Key result
Anoxia and acidosis significantly inhibited maximum isometric force (to 40% and 81% of control) and maximal power output of turtle cardiac muscle strips, while maximum velocity of shortening was unaffected.
Population
Cardiac ventricular muscle strips from the anoxia-tolerant turtle Chrysemys picta bellii
Comparison
Exposure to anoxia, lactate acidosis, and anoxic… vs Control conditions (normoxia, non-acidosis)
Design
Preclinical
Authors
Loading...
Turtle cardiac findings warrant caution extrapolating to mammals; leaves open whether preserved shortening velocity confers ischemic protection in human myocardium.
Acidosis and anoxia inhibit isometric force production and maximal power output in turtle cardiac muscle without affecting the maximum velocity of shortening, indicating cross-bridge cycling rate is preserved.
Shi et al. (1997) studied Anoxia and acidosis in turtle cardiac muscle. Anoxia, acidosis, and temperature reduction vs. Control conditions (normoxia, non-acidosis) was evaluated on Maximum isometric force (P0), maximum velocity of shortening (Vmax), and maximal power output (Powermax). Anoxia and acidosis significantly inhibited maximum isometric force (to 40% and 81% of control) and maximal power output of turtle cardiac muscle strips, while maximum velocity of shortening was unaffected.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: