Analyses of [Ca2+]iin the isolated beating rat heart (using Indo-1 dye) demonstrated a direct relationship between developed pressure and each of the following: (a) systolic [Ca2+]i; (b) amplitude of [Ca2+]itransients; and (c) diastolic level of [Ca2+]i. Agents which increased cAMP levels, augmented amplitude of [Ca2+]itranslents, and lowered the resting level of [Ca2+]i, thereby shifting the relationship between developed preesure and diastolic as well as systolic [Ca2+]iconcentrations towards lower [Ca2+]ilevels for comparable peak systolic pressure measurements at constant end-diastolic pressure. Addition of adenosine to the perfusate containing isoproterenol completely prevented any cAMP-induced cytosolic changes. Interventions which altered [Ca2+]iand developed pressure, but did not increase cAMP (e.g., perfusion pressure, extracellular calcium, calcium entry blockers, and alpha agonist), caused an increase in diastolic levels of [Ca2+]icommensurate with the augmentation in developed pressure and amplitude of [Ca2+]itranslents. When the diastolic [Ca2+]irose to 400 nmoles and the cAMP was below 4 nmolus the heart fibrillated. The heart fibrillated at a diastolic [Ca2+]iof 350 nmoles when the cAMP was elevated to 6 nmoles. The diastolic level of [Ca2+]iat which the heart begins to fibrillate is indicative of the effect contraction threshold. © 1991.
Wikman-Coffelt, J., Wu, S. T., & Parmley, W. W. (1991). Intracellular endocardial calcium and myocardial function in rat hearts. Cell Calcium, 12(1), 39–50. https://doi.org/10.1016/0143-4160(91)90083-Q