Occurrence of intramitochondrial glycogen in canine myocardium after prolonged anoxic cardiac arrest

Abstract

Intramitochondrial glycogen deposits were observed in viable cardiac muscle cells of dogs sacrificed 2 to 4 weeks following prolonged periods of normothermic anoxic cardiac arrest induced by aortic cross-clamping during total cardiopulmonary bypass. These deposits were not observed in control dogs, in dogs which died several hours to 8 days after the anoxic period, or in cardiac biopsies taken immediately before and immediately after the anoxic period. The intramitochondrial glycogen deposits were located in the outer mitochondrial compartment, and varied from few to large numbers of granules that almost completely filled the mitochondria. These granules occurred in the monoparticulate (β) form and usually were slightly larger than the extramitochondrial β glycogen granules. Both intra- and extramitochondrial glycogen gave a strongly positive reaction with the periodic acid-thiosemicarbazide-silver proteinate method of Thiéry for the demonstration of polysaccharides; glycogen granules in both locations were extracted from ultrathin sections by amylase. Although intramitochondrial glycogen deposits have been described in a few patients with cardiomyopathies, the present study suggests that such deposits indicate a type of response to injury rather than a specific type of cardiomyopathy. It is suggested that the three factors responsible for the occurrence of intramitochondrial glycogen deposits in cardiac muscle cells following anoxic cardiac arrest are: (i) solubilization of the enzymes of glycogen metabolism during the anoxic period: (ii) increased permeability, due to anoxic damage, of the outer mitochondrial membrane; and (iii) diffusion of the solubilized enzymes of glycogen synthesis into the mitochondria with subsequent formation of glycogen.