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首页> 外文期刊>The Journal of Experimental Biology >ACID-BASE REGULATION IN TADPOLES OF RANA CATESBEIANA EXPOSED TO ENVIRONMENTAL HYPERCAPNIA
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ACID-BASE REGULATION IN TADPOLES OF RANA CATESBEIANA EXPOSED TO ENVIRONMENTAL HYPERCAPNIA

机译:暴露于环境高碳酸的水生林蛙水仙中的酸碱调节

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摘要

Tadpoles of Rana catesbeiana were exposed to different levels of environmental hypercapnia. The acid-base regulatory response differed from that in adult amphibians in showing a high degree of pH compensation in the extracellular fluid (65-85%) and complete compensation in the intracellular fluid (tail muscle and liver) within 24h. Hypercapnia induced a massive transfer of HCO3- equivalents and Ca2+ from the tadpoles to the environment, which lasted some 4-6h. Bicarbonate accumulated in the body fluids came mainly from internal buffer sources (probably CaCO3 in lime sacs and/or skin deposits). It is suggested that the large bicarbonate efflux from the animal is a consequence of the dissolution of CaCO3 stores and the delayed adjustment of bicarbonate-retaining mechanisms. Re-exposure of tadpoles to hypercapnia after 1-3 weeks of normocapnic recovery only affected transepithelial fluxes of acid-base equivalents marginally, suggesting that mobilisable CaCO3 stores were depleted during the first exposure to hypercapnia and that they were not refilled. The CaCO3 stores may normally be mobilised during the slowly developing internal hypercapnia that occurs during metamorphosis. [References: 23]
机译:es蛙的暴露于不同水平的环境高碳酸血症。酸碱调节反应与成年两栖动物不同,其表现为在24小时内细胞外液中有高度的pH补偿(65-85%),细胞内液中有完全的pH补偿(尾部肌肉和肝脏)。高碳酸血症导致H中的HCO3-当量和Ca2 +大量转移到环境中,持续约4-6h。体液中积累的碳酸氢盐主要来自内部缓冲源(可能是石灰囊和/或皮肤沉积物中的CaCO3)。有人认为,动物碳酸氢盐的大量流出是CaCO3储存溶解和碳酸氢盐保留机制调整延迟的结果。 nor在正常碳酸血症恢复1-3周后再次暴露于高碳酸血症,仅轻微影响酸碱当量的跨上皮通量,这表明可动性CaCO3储存在首次暴露于高碳酸血症的过程中被耗尽,并且没有被补充。通常,在变态过程中发生的缓慢发展的内部高碳酸血症期间,通常可以调动CaCO3存储。 [参考:23]

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