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酸中毒和碳酸酐酶抑制对板鳃类直肠腺的影响。

Effects of acidosis and carbonic anhydrase inhibition in the elasmobranch rectal gland.

作者信息

Swenson E R, Maren T H

出版信息

Am J Physiol. 1984 Jul;247(1 Pt 2):F86-92. doi: 10.1152/ajprenal.1984.247.1.F86.

Abstract

We studied the effects of acidosis and carbonic anhydrase inhibition on rectal gland fluid secretion. In the anesthetized dogfish shark, Squalus acanthias, volume expanded by a constant infusion of Ringer solution, fluid formation was halved by severe systemic metabolic and respiratory acidosis (pH approximately 7.10) and carbonic anhydrase inhibition. Mild respiratory acidosis (pH approximately 7.6) equivalent to the measured systemic pH during carbonic anhydrase inhibition was without effect. Inhibition of rectal gland enzyme produced severe glandular acidosis, which is indicated by an increase in gland fluid PCO2 (from 7 to 26 mmHg) and HCO3- (from 1.2 to 2.4 mM) and a decrease in pH (from 6.7 to 6.4). Gland tissue total CO2 dropped from 18 to 11 mmol/kg. These changes occurred despite nearly 50% reduction in fluid formation, O2 consumption, and CO2 output. We propose that carbonic anhydrase facilitates CO2 transfer from sites of metabolism to capillary blood by its conversion to HCO3-. This maintains a tolerable intracellular acid-base milieu during stimulated fluid secretion.

摘要

我们研究了酸中毒和碳酸酐酶抑制对直肠腺液分泌的影响。在麻醉的角鲨(Squalus acanthias)中,通过持续输注林格氏液使血容量增加,严重的全身性代谢性和呼吸性酸中毒(pH约为7.10)以及碳酸酐酶抑制可使液体生成减少一半。与碳酸酐酶抑制期间测得的全身性pH值相当的轻度呼吸性酸中毒(pH约为7.6)则无影响。直肠腺酶的抑制导致严重的腺性酸中毒,这表现为腺液PCO2升高(从7 mmHg升至26 mmHg)、HCO3-升高(从1.2 mM升至2.4 mM)以及pH降低(从6.7降至6.4)。腺组织总CO2从18 mmol/kg降至11 mmol/kg。尽管液体生成、氧气消耗和二氧化碳排出量减少了近50%,这些变化仍会发生。我们提出,碳酸酐酶通过将CO2转化为HCO3-,促进了CO2从代谢部位向毛细血管血液的转运。这在刺激液体分泌期间维持了可耐受的细胞内酸碱环境。

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