Gastrectomized Rats Respond with Exaggerated Hypercalcemia to Oral and Intravenous Calcium Loads because of Impaired Ability of Bone to Take Up Ca 2+

Abstract

Background: Gastrectomy (GX) causes osteopenia. The hypothesis tested in the present study is that GX affects Ca homeostasis and that an impaired ability to handle Ca contributes to the GX-evoked osteopenia. Methods: SHAM-operated and GX rats were compared with respect to changes in blood Ca 2+ after oral or intravenous loads of CaCl 2 1-2 weeks or 2-4 months after the operations. Results: Different doses of oral CaCl 2 raised blood Ca 2+ more in GX than in SHAM rats, more so after 2-4 months than after 1-2 weeks. The rise was greater in fasted (48 h) rats than in fed rats regardless of whether they were SHAM or GX. While SHAM rats tolerated high doses of CaCl 2 well, GX rats died when exposed to quite modest doses, particularly 2-4 months after GX. Intravenous infusion of CaCl 2 (2500 &#119 mol/kg/h) induced a greater and steeper rise in blood Ca 2+ in GX rats than in SHAM rats. Kinetic analysis of the blood Ca 2+ data showed GX rats to display: 1) a decreased Ca 2+ elimination clearance from the central distribution compartment (blood), 2) a reduced size of the peripheral distribution compartment (the so-called bone fluid compartment), and 3) a spectacular decrease in the intercompartmental clearance (transfer of Ca 2+ from blood to bone). These effects were notably apparent after 2-4 months. At sacrifice, the GX-evoked osteopenia was confirmed by planimetric analysis of the calvariae, revealing 40% reduction of bone tissue after 2-4 months. Conclusions: Based on the present data we argue that GX rats respond with exaggerated hypercalcemia to oral and intravenous CaCl 2 loads because of a greatly impaired transfer of Ca 2+ from blood to bone. We suggest that with time this impairment results in osteopenia.

• Blood Ph-ACIDOSIS
• Calcium
• Calcium Metabolism
• Gastrectomy
• Hypercalcemia