慢性血液透析患者の低血圧発症に関する臨床的研究

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  • Studies on the Mechanism of Hypotension in Chronic Hemodialysis Patients
  • マンセイ ケツエキ トウセキ カンジャ ノ テイ ケツアツ ハッショウ ニ カ

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The control of blood pressure is of crucial importance for successful hemodialysis, especially in hypotensive patients. The mechanism of hypotension is not yet completely understood. It is commonly beleived that one of the major causative factors of hypotension is dehydration. Although dehydration stimulates such pressor mechanisms as sympathetic nervous activity and renin angiotensin (R-A) axis, hypotension nevertheless results. In this paper I investigated the mechanism by which this seemingly paradoxical effect may be produced. In particular, I have examined the implication of R-A axis and plasma level of prostaglandin (PG) on the mechanism. In hypotensive patients contrast to normal adults, the infusion of 1-Sar, 8-Ile angiotensin II (A II) resulted in lowering of blood pressure. This fact suggests that the circulating A II plays a role in maintenance of blood pressure in these patients. PRA, plasma aldosterone concentration and immunoreactive plasma prostaglandin E1 (I-PGE1) level, all exceeded the normal range for adult. Sensitivity to infused A II and norepinephrine also decreased significantly in these patients. PRA, I-PGE1 and the critical pressor dose of A II decreased by 28%, 46% and 39% respectively upon adminlstration of 75 mg of indomethacin (IND) on each of seven consecutive days. PRA and I-PGE1 increased significantly during the time course of hemodialysis, but the sensitivity to infused A II decreased. The hypotensive episodes developed in three out of six cases. Elevation of PRA and I-PGE1 due to hemodialysis was inhibited completely after pretreatment with 75mg of IND on each three consecutive days. On the other hand, sensitivity to infused angiotensin II remained favorrably and no cases of hypotensive episodes were observed in the time course of hemodialysis. These results suggest that the hypotension which has sometimes been observed during hemodialysis may be accounted for the inhibition of such pressor mechanisms as R-A axis and sympathetic nervous activity by the elevated level of plasma prostaglandins.

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