Effects of perfusion pressure on intracellular calcium, energetics, and function in perfused rat hearts
Kojima, S.; Wu, S.T.; Watters, T.A.; Parmley, W.W.; Wikman-Coffelt, J.
American Journal of Physiology 264(1 Pt 2): H183-H189
1993
ISSN/ISBN: 0002-9513 PMID: 8430845 Document Number: 413520
Effects of perfusion pressure in a range from 50 to 140 cmH-2O on intracellular Ca-2+ concentration ((Ca-2+)-i) were evaluated along with cardiac function, energy metabolism, and left ventricular geometry in a concentration of 2 or 4 mM of extracellular Ca-2+ ((Ca-2+)-o) in isovolumic perfused rat hearts (Ca-2+)-i was evaluated with a surface fluorometry technique in hearts loaded with indo-1/AM. The systolic and diastolic values and the amplitude (difference between systolic and diastolic values) of indo-1 fluorescence ratio (an index of (Ca-2+)-i) were linearly related to perfusion pressure. Changes in the fluorescence ratio were harmonious with rapid changes in left ventricular pressure and stabilized within 30-40 s after changes in perfusion pressure. Developed pressure and O-2 consumption were closely, linearly correlated with the fluorescence ratio irrespective of (Ca-2+)-o. Left ventricular end-diastolic wall thickness, measured by 2-dimensional echocardiography, paralleled perfusion pressure and showed a good correlation with the fluorescence ratio. Diastolic myocardial adenosine 3',5'-cyclic monophosphate significantly decreased only at the lowest perfusion pressure. The ln(phosphocreatine)/(P-i) also changed with altered perfusion pressure. In conclusion, perfusion pressure modulates (Ca-2+)-i, which in turn regulates myocardial contraction and associated O-2 utilization.