The changes in the rat parotid glands following total parenteral nutrition and pancreatico-biliary diversion are not mediated by cholecystokinin.
CONCLUSIONS
The results of the present study suggest that the pancreas and parotid glands both respond with hypoplasia during absence of food in the digestive tract and with hyperplasia following pancreatico-biliary diversion (PBD). Factors other than cholecystokinin (CCK) are, however, involved in the effects on the parotid glands, since infusion of CCK-8S and devazepide was without influence.


OBJECTIVE
Total parenteral nutrition (TPN) causes reduced pancreatic weight, whereas PBD evokes hyperCCKemia and enlargement of the rat pancreas. The pancreas and parotid glands have in part similar morphology and function. Therefore, we studied the possible presence of alterations also in the parotid glands during TPN, after PBD and during infusion of sulfated cholecystokinin (CCK-8S) and the CCK-A receptor antagonist devazepide, respectively.


RESULTS
Rats either received TPN for 7 d, or were kept under otherwise identical conditions with free access to food and water. TPN markedly reduced both pancreatic and parotid wet weight and thereby also the protein and amylase contents, and pancreatic DNA content was decreased. There was a significant correlation between the pancreas and parotid glands when comparing these parameters. The concentration of plasma CCK was unaffected by TPN. PBD caused a sevenfold increase in plasma CCK and a three fold increase in the pancreatic weight compared to control rats 28 d after the operation. The protein and DNA contents in the pancreas were found to be increased. The parotid glands increased twofold in weight, but their protein and amylase contents were not affected. There was a significant correlation between the pancreas and parotid glands when comparing weight, and protein and amylase concentrations. Infusion of CCK-8S during 28 d caused a marked increase in pancreatic wet wt and protein and DNA contents. The CCK-A receptor antagonist devazepide induced a reduction in protein and DNA contents in the pancreas. The parotid glands were not affected by either treatment. No effect on the labeling index of serous and ductal cells of the parotid gland was seen at 36 h, 3, 7, and 28 d of infusion with CCK-8S or devazepide.
Axelson
J
J
Department of Surgery, University Hospital, Lund, Sweden.
Fan
B G
BG
Ohlsson
B
B
Rehfeld
J
J
Ekelund
M
M
Ihse
I
I
D000681:Amylases / Q000032:analysis; D000818:Animals; D001570:Benzodiazepinones / Q000494:pharmacology; D001652:Bile Ducts / Q000601:surgery; D002766:Cholecystokinin / Q000097:blood / Q000502:physiology*; D004247:DNA / Q000032:analysis; D020109:Devazepide; D006727:Hormone Antagonists / Q000494:pharmacology; D008297:Male; D009929:Organ Size; D010179:Pancreas / Q000033:anatomy & histology / Q000737:chemistry / Q000187:drug effects / Q000502:physiology*; D010183:Pancreatic Ducts / Q000601:surgery; D010289:Parenteral Nutrition, Total; D010306:Parotid Gland / Q000033:anatomy & histology / Q000737:chemistry / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012844:Sincalide / Q000031:analogs & derivatives / Q000494:pharmacology
C090019:8-sulfocholecystokinin octapeptide; D001570:Benzodiazepinones; D006727:Hormone Antagonists; D004247:DNA; D002766:Cholecystokinin; D000681:Amylases; D020109:Devazepide; D012844:Sincalide