This study was carried out to investigate the mechanisms of acinar cell deletion, leading to the pancreatic atrophy of rat pancreas after experimental duct ligation. Fifty-seven male Sprague-Dawley rats, maintained on a stock diet, weighing 200gm, in average, were divided into 2 experimental groups. Group 1. Control group. Six rats. Abdominal cavity was opened and closed without further treatment. Group 2. Fifty-one rats. Animals were treated with partial ligation of the pancreatic ducts according to the procedure developed by Hultquist followed by sequential sacrifices at: 1 hour (3 rats), 3 hour (3 rats) 6 hours (6 rats), 12 hours (3 rats) and 24 hours (8 rats); 2 days (8 rats), 3 days(3 rats), 4 days (3 rats), and 5 days(5 rats); 1 week (3 rats), 2 weeks (3 rats), 2 weeks (3 rats) and 8 weeks (3 rats); after ligation. Distal part of the pancreas of the animals after partial ligation was extirpated and examined by both light and electron microscopy. The results obtained were as follows: Light microsopically, noted were and interstial edema and focal necrosis of the pancreatic tissue along with fine vacuolization and depletion of the zymogen granules in the acinar cell cytoplasms and condensation of the acinar cell nucleus. These changes were observed by 2 days after ligation. At about the same time, one can observe the dense body, identified to be apoptotic body, in the acinar cells which were found to be decreased in quantity. By 5 days affer ligation, no recognizable acinar cells left in the collagenous stroma exdept intercalated ducts. Conspicuous stroma except intercalated ducts. Conspicuous stromal hyalinization, thereafter. Electron microscopically (TEM and SEM), nuclear condensation and margination toward the nuclear membrane was noted by 6 hours after duct ligation. By 24 hours sporadic membrane-bounded apoptotic bodies appeared in the acinar cells, the number of which reaching to the peak by 3 days after ligation. These apoptotic bodies were found to be phagocytosed by either intraepithlial mononclear phagocytes or adjoinging acinar cells. It can be concluded, therefore: That orderly remodeling of pancreatic exocrine tissue during atrophy is effected by rapid deletion of acinar cells by apoptosis.