The course and nature of acinar cell death following pancreatic ligation in the guinea pig.
The course and nature of acinar cell death (ACD) following pancreatic ligation in the guinea pig was studied as a possible model for human disease. Ultrastructural studies after various periods of ligation suggested a biphasic pattern of ACD. Early phase ACD involved only a small portion of acinar cells and occurred within a few hours of ligation. It was preceded by swelling and vesiculation of the rough endoplasmic reticulum. Morphometric measurements disclosed celular swelling at this time, and NaCl equilibration studies demonstrated a change in cellular osmoregulation. Late phase ACD, characterized by cellular wasting and autophagic vacuole formation, became prominent several days after ligation. Marked increases in lysosomal enzyme activities were found in tissue homogenates at this time, and acid phosphatase electron histochemistry localized the majority of this increased activity to lysosomes and autophagic vacuoles within the acinar cells. The etiology and nature of both phases of ACD are discussed.
D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D002470:Cell Survival; D004247:DNA / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D005260:Female; D005966:Glucuronidase / Q000378:metabolism; D006168:Guinea Pigs; D006651:Histocytochemistry; D002479:Inclusion Bodies / Q000648:ultrastructure; D008026:Ligation; D008247:Lysosomes / Q000201:enzymology; D008854:Microscopy, Electron; D010179:Pancreas / Q000201:enzymology / Q000473:pathology* / Q000648:ultrastructure; D010183:Pancreatic Ducts / Q000601:surgery; D012965:Sodium Chloride; D013997:Time Factors; D014882:Water-Electrolyte Balance
D012965:Sodium Chloride; D004247:DNA; D000135:Acid Phosphatase; D005966:Glucuronidase