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Brain and Nerve No to Shinkei Volume 38, Issue 4 （April 1986）

Brain and Nerve 脳と神経 38巻4号（1986年4月発行）

Japanese English

原著

慢性低酸素症の脳循環 CEREBRAL HEMODYNAMICS IN CHRONIC-HYPDXIC HYPDXIA 有竹康一 ¹ , 高倉公朋 ¹ Koichi Aritake ¹ , Hans-Michael Mayer ² , Emanuel Fritschka ² , Jorg Cervós-Navarro ² , Kintomo Takakura ¹ ¹東京大学附属病院脳神経外科 ¹Department of Neurosurgery, University of Tokyo Hospital ²Institute of Neuropathology, Free University of Berlin pp.363-369

発行日 1986年4月1日 Published Date 1986/4/1

DOI https://doi.org/10.11477/mf.1406205693

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Abstract 文献概要
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　抄録　吸入酸素濃度を4.5月間にわたり段階的に低下させ，最終的に8vol％吸入酸素濃度下に置かれた雑種成猫を用い，慢性低酸素症の脳微小循環，およびその調節能に与える影響を検討した。Radioactivemicrosphere法で血中酸素分圧（PaO₂），体血圧（SAP）の変化に対する脳血流量変化を調べ，脳循環反応性について正常動物と慢性低酸素症動物の両群で比較検討した。脳血流量測定は，正常PaO₂正常SAP（PaO₂＞100mmHg,SAP＞100mmHg），低PaO2正常SAP （PaO₂＝30mmHg,SAP＞100mmHg），正常PaO₂低SAP （PaO₂＞100mmHg,SAP＝60mmHg）の3条件下で行った。慢性低酸素症動物では，高ヘマトクリット値と高心拍出が認められ，血液性状と心機能の慢性低酸素症への適応が見られた。慢性低酸素症動物では正常PaO₂下と低PaO₂下での脳血流量は正常動物と比較し増加していた。脱血によるSAP低下は慢性低酸素症の脳血流量を正常SAP時に比べ減少させたが，低SAP時の脳血流量は正常動物と比べ低下していなかった。今回作成された慢性低酸素症動物のPaO₂,SAP変化に対する脳血管反応性は残存していると思われた。

The effects of chronic-hypoxic hypoxia on ce-rebral blood flow and its regulating mechanisms were investigated by means of intracardiac injec-ion of radioactively labelled microspheres. In a gas chamber designed and constructed for the purpose, adult cats were exposed to stepwise decreasing inspiratory oxygen concentrations (for 4.5 months with a final O₂ concentration of 8 vol%). Using animals adapted to hypoxic hypoxia, responsiveness of cerebral blood flow either to alterations in sys-temic arterial pressure (SAP) or to alterations in arterial blood oxygen tension (PaO₂) were assessed. Flow measurement was done under three different conditions : normoxic normotension (PaO₂>100 mmHg ; SAP>100 mmHg), hypoxic normotension (PaO₂= 30 mmHg ; SAP >100 mmHg), or normoxic hypotension (PaO₂> 100 mmHg ; SAP= 60 mmHg).

Hematocrit values continuously increased to 56 % during the process of adaptation to hypoxia. There was also a remarkable increase in cardiac output of hypoxia-adapted animals subjected to hypoxia and to normoxia. Chronic-hypoxic hypoxia led to increased cerebral blood flow, which per-sisted even when animals were returned to normo-xia. Under hemorrhagic hypotension, cerebral blood flow fell significantly in animals adapted to chronic-hypoxic hypoxia but did not fall short of the absolute values in controls. The relative reduc-tion in cerebral blood flow might be attributable to the decrease in cardiac output and to altered blood viscosity. This implied that, even in animals subjected to long-standing graded hypoxic hypoxia, autorgulatory capacity might be partly preserved.