Underlying mechanism of ASIC1a involved in acidosis-induced cytotoxicity in rat C6 glioma cells. (49/110)

AIM: To investigate the underlying mechanism of acid-sensing ion channel (ASIC) 1a involved in the acidosis-induced cytotoxicity of rat C6 glioma cells. METHODS: The stable ASIC1a-silenced C6 cells built with the RNA interference technology were confirmed by RT-PCR and Western blot analysis. Intracellular calcium ([Ca2+]i) in both the wild-type rat C6 glioma cells and the ASIC1a-silenced C6 cells were analyzed before and after acid application/exposure with the calcium imaging experiment. RESULTS: The rapid extracellular pH drop induced the increase of [Ca2+]i in the wild-type C6 cells, but not in the ASIC1a-silenced C6 cells. During the prolonged acid exposure, [Ca2+]i was lower in the ASIC1a-silenced C6 cells than that in the control cells. CONCLUSION: The resultant toxicity of [Ca2+]i might contribute to the acidosis-induced cytotoxicity.  (+info)

Ethylene glycol ingestion treated only with fomepizole. (50/110)

INTRODUCTION: Ethylene glycol is a widely used chemical that is capable of causing significant injury if ingested. Treatment for ethylene glycol poisoning typically includes basic supportive care, alcohol dehydrogenase inhibition, and hemodialysis. Recent data have suggested that hemodialysis may not be necessary for cases of ethylene glycol poisoning that can be treated with fomepizole as blocking therapy before acidosis or renal dysfunction develops. CASE REPORT: A 33-year-old man presented to the emergency department 1 hour after drinking approximately 1/2 gallon of ethylene glycol antifreeze and an unknown quantity of beer. On arrival he was mildly inebriated but otherwise displayed no other features of ethylene glycol poisoning. Fomepizole therapy was initiated and initial laboratory studies later revealed an osmol gap of 157 mOsm and an ethylene glycol concentration of 706 mg/dL. Nephrology and toxicology services were consulted. Over the next 3 days, fomepizole therapy was continued while the patient's acid-base status and renal function were closely monitored. No evidence of acid-base abnormalities or renal impairment was ever observed and the patient was discharged to psychiatric care on the fourth hospital day. DISCUSSION: This report describes the case of a patient who presented soon after a massive ingestion of ethylene glycol with very high serum concentrations. He was successfully treated using fomepizole and basic supportive care. Our patient developed neither renal insufficiency nor metabolic acidosis. His concomitant ethanol consumption, early presentation, and treatment likely contributed to his favorable outcome. This case report underscores the effectiveness of supportive care and fomepizole in the treatment of ethylene glycol poisoning.  (+info)

Acid-base analysis: a critique of the Stewart and bicarbonate-centered approaches. (51/110)

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A practical approach to acid-base disorders. (52/110)

This discussion was selected from the weekly staff conferences in the Department of Medicine, University of California, San Francisco. Taken from a transcription, it has been edited by Homer A. Boushey, MD, Professor of Medicine, and Nathan M. Bass, MD, PhD, Associate Professor of Medicine, under the direction of Lloyd H. Smith, Jr, MD, Professor of Medicine and Associate Dean in the School of Medicine.  (+info)

Excess dietary L-cysteine causes lethal metabolic acidosis in chicks. (53/110)

A 72-h time-course study was conducted to elucidate the physiological mechanism underlying cysteine (Cys) toxicity in chicks beginning at 8-d posthatch. Biochemical markers quantified in plasma and liver samples collected from chicks receiving 30 g/kg excess dietary Cys were compared with baseline measurements from chicks receiving an unsupplemented corn-soybean meal diet over a 72-h feeding period. Concomitant with chick mortality were indices of acute metabolic acidosis, including a rapid increase (P < 0.001) in anion gap that resulted from a reduction (P < 0.001) in plasma HCO(3)(-) of approximately 40% and a 2.8-fold increase (P < 0.001) in plasma sulfate in chicks receiving excess Cys. Additionally, provision of 30 g/kg excess Cys resulted in a 1.5-fold increase (P < 0.05) in hepatic oxidized glutathione compared with the 0-h control time-point. Excess dietary Cys did not affect plasma free Met, but plasma free Cys increased (P < 0.05) from 89 to 107 mumol/L at 12 h and remained elevated through 36 h. Strikingly, ingestion of 30 g/kg excess Cys caused more than a doubling (P < 0.001) of plasma free cystine, the oxidized form of Cys, beginning 12 h after initiating the study, and it remained elevated throughout the 72-h feeding period. Taken together, these data suggest that ingestion of 30 g/kg excess l-Cys causes both acute metabolic acidosis and oxidative stress in young chicks when fed a nutritionally adequate, corn-soybean meal diet.  (+info)

Bicarbonate buffered ultrafiltration leads to a physiologic priming solution in pediatric cardiac surgery. (54/110)

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Meta-analysis of the quantity of calcium excretion associated with the net acid excretion of the modern diet under the acid-ash diet hypothesis. (55/110)

BACKGROUND: The acid-ash diet hypothesis of osteoporosis suggests that acid from the modern diet causes a demineralization of the skeleton, and mobilized bone calcium is excreted. A systematic approach has not been used to summarize the findings of the numerous studies about the hypothesis. OBJECTIVES: The purpose of this meta-analysis was to estimate the quantity of net acid excretion and calciuria associated with the modern diet, to assess the association between acid excretion and calcium excretion, and to assess the influence of urine preservatives on calcium measurement. DESIGN: We systematically searched for trials of the acid-ash hypothesis and conducted a meta-analysis. RESULTS: Twenty-five of 105 studies met the inclusion criteria. The estimated quantity of net acid excretion from the weighted average of the control diets from 11 studies was 47 mEq/d. The increase in urinary calcium with a change in renal net acid excretion depended on whether the urine was acidic or alkaline (P < 0.001). A significant linear relation was observed between net acid excretion and calcium excretion for both acidic and alkaline urine (P < 0.001). The estimated change in urine calcium associated with a change of 47 mEq of net acid excretion in acidic urine was 1.6 mmol/d (66 mg/d) of calcium. CONCLUSION: Evidence suggests a linear association between changes in calcium excretion in response to experimental changes in net acid excretion. However, this finding is not evidence that the source of the excreted calcium is bone or that this calciuria contributes to the development of osteoporosis.  (+info)

Head CT in patient with metabolic acidosis. (56/110)

An unresponsive 30-year-old female with a history of anxiety and chronic alcohol abuse presented to an emergency department with altered mental status and a severe metabolic acidosis. The patient was intubated for airway protection, and she empirically received folic acid, bicarbonate, and 5% ethanol continuous infusion for suspected ingestion of toxic alcohol. Following transfer to our institution, the patient was minimally responsive to noxious stimuli. She received fomepizole at dosing corrected for hemodialysis(HD), and bicarbonate via multiple boluses and continuous infusion. The ethanol drip was stopped. The nephrology service had been alerted to this patient's arrival and condition; hemodialysis via a standard heparinized circuit was initiated immediately after her arrival, which produced a marked improvement in the patient's acid-base status. Her serum methanol concentration subsequently returned at > 200 mg/dL. After 12 hours and 2 sessions of hemodialysis, the patient remained unresponsive despite minimal sedation. Anisocoria was noted on exam. Computed tomography of the brain demonstrated a large hematoma in the left basal ganglia that extended into the left frontal and parietal white matter accompanied by intraventricular extension, midline shift, loss of grey-white differentiation throughout, suggesting tonsillar herniation (Figure 1). Forty-eight hours after presentation, radionuclide imaging of the brain revealed no intracranial blood flow; heart, lungs, liver, kidneys, and pancreas were subsequently harvested for transplantation.  (+info)