| Japanese |
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| Title | 敗血症性ショック初期動物モデルにおける心筋βアドレナリン受容体を介した陽性変力作用減弱に関する検討 |
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| Subtitle | 特集 第19回日本循環制御医学会総会 若手研究者によるシンポジウム |
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| Authors | 松田直之*, 丸藤哲*, 服部裕一**, 菅野盛夫**, 劒物修* |
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| Authors(kana) | |
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| Organization | *北海道大学医学部麻酔学講座, **北海道大学医学部情報薬理学講座細胞薬理学分野 |
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| Journal | 循環制御 |
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| Volume | 20 |
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| Number | 1 |
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| Page | 18-25 |
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| Year/Month | 1999/ |
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| Article | 報告 |
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| Publisher | 日本循環制御医学会 |
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| Abstract | 「要旨」敗血症性ショックにおける血圧低下の主因は, Nitric oxide(NO)の過剰産生により血管拡張が生じるためと考えられてきた. しかしながら, 敗血症性ショックで認められる心収縮性低下が敗血症のどの時期より, どのような機序で生じるかについては, いまだ十分な解明が得られていない. 本研究では, 初期敗血症モデルとしてlipopolysaccharide(LPS)100μg/kgを静脈内投与したウサギを用いて, 摘出乳頭筋標本でのisoproterenolによる陽性変力作用を検討した. その結果, 乳頭筋標本の基礎収縮力に対照群と敗血症群に差は見られなかったが, LPS投与3時間後で既にisoproterenolによる濃度反応曲線が右方移動し, さらに6時間後では最大反応が減弱した. この陽性変力作用減弱は, NG-nitro-L-arginine(L-NNA)前処置によりNO産生を阻害しても改善されず, また, 受容体結合飽和実験より求めたβアドレナリン受容体数や親和性に低下を認めなかった. 敗血症では病初期より陽性変力作用の減弱が生じており, その原因として過剰に産生されたNO以外の要因が関与する. |
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| Practice | 基礎医学・関連科学 |
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| English |
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| Title | Depressed Positive Inotropic Effect of Myocardial β-Adrenoceptor Stimulation in Animal Models as an Early Phase of Septic Shock |
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| Subtitle | |
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| Authors | Naoyuki Matsuda*, Satoshi Gando*, Yuich Hattori**, Morio Kanno**, Osamu Kemmotsu* |
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| Organization | *Departments of Anesthesiology and Pharmacology, Hokkaido University School of Medicine, **Departments of Anesthesiology, Hokkaido University School of Medicine |
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| Journal | Circulation Control |
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| Volume | 20 |
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| Number | 1 |
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| Page | 18-25 |
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| Year/Month | 1999/ |
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| Article | Report |
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| Publisher | Japan Society of Circulation Control |
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| Abstract | Endotoxin-induced septic shock is associated with hypotension due to vasodilation by nitric oxide overproduction. However, it is poorly understood whether cardiac dysfunction observed in septic shock is related to hypotension. The aim of this study was to investigate possible mechanisms underlying the impaired contractile response to β-adrenoceptor stimulation at an early phase of septic shock. Septic shock was induced in Newzealand White rabbits by administration of lipopolysaccharide (LPS : 100 μg/kg iv). Papillary muscles isolated from the septic hearts 3 and 6 hours after LPS administration exhibited marked reductions in the positive inotropic response to isoproterenol regardless of whether 100μM Nω-nitro-L-arginine was present. The density of myocardial β-adrenoceptors and the affinity of myocardial β-adrenoceptors to catecholamine were unaffected by LPS pretreatment. These results suggest that the impaired contractile response to β-adrenoceptor stimulation observed in septic myocardium is not caused by the direct inhibition of NO. Alterations in coupling of β-adrenoceptors to the signaling pathways rather than the decreased density of the receptors may contribute to the impaired response. |
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| Practice | Basic medicine |
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| Keywords | Septic shock, LPS, β-adrenoceptors, Nitric oxide |
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