Gilmour K M, Euverman R M, Esbaugh A J, Kenney L, Chew S F, Ip Y K, Perry S F
Department of Biology and Centre for Advanced Research in Environmental Genomics, University of Ottawa, Ottawa, ON, Canada.
J Exp Biol. 2007 Jun;210(Pt 11):1944-59. doi: 10.1242/jeb.02776.
African lungfish Protopterus annectens utilized both respiratory and metabolic compensation to restore arterial pH to control levels following the imposition of a metabolic acidosis or alkalosis. Acid infusion (3 mmol kg(-1) NH(4)Cl) to lower arterial pH by 0.24 units increased both pulmonary (by 1.8-fold) and branchial (by 1.7-fold) ventilation frequencies significantly, contributing to 4.8-fold and 1.9-fold increases in, respectively, aerial and aquatic CO(2) excretion. This respiratory compensation appeared to be the main mechanism behind the restoration of arterial pH, because even though net acid excretion (J(net)H(+)) increased following acid infusion in 7 of 11 fish, the mean increase in net acid excretion, 184.5+/-118.5 micromol H(+) kg(-1) h(-1) (mean +/- s.e.m., N=11), was not significantly different from zero. Base infusion (3 mmol kg(-1) NaHCO(3)) to increase arterial pH by 0.29 units halved branchial ventilation frequency, although pulmonary ventilation frequency was unaffected. Correspondingly, aquatic CO(2) excretion also fell significantly (by 3.7-fold) while aerial CO(2) excretion was unaffected. Metabolic compensation consisting of negative net acid excretion (net base excretion) accompanied this respiratory compensation, with J(net)H(+) decreasing from 88.5+/-75.6 to -337.9+/-199.4 micromol H(+) kg(-1) h(-1) (N=8). Partitioning of net acid excretion into renal and extra-renal (assumed to be branchial and/or cutaneous) components revealed that under control conditions, net acid excretion occurred primarily by extra-renal routes. Finally, several genes that are involved in the exchange of acid-base equivalents between the animal and its environment (carbonic anhydrase, V-type H(+)-ATPase and Na(+)/HCO (-)(3) cotransporter) were cloned, and their branchial and renal mRNA expressions were examined prior to and following acid or base infusion. In no case was mRNA expression significantly altered by metabolic acid-base disturbance. These findings suggest that lungfish, like tetrapods, alter ventilation to compensate for metabolic acid-base disturbances, a mechanism that is not employed by water-breathing fish. Like fish and amphibians, however, extra-renal routes play a key role in metabolic compensation.
非洲肺鱼原鳍鱼（Protopterus annectens）在代谢性酸中毒或碱中毒后，利用呼吸和代谢补偿机制将动脉血pH值恢复到正常水平。注入酸（3 mmol kg⁻¹ NH₄Cl）使动脉血pH值降低0.24个单位，显著增加了肺通气频率（增加1.8倍）和鳃通气频率（增加1.7倍），分别使空气中和水中的二氧化碳排出量增加了4.8倍和1.9倍。这种呼吸补偿似乎是动脉血pH值恢复的主要机制，因为尽管在11条鱼中有7条在注入酸后净酸排出量（J(net)H⁺）增加，但净酸排出量的平均增加量为184.5±118.5 μmol H⁺ kg⁻¹ h⁻¹（平均值±标准误，N = 11），与零无显著差异。注入碱（3 mmol kg⁻¹ NaHCO₃）使动脉血pH值升高0.29个单位，虽然肺通气频率未受影响，但鳃通气频率减半。相应地，水中的二氧化碳排出量也显著下降（下降3.7倍），而空气中的二氧化碳排出量未受影响。这种呼吸补偿伴随着由负净酸排出（净碱排出）组成的代谢补偿，J(net)H⁺从88.5±75.6降至 -337.9±199.4 μmol H⁺ kg⁻¹ h⁻¹（N = 8）。将净酸排出量分为肾脏和肾外（假定为鳃和/或皮肤）成分，结果显示在对照条件下，净酸排出主要通过肾外途径进行。最后，克隆了几个参与动物与其环境之间酸碱当量交换的基因（碳酸酐酶、V型H⁺ -ATP酶和Na⁺/HCO₃⁻共转运体），并检测了注入酸或碱前后鳃和肾脏中这些基因的mRNA表达。在任何情况下，代谢性酸碱紊乱均未显著改变mRNA表达。这些发现表明，肺鱼与四足动物一样，通过改变通气来补偿代谢性酸碱紊乱，而这一机制是水生呼吸鱼类所不具备的。然而，与鱼类和两栖动物一样，肾外途径在代谢补偿中起关键作用。
