Relationships between cytosolic phosphorylation potential, low-flow ischemic purine release and post-ischemic left ventricular developed pressure were examined in perfused working guinea-pig heart. During moderate ischemic acidification, metabolic intervention by pyruvate attenuated cytosolic NADH accumulation and (ATP+ADP+AMP) degradation. In reperfusion, spontaneously developed ventricular pressure increased in parallel with the phosphorylation potential (R2 = 0.71), but forced restoration of function by inotropic measures occurred at the expense of the phosphorylation potential.
CITATION STYLE
Mallet, R. T., Bunger, R., Prinzen, F., Allen, D., & Bassingthwaighte, J. (1993). Metabolic protection of post-ischemic phosphorylation potential and ventricular performance. In Advances in Experimental Medicine and Biology (Vol. 346, pp. 233–241). Springer Science and Business Media, LLC. https://doi.org/10.1007/978-1-4615-2946-0_22
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