CA2-DEPENDENT FLUORESCENCE TRANSIENTS AND PHOSPHATE-METABOLISM DURINGLOW-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 contrac tile dysfunction, isolated rat hearts were studied during graded reduc tions of coronary flow. Indo1 fluorescence at 385- and 456-nm waveleng ths (F385/456) Was used as an index of [Ca2+]i. P-31-magnetic resonanc e spectroscopy (MRS) was used to measure free energy of ATP hydrolysis (DELTAG(ATP)), intracellular pH (pH(i)), and P(i) in parallel experim ents to determine whether these factors may be responsible for increas ing diastolic [Ca2+]i or altering the [Ca2+]i-pressure relationship. W hen coronary flow was reduced to 20 and 10% of control, diastolic F385 /456 increased by 14 +/- 3 and 39 +/- 5%, respectively. Although devel oped pressure markedly decreased when coronary flow was reduced, there was no change of the F385/456 transient amplitude (systolic minus dia stolic). During low-flow ischemia there was a significant decrease of DELTAG(ATP) and increase of P(i) that may lead to increased [Ca2+]i. F urthermore, there was a close inverse relationship between P(i) and de veloped pressure, suggesting that P(i) is an important regulator of co ntractility.