PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
March 6, 20260 citationsOpen Access

Respiratory physiology of the hellbender, Cryptobranchus A. Alleganiensis

View Full Paper
BGBoutilier, R G 1953-2003 (Robert Graeme),

Key Points

  • This research aims to explore the blood properties and physiological responses to high carbon dioxide levels in the hellbender.
  • In vitro blood property measurements in Cryptobranchus a. alleganiensis
  • In vivo responses to chronic hypercapnic exposure
  • Assessment of oxygen binding affinity and Bohr effect
  • Quantification of bicarbonate and chloride levels in blood and plasma
  • Evaluation of blood buffering capacity and CO₂ combining power
  • Blood shows high oxygen binding affinity (P₅₀ = 21 mm Hg at pH 7.850)
  • A significant Bohr effect is observed (-0.28 Δlog PP₅₀/ΔpH)
  • A large chloride shift occurs as Pco₂ increases
  • Hypercapnia initially induces respiratory acidosis, compensated by increased plasma [HCO⁻₃]
  • Arterial blood Pco₂ slowly returns to normal after normocapnic conditions, with incomplete restoration of plasma [HCO⁻₃] over several days.

Abstract

The in vitro properties of blood and the in vivo responses to chronic hypercapnic exposure in the exclusively aquatic urodele amphibian Cryptobranchus a. alleganiensis (Daudin) are described. Typical of other aquatic breathers, the oxygen binding affinity of the blood is high (P₅₀ = 21 mm Hg at pH 7.850) and there is an appreciable Bohr effect (-0.28 Δlog PP₅₀/ΔpH). Carbon dioxide combining curves revealed a Haldane effect in the physiological range of arterial blood Pco₂. Measurements of blood buffering capacity (Δ HCO⁻₃ /ΔpH) and CO₂ combining power (mM/litre) reveal a large intraspecific variability which is correlated with haematocrit. Measurements of bicarbonate and chloride in whole blood and plasma indicate that a large Cl⁻/HCO⁻₃ exchange (Chloride shift) occurs across the erythrocytic membrane as Pco₂ increases. This phenomenon has not previously been quantified in aquatic or amphibious vertebrates. Hypercapnic exposure induces in Cryptobranchus an initial respiratory acidosis which is progressively compensated for over a prolonged time course by increases in plasma HCO⁻₃. The source of this added bicarbonate is thought to be a redistribution of body buffer stores. Upon return to normocapnic conditions, arterial blood Pco₂ returns slowly to normal levels but the restoration of pre-exposure plasma HCO⁻₃ is incomplete over several days of recovery. Other aspects examined and discussed include, blood oxygenation characteristics and the partitioning of CO₂ between the red cells and plasma during both normocapnic and hypercapnic conditions.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Boutilier, R G 1953-2003 (Robert Graeme), (1978) studied this question.

synapsesocial.com/papers/69aa70f8531e4c4a9ff5b36fhttps://doi.org/10.26108/qv3y-4x13
Ask AI
Helpful
Bookmark
Share
View Full Paper