Renal Phosphate Excretion during Postsurgical Hypoxia
Grant-in-Aid for Scientific Research (C)
|Allocation Type||Single-year Grants|
|Research Institution||The University of Tokyo|
MIMURA Yoshikazu Branch Hospital, Faculty of Medicine, Associate Professor, 医学部・附属病院分院, 助教授 (10175614)
KANAUCHI Hajime Branch Hospital, Faculty of Medicine, Assistant Professor, 医学部・附属病院分院, 助手 (20242141)
OGAWA Toshihisa Branch Hospital, Faculty of Medicine, Assistant Professor, 医学部・附属病院分院, 助手 (80224111)
中村 卓郎 東京大学, 医学部・附属病院(分), 助手 (10251208)
宇納 恵三 東京大学, 医学部・附属病院(分), 助手 (10272593)
|Project Period (FY)
1996 – 1997
Completed(Fiscal Year 1997)
|Budget Amount *help
¥1,500,000 (Direct Cost : ¥1,500,000)
Fiscal Year 1997 : ¥500,000 (Direct Cost : ¥500,000)
Fiscal Year 1996 : ¥1,000,000 (Direct Cost : ¥1,000,000)
|Keywords||Hypoxia / Endotoxemia / Phosphate excretion / Parathyroid hormone / Renal nerves / Catecholamines excretion / エッドトキシン血症|
Since phosphate is essential for energy consuming metabolic processes in the cells of the body, the magnitude of renal phosphate excretion may affect the energy metabolism. Phosphate homeostasis is regulated mainly by PTH and other renal hormones which control the rate of phosphate excretion in the kidney. Few information is available as to PTH function and phosphate excretion after surgical injury.
The objective of the present study was to investigate the renal phosphate excretion during surgical stress, such as hypoxia and/or endotoxemia.
3. Methods & Results
(1) Hypoxia produced by inhalation of 10% oxygen for 12 h or less reduced phosphate excretion in rats. (2) This effect is reveresd by reoxygenation. (3) Hypoxia resulted in nephiogenous cyclic AMP production with stabel PTH level. (4) Hypoxia elicited a parallel increase in norepinephrine excretion and a decrease in dopamine excretion. (5) Escherichia coli endotoxin 4 mg/kg administration resulted in a decrease in phosphate excretion in rats. (6) This is not reversed to saline-treated rats by renal denervation procedures.
Pathophysilogy responsible for hypoxemia and endotoxemia after surgery produces phosphate retention in the boldy : (1) Hypoxia specifically attenuates the renal responsiveness to parathyroid glands ; (2) This is due to at steps before PTH-siimulated cyclic AMP production ; (3) A parallel increase in norepinephrine production and a decrease in dopamine production in the kidney may be responsible for the phosphate retention after surgery ; (4) However, renal sympathetic nerves have a minor contribution to renal phosphate rentention during endotoxemia, characterized by cellular hypoxia. Further studies will be needed to clarigy the relation between these observed phosphate retention arid energy metabolism after surygery.
Research Output (7results)