THE INFLUENCES OF METHOD OF SACRIFICING THE ANIMALS MEDULLA-SHOCK AND CALCIUM-BLOCK ON THE TOPOGRAPHIC DISTRIBUTION OF NORMAL AND ABNORMAL GLYCOGEN INRABBIT’S LEFT VENTRICLE

A total of 23 adult rabbits were used in this study. Six were used as control andthe remaining 17 rabbits were injected with adrenaline to produce cardiac lesion. Theseanimals were sacrificed alternatively either by medullary-shock or clacium block after 1,3, 5, 7, 10, 14 and 21 days of experiment. The left ventricle was excised and fixed inCarnoy fixative, embedded in paraffin, stained with either H-E or PAS (McManus)method. Slides of saliva digestion and PAS staining were used for the identificationof glycogen. The following points of conclusion were drawn: 1. More glycogen was present in the left ventricle of animals killed by calciumblock than those killed by medulla-shock. 2. The glycogen content in the outer and inner myocardial layers of the normalanimal killed by calcium block was identical and that of the middle layer was lesser.Since these myocardial layers perform different functions in ventricular contraction, theauthors suggest that the glycogen content of the different normal myocardial layers wasassociated with its function. 3. Medulla-shock causes anoxia of the heart. There were severe exhaustion ofglycogen in the outer layer during anoxia. The influence of anoxia was restricted to theintersinusal region (the parasinusal region was less influenced) of the middle layer. Theinfluence of anoxia to the inner layer was minimal. These phenomena were interpretedas due to the different blood sources of each layer. 4. In the myocardium of the shocked animals, glycogen was constantly stagnatedat the following places: the perisinusal fibers of the middle layer, the lateral boundariesof the papillary muscle, and the inner layer of the myocardium. These phenomena fur-ther proved the relationship between the glycogen distribution and the blood supply. 5. The perilesion deposition of glycogen due to adrenaline was not influenced bythe process of anoxia in any layer of the myocardium. The abnormal glycogen disap-peared coincidentally with other cytoplasmic material during degeneration. So, it wasbelieved that this glycogen probably was combined with the protein. The range ofabnormal glycogen distribution was in accordance with the severity of the lesion. 6. Within the first 5 days of our experiment, the focal lesion had not yet form-ed, the injury of individual fiber was variable and so did glycogen distribution. Afterthe 14th experimental day, the lesion was replaced by scar tissue and the perilesion car-diac fibers reappeared to normal. Thus, there was no abnormal glycogen deposit in thatregion. Only between the 5th and 14th experimental days, the abnormal glycogen de-position was distinct.