AJP - Regulatory, Integrative and Comparative Physiology, Vol 268, Issue 3 683-R689, Copyright © 1995 by American Physiological Society
Effects of input pressure on in vitro turtle heart during anoxia and acidosis: a 31P-NMR study
D. C. Jackson, H. Shi, J. H. Singer, P. H. Hamm and R. G. Lawler
Department of Physiology, Brown University, Providence, Rhode Island 02912.
In vitro working hearts of the turtle, Chrysemys picta bellii, paced at 30
beats/min, were studied over a range of input pressures in the following
sequence of perfusion conditions: control normoxia, control anoxia,
lactacidotic normoxia, and lactacidotic anoxia. Two such series of
experiments were performed. In series 1 (n = 12), ventricular pressure (PV)
and cardiac output were measured, and power output and dPV/dt were
calculated. In series 2 (n = 5), intracellular phosphorus metabolites and
intracellular pH (pHi) were also measured using 31P-nuclear magnetic
resonance (31P-NMR) spectroscopy. In series 1 all mechanical variables
increased with input pressure in generally similar fashion, except during
anoxic acidosis, during which mechanical performance was depressed and was
increased less or not at all by input pressure. Creatine phosphate (CP) and
pHi fell significantly in anoxia and anoxic acidosis, but neither these
variables, ATP, CP/ATP, nor, presumably, ADP changed as a function of input
pressure with any perfusate despite often large increments in mechanical
output. We conclude that anoxia and acidosis act synergistically to depress
cardiac function in turtle hearts. Also, the insensitivity of NMR variables
to changes in input pressure and cardiodynamics suggests that changes in
these variables are unimportant for controlling energy turnover in this
preparation.
