摘要
Hagfish are capable of tolerating extreme hypercapnia (> 30 Torr) by mounting substantial plasma [HCO3 (-)] (hypercarbia) to compensate for CO2-mediated acidosis. The goal of this study was to characterize the mechanistic hypercarbia-recovery strategies in the highly CO2 tolerant hagfish. We exposed hagfish to hypercapnia (30 Torr) for 48 h and allowed a 24 h recovery period in normocapnic seawater. Within 8 h of the recovery period, the compensatory plasma [HCO3 (-)] load (similar to 70 mmol L-1) was rapidly offloaded. While increases in both whole-animal HCO3 (-) excretion and glomerular filtration were observed throughout recovery (2-8 h), neither can fully account for the observed rates of whole-animal HCO3 (-) loss, which peaked at similar to 3.5 mmol kg(-1) h(-1). Inhibition of carbonic anhydrase via acetazolamide revealed that the restoration of plasma [HCO3 (-)] from hypercapnia-induced hypercarbia is likely facilitated in a dualistic manner, initially relying on both carbonic anhydrase mediated CO2 offloading and Cl-/HCO3 (-) exchange processes, both of which are likely either upregulated or further activated as recovery progresses.
- 出版日期2018-5