Ca(2+)-dependent fluorescence transients and phosphate metabolism during low-flow ischemia in rat hearts.

To determine whether cytosolic free calcium ([Ca2+]i) rises during low-flow ischemia and to determine the mechanisms responsible for contractile dysfunction, isolated rat hearts were studied during graded reductions of coronary flow. Indo1 fluorescence at 385- and 456-nm wave-lengths (F385/456) was used as an index of [Ca2+]i. 31P-magnetic resonance spectroscopy (MRS) was used to measure free energy of ATP hydrolysis (delta GATP), intracellular pH (pHi), and Pi in parallel experiments to determine whether these factors may be responsible for increasing diastolic [Ca2+]i or altering the [Ca2+]i-pressure relationship. When coronary flow was reduced to 20 and 10% of control, diastolic F385/456 increased by 14 +/- 3 and 39 +/- 5%, respectively. Although developed pressure markedly decreased when coronary flow was reduced, there was no change of the F385/456 transient amplitude (systolic minus diastolic). During low-flow ischemia there was a significant decrease of delta GATP and increase of Pi that may lead to increased [Ca2+]i. Furthermore, there was a close inverse relationship between Pi and developed pressure, suggesting that Pi is an important regulator of contractility.