Information and misinformation regarding ischemia of heart muscle tissue. The cause of cell death during blood reperfusion and reactivation of heart muscle tissue after prolonged ischemia.

An electron microscopic study of heart muscle tissue exposed to six hours ischemia and prepared according to the low denaturation embedding technique revealed a structural modification confined to the mitochondrial cristae. The modification consisted of a removal of Krebs cycle enzymes from the cristae. Reperfusion of the ischemic tissue after four hours ischemia led to extensive breakdown of the mitochondrial structure and contractility could not be restored. However, when after six hours ischemia the ischemic tissue was reperfused with blood, the composition of which had been modified to stimulate mitochondrial function, no additional structural changes were observed and contractility was restored. The structural damage caused by reperfusion with non modified blood is explained by a loss of control of plasma membrane permeability caused by impaired ATP production which makes the ionic composition of the cytosol approach that of blood plasma, stopping oxidative phosphorylation. A treatment to restore heart muscle function after long periods of ischemia and after heart transplantation is proposed. The structural damage revealed that the Krebs cycle and the respiratory chain enzymes are associated according to a regular periodic pattern and that the enzyme molecules are closely aggregated three-dimensionally. Earlier electron microscopic studies revealing massive structural deterioration of heart muscle cells already after 45 to 60 minutes ischemia leading to the conclusion that the cells are irreversibly damaged, is based on fixation artifacts caused by osmium fixation. This study has been carried out in collaboration with the research team of Gerald D. Buckberg at the Thoracic Surgery Division at University of California at Los Angeles.