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RELATION OF THE LIVER TO ASPHYXIAL HYPER‐GLYCZEMIA IN FISHES
Author(s) -
Simpson W. W.
Publication year - 1928
Publication title -
quarterly journal of experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0370-2901
DOI - 10.1113/expphysiol.1928.sp000463
Subject(s) - asphyxia , blood sugar , fish <actinopterygii> , physiology , sugar , medicine , biology , endocrinology , anesthesia , chemistry , food science , fishery , diabetes mellitus
1. The normal blood‐sugar of the ling cod, when conditions are standardized, is quite constant and of the same order of magnitude as that of other Teleosts, (1), (2). 2. In the few cases in which fish died under operation no hyperglycæmia developed during the twenty minutes that it occupied, thus confirming previous observations in showing that a delay occurs between asphyxiation and the onset of the hyperglycæmia, (1), (2), (3). 3. Asphyxia, following complete heparectomy in fish, does not cause hyperglycæmia. 4. Under control operation, “mock heparectomy,” asphyxia causes the development of the usual high blood‐sugar. 5. These results show that the presence of the liver is essential to the development of asphyxial hyperglycæmia, and they contradict the view that “masked carbohydrates” present in normal blood are a source of the excess of blood‐sugar after asphyxia.