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癫痫大发作后乳酸酸中毒的自然史。一种用于研究与高钾血症无关的阴离子间隙酸中毒的模型。

Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated with hyperkalemia.

作者信息

Orringer C E, Eustace J C, Wunsch C D, Gardner L B

出版信息

N Engl J Med. 1977 Oct 13;297(15):796-9. doi: 10.1056/NEJM197710132971502.

Abstract

To define the time course of the metabolic acidosis that follows a single grand-mal seizure, we obtained serial blood samples from eight consecutive patients. Immediately after a seizure, the mean (+/- S.E.M.) venous lactate concentration was 12.7 +/- 1.0 meq per liter, the mean carbon dioxide content 17.1 +/- 1.1 mmol per liter, and the mean arterial pH 7.14 +/- 0.06. Sixty minutes later their values were 6.6 +/- 0.7 meq per liter (P less than 0.005), 23.6 +/- 1.1 mmol per liter (P less than 0.005) and 7.38 +/- 0.04 (P less than 0.005) respectively. The spontaneous resolution of the acidosis was due, in large part, to the metabolism of lactate and to the concomitant removal of hydrogen ion. There was no change in the serum potassium concentration, despite the development of a severe systemic acidemia and the subsequent return to normal of the pH. We suggest that the patient with seizures may serve as a unique model of lactic acidosis.

摘要

为了明确单次癫痫大发作后代谢性酸中毒的时间进程,我们连续采集了8例患者的系列血样。癫痫发作后即刻,平均(±标准误)静脉血乳酸浓度为12.7±1.0mEq/L,平均二氧化碳含量为17.1±1.1mmol/L,平均动脉血pH值为7.14±0.06。60分钟后,这些数值分别为6.6±0.7mEq/L(P<0.005)、23.6±1.1mmol/L(P<0.005)和7.38±0.04(P<0.005)。酸中毒的自然缓解在很大程度上归因于乳酸的代谢以及随之而来的氢离子清除。尽管出现了严重的全身性酸血症且随后pH值恢复正常,但血清钾浓度并未改变。我们认为癫痫患者可能是乳酸酸中毒的独特模型。

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