Dropping the base: Characterizing the hypercarbia recovery strategies following extreme hypercapnia in the highly CO2 tolerant hagfish (Eptatretus stoutii)

Abstract

As scavengers that feed on decaying carrion (e.g. fish, large marine mammals), hagfish (Eptatretus stoutii) can be subjected to noxious environmental stresses such as high ammonia, anoxia and hypercapnia. While the physiological impacts and the hagfishes' tolerance of these stressors have been well characterized, little data exists on the mechanisms and strategies for recovery from these stressors that would be mandatory in the natural environment. Indeed, hagfish are capable of tolerating extreme hypercapnia (>30 Torr; 72h) by building up plasma [HCO3−] over 24 – 48 h of exposure, attaining the highest plasma [HCO3−] levels ever observed in any organism (~70 mmol HCO3− L−1). The goal of this study was to characterize the hypercarbia recovery strategies of the highly CO2 tolerant following hypercapnia exposure. In a series of experiments, hagfish were exposed to hypercapnia (4% CO2) for 48 h to induce hypercarbia before being allowed to recover in normocapnic seawater. During this recovery period, measurements of blood acid/base status, plasma [Cl−] and net H+/HCO3− flux were made to elucidate the recovery strategies of the hagfish. Upon reintroduction into nonromantic conditions, hagfish rapidly (<8h) offloaded the compensatory base load (65.8 ± 2.1 mmol HCO3− L−1) while sustaining an incredible blood alkalosis of ~0.8 pH units compared to post‐exposure conditions, to a blood pH 8.67 ± 0.03 within 4h of recovery. 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 ~3.5 mmol kg−1 h−1. Inhibition of carbonic anhydrase using acetazolamide revealed that 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.Support or Funding InformationNSERC (GGG: 203736)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.