 있었다.

• The Korean Journal of Physiology and Pharmacology
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• 제24권2호
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• pp.173-183
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• 2020

An in vitro model for ischemia/reperfusion injury has not been well-established. We hypothesized that this failure may be caused by serum deprivation, the use of glutamine-containing media, and absence of acidosis. Cell viability of H9c2 cells was significantly decreased by serum deprivation. In this condition, reperfusion damage was not observed even after simulating severe ischemia. However, when cells were cultured under 10% dialyzed FBS, cell viability was less affected compared to cells cultured under serum deprivation and reperfusion damage was observed after hypoxia for 24 h. Reperfusion damage after glucose or glutamine deprivation under hypoxia was not significantly different from that after hypoxia only. However, with both glucose and glutamine deprivation, reperfusion damage was significantly increased. After hypoxia with lactic acidosis, reperfusion damage was comparable with that after hypoxia with glucose and glutamine deprivation. Although high-passage H9c2 cells were more resistant to reperfusion damage than low-passage cells, reperfusion damage was observed especially after hypoxia and acidosis with glucose and glutamine deprivation. Cell death induced by reperfusion after hypoxia with acidosis was not prevented by apoptosis, autophagy, or necroptosis inhibitors, but significantly decreased by ferrostatin-1, a ferroptosis inhibitor, and deferoxamine, an iron chelator. These data suggested that in our SIR model, cell death due to reperfusion injury is likely to occur via ferroptosis, which is related with ischemia/reperfusion-induced cell death in vivo. In conclusion, we established an optimal reperfusion injury model, in which ferroptotic cell death occurred by hypoxia and acidosis with or without glucose/glutamine deprivation under 10% dialyzed FBS.