Open AccessA Portal Factor Influences Serum Calcium Homeostasis
Author(s) -
ChenHsen Lee,
Edwin L. Kaplan,
Jeffrey T. Sugimoto,
Hunter Heath
Publication year - 1980
Publication title -
annals of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.153
H-Index - 309
eISSN - 1528-1140
pISSN - 0003-4932
DOI - 10.1097/00000658-198010000-00004
Subject(s) - portacaval shunt , medicine , endocrinology , parathyroidectomy , calcium , hypoparathyroidism , parathyroid hormone , hyperphosphatemia , homeostasis , calcium metabolism , portal hypertension , cirrhosis
In order to evaluate the importance of a portal factor in serum calcium homeostasis, end-to-side portacaval shunts were performed in groups of adult, male Lewis rats either before or after parathyroidectomy. Subsequent changes in serum calcium values were followed. When parathyroidectomy was performed one day or 28 days after a portacaval shunt, hypocalcemic changes occurred soon after. However, in these shunted, parathyroidectomized animals which were maintained on a normal calcium diet the serum calcium concentrations soon began to rise and by three weeks after operationthe rats became normocalcemic. In animals which had a portacaval shunt performed three days after parathyroidectomy, the serum calcium levels again rose and became normal in approximately three weeks. In the shunted, parathyroidectomized animals, both the serum calcium and phosphorus concentrations remained normal as long as the rats were maintained ona normal calcium diet. When a low calcium diet was introduced, marked hypocalcemia occurred and serum parathyroid hormone values were barely detectable, both of which attest to the completeness of parathyroidectomy. These data support the hypothesis that following portacaval shunt, a calcium elevating factor, which is similar in action to parathyroid hormone but is not PTH itself, bypasses the liver and becomes effective in the systemic circulation. It acts to correct the hypocalcemia and hyperphosphatemia of parathyroidectomized rats. The possible role of various known gastrointestinal factors in this process is discussed.