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- 검색키워드
- 저자 : 羅信愛 (검색결과 2 건)
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家兎腎臟의 Sodium 排泄機能에 對한 交感神經의 影響에 關한 實驗的 硏究
羅信愛 우석대학교 의과대학 1968 우석의대잡지 Vol.5 No.1
It has been reported that epinephrine and norepinephrine inhibit the urinary excretion of sodium and also denervation of kidney produces naturesis. However it is not yet clear which receptor of the sympathetic nerve inhibit the renal sodium excretion and the effect of sympathetic nerve in rabbit, since a species difference of the effect of sympathetic nerve on renal sodium excretion has been reported. Author carried out an experiment to clearify which receptor of the sympathetic nerve has an inhibitory effect on renal sodium excretion as well as an effect of sympathetic nerve on the diuretic action of lasix in rabbit. Fourty rabbits were studied on their alteration of urinary sodium, chloride and potassium according to the following experiments, namely 1. stimulation of the α-receptor of sympathetic nerve with epinephrine and norepinephrine 2. stimulation of the α-receptor in reserpinized rabbit 3. stimulation of the α-receptor, blocked with ergotamine 4. stimulation of the β-receptor with isoproterenol(Isuprel®) 5. effect of β-receptor blocking and stimulation of the β-receptor, blocked with propranolol(Inderal®). All rabbits, used were matured and weighed about 2㎏. They were given 0.3% saline intravenously with a speed of 4 drops per minute under urethane anesthesia in order to keep adequate urine flow and urine samples were collected in every 30 minutes throughout the experiment. The control urine samples were collected for 60 to 90 minutes in all experiments. A 20 γ/㎏ of epinephrine and norepinephrine were given intravenously in 4 and 2 rabbits respectively and followed by furosemide(lasix®) injection 60 to 90 minutes later. In 2 rabbits epinephrine and furosemide injected simultaneously. In all rabbits, the urinary excretion of sodium, potassium and chloride were decreased markedly following the epinephrine and norepinephrine injection and the diuresis occured in all rabbits promptly and lasted for about one hour following the injection of furosemide. However the simultaneous injection of these two drugs caused a mild diuresis which occurred less promptly and lasted longer than one hour. In reserpinized rabbits the injection of epinephrine caused an increase of urinary sodium excretion which was considered to be due to unknown mechanism instead of depletion of catecholamine in tissue by reserpine. In ergotamine treated rabbits, the effects of epinephrine and norepinephrine were inconsistent and unremarkable. In 6 rabbits 4 drops of 0.5 % isoproterenol were inhalated and in 2 rabbits 5㎎/㎏ of isoproterenol were given intravenously. The changes in urinary sodium excretion were variable and also the changes were not remarkable. A 0.5㎎/㎏ of propranolol(Inderal®) was given in 5 rabbits and followed by lasix injection. There was no noticiable changes on urinary electrolytes excretion and the responses to lasix injection were as usual. The isoproterenol was given in 5 rabbits, treated with propranolol previously and there was neither remarkable nor consistent changes in urinary electrolytes. These data indicated that the sympathetic nerve has an inhibitory effect of urinary sodium excretion and the a-receptor of sympathetic nerve is the predominently responsible site of inhibitory effect on urinary sodium excretion. It appears also that the epinephrine is able to decrease and changes the diuretic action of furosemide.
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