メチレンブルーが敗血症性ショックの呼吸・循環に及ぼす影響
敗血症性ショックでは一酸化窒素(NO)に起因するcyclic 3',5'-guanosine monophosphate(cGMP)の増加が末梢血管抵抗低下の原因となっている。われわれは敗血症性ショック患者にcGMP産生を抑制するmethylene blue(MB;可溶性グアニール酸シクラーゼ阻害剤)を投与して循環とガス交換への影響を調べた。Hyperdynamic state (CI>3.5l・min-1・m-2)を示した敗血症患者8例を対象として,MB2mg・kg-1を30分間で投与した。投与前,投与直後,投与終了1,2,24時間後に呼吸,循環の各パラメータ,血中...
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Published in | 日本集中治療医学会雑誌 Vol. 2; no. 3; pp. 87 - 91 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | Japanese |
Published |
一般社団法人 日本集中治療医学会
01.07.1995
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Online Access | Get full text |
ISSN | 1340-7988 1882-966X |
DOI | 10.3918/jsicm.2.87 |
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Abstract | 敗血症性ショックでは一酸化窒素(NO)に起因するcyclic 3',5'-guanosine monophosphate(cGMP)の増加が末梢血管抵抗低下の原因となっている。われわれは敗血症性ショック患者にcGMP産生を抑制するmethylene blue(MB;可溶性グアニール酸シクラーゼ阻害剤)を投与して循環とガス交換への影響を調べた。Hyperdynamic state (CI>3.5l・min-1・m-2)を示した敗血症患者8例を対象として,MB2mg・kg-1を30分間で投与した。投与前,投与直後,投与終了1,2,24時間後に呼吸,循環の各パラメータ,血中cyclic 3',5'-adenosine monophosphate (cAMP),cGMP濃度を測定した。その結果,平均動脈圧,全身血管抵抗係数はMB投与終了直後に著明な増加を認め,1時間後にはやや低下したが24時間後まで有意な増加が持続した。平均肺動脈圧,肺内シャント率,呼吸係数は投与前後で有意に変化しなかった。cGMPは投与終了2時間後に有意に低下したがcAMPは変化しなかった。以上よりMBは敗血症性ショックに対して全身循環動態を改善させるがガス交換には影響を与えないことがわかった。 |
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AbstractList | 敗血症性ショックでは一酸化窒素(NO)に起因するcyclic 3',5'-guanosine monophosphate(cGMP)の増加が末梢血管抵抗低下の原因となっている。われわれは敗血症性ショック患者にcGMP産生を抑制するmethylene blue(MB;可溶性グアニール酸シクラーゼ阻害剤)を投与して循環とガス交換への影響を調べた。Hyperdynamic state (CI>3.5l・min-1・m-2)を示した敗血症患者8例を対象として,MB2mg・kg-1を30分間で投与した。投与前,投与直後,投与終了1,2,24時間後に呼吸,循環の各パラメータ,血中cyclic 3',5'-adenosine monophosphate (cAMP),cGMP濃度を測定した。その結果,平均動脈圧,全身血管抵抗係数はMB投与終了直後に著明な増加を認め,1時間後にはやや低下したが24時間後まで有意な増加が持続した。平均肺動脈圧,肺内シャント率,呼吸係数は投与前後で有意に変化しなかった。cGMPは投与終了2時間後に有意に低下したがcAMPは変化しなかった。以上よりMBは敗血症性ショックに対して全身循環動態を改善させるがガス交換には影響を与えないことがわかった。 |
Author | 小野, 知美 星屋, 博信 岡本, 光明 中, 敏夫 森永, 俊彦 友渕, 佳明 篠崎, 正博 川崎, 貞男 |
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References | 7) Ferrari-Baliviera E, Mealy K, Smith RJ, et al. Tumor necrosis factor induces adult respiratory distress syndrome in rats. Arch Surg 1989; 124: 1400-5. 12) Persson MG, Gustafsson LE, Wiklund NP, et al. Endogenous nitric-oxide as a probable modulator of pulmonary circulation and hypoxic pressure response in vivo. Acta Physiol Scand 1990; 140: 449-57. 14) Schilling J, Cakmakci M, Baettig U, et al. A new approach in the treatment of hypotension in human septic shock by NG-monomethyl-L-arginine, an inhibitor of the nitric oxide synthetase. Intensive care Med 1993; 19: 227-31. 13) Liew FY, Cox FE. Non-specific defence mechanism: the role of nitric oxide. Immunol Today 1991; 12: A 17-21. 6) Donnelly SC, Strieter RM, Kunkel SL, et al. Interleukin-8 and development of adult respiratory distress syndrome in at-risk patient. Lancet 1993; 341: 643-7. 10) 渡辺正弘,浜野哲夫,松本剛.ワゴステインの吸収・分布・代謝および排泄.新薬と臨床1974;23:691-7. 9) Shneider F, Lutun P, Hasselmann M, et al. Methylene blue increases systemic resistance in human septic shock. Intensive Care Med 1992; 18: 309-11. 16) Schneider F, Lutun Ph, Couchot A, et al. Plasma cyclic guanosine 3'-5' monophosphate concentrations and low vascular resistance in human septic shock. Intensive care Med 1993; 19: 99-104. 4) Besaley D. Interleukin 1 and endotoxin activate soluble guanylate cyclase in vascular smooth muscle. Am J Physiol 1990; 259: r38-r44. 2) Fleming I, Gray GA, Julou-Schaeffer G, et al. Impaired vascular reactivity in the rat following endotoxin treatment can be endothelium-imdependent, yet involves the L-arginine pathway. J Physiol London (proceeding) 1990; 423: 18. 1) Parratt JR. Alterations in vascular reactivity in sepsis and endotoxemia. In: Vincent JL. Update in Intensive Care and Emergency Medicine. Berlin: Springer 1973; 8: 299-308. 15) Harvey SC. Antiseptics and disinfectants; fungcides, ectoparasiticides. In: Goodman LS, Gilman A, editors. The Pharmacological Basis of Therapeutics 3rd ed. New York: The MacMillan Co, 1970; 1003-4. 8) Hutcheson IR, Whittle BRJ, Boughton-Smith NK. Role of nitric oxide in maintaining vascular integrity in endotoxin-induced acute intestinal damage in the rat. Br J Pharmacol 1990; 101: 815-20. 5) Martin W, Furchgott RF, Villani GM, et al. Depression of contractile responses in rat aorta by spontaneously released endothelium-derived relaxing factor (EDRF). J Pharmacol Exp. Ther 1989; 237: 529-38. 3) Parratt JR, Stoclet JC. Nitric oxide as a mediator of the vascular derangements of sepsis and endotoxemia. In: Lamy M, Thijs LG, editors. Mediators of Sepsis. Berlin: Springer-Verlag, 1992: 174-89. 11) Sprague RS, Thiemermann C, Vane JR. Endogenous nitric oxide maintains blood flow to hypoxic alveoli in anaesthetized rabbits. J Vasc Res 1992; 29: 202. |
References_xml | – reference: 14) Schilling J, Cakmakci M, Baettig U, et al. A new approach in the treatment of hypotension in human septic shock by NG-monomethyl-L-arginine, an inhibitor of the nitric oxide synthetase. Intensive care Med 1993; 19: 227-31. – reference: 7) Ferrari-Baliviera E, Mealy K, Smith RJ, et al. Tumor necrosis factor induces adult respiratory distress syndrome in rats. Arch Surg 1989; 124: 1400-5. – reference: 16) Schneider F, Lutun Ph, Couchot A, et al. Plasma cyclic guanosine 3'-5' monophosphate concentrations and low vascular resistance in human septic shock. Intensive care Med 1993; 19: 99-104. – reference: 1) Parratt JR. Alterations in vascular reactivity in sepsis and endotoxemia. In: Vincent JL. Update in Intensive Care and Emergency Medicine. Berlin: Springer 1973; 8: 299-308. – reference: 9) Shneider F, Lutun P, Hasselmann M, et al. Methylene blue increases systemic resistance in human septic shock. Intensive Care Med 1992; 18: 309-11. – reference: 2) Fleming I, Gray GA, Julou-Schaeffer G, et al. Impaired vascular reactivity in the rat following endotoxin treatment can be endothelium-imdependent, yet involves the L-arginine pathway. J Physiol London (proceeding) 1990; 423: 18. – reference: 8) Hutcheson IR, Whittle BRJ, Boughton-Smith NK. Role of nitric oxide in maintaining vascular integrity in endotoxin-induced acute intestinal damage in the rat. Br J Pharmacol 1990; 101: 815-20. – reference: 11) Sprague RS, Thiemermann C, Vane JR. Endogenous nitric oxide maintains blood flow to hypoxic alveoli in anaesthetized rabbits. J Vasc Res 1992; 29: 202. – reference: 15) Harvey SC. Antiseptics and disinfectants; fungcides, ectoparasiticides. In: Goodman LS, Gilman A, editors. The Pharmacological Basis of Therapeutics 3rd ed. New York: The MacMillan Co, 1970; 1003-4. – reference: 5) Martin W, Furchgott RF, Villani GM, et al. Depression of contractile responses in rat aorta by spontaneously released endothelium-derived relaxing factor (EDRF). J Pharmacol Exp. Ther 1989; 237: 529-38. – reference: 10) 渡辺正弘,浜野哲夫,松本剛.ワゴステインの吸収・分布・代謝および排泄.新薬と臨床1974;23:691-7. – reference: 4) Besaley D. Interleukin 1 and endotoxin activate soluble guanylate cyclase in vascular smooth muscle. Am J Physiol 1990; 259: r38-r44. – reference: 6) Donnelly SC, Strieter RM, Kunkel SL, et al. Interleukin-8 and development of adult respiratory distress syndrome in at-risk patient. Lancet 1993; 341: 643-7. – reference: 13) Liew FY, Cox FE. Non-specific defence mechanism: the role of nitric oxide. Immunol Today 1991; 12: A 17-21. – reference: 3) Parratt JR, Stoclet JC. Nitric oxide as a mediator of the vascular derangements of sepsis and endotoxemia. In: Lamy M, Thijs LG, editors. Mediators of Sepsis. Berlin: Springer-Verlag, 1992: 174-89. – reference: 12) Persson MG, Gustafsson LE, Wiklund NP, et al. Endogenous nitric-oxide as a probable modulator of pulmonary circulation and hypoxic pressure response in vivo. Acta Physiol Scand 1990; 140: 449-57. |
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Snippet | 敗血症性ショックでは一酸化窒素(NO)に起因するcyclic 3',5'-guanosine monophosphate(cGMP)の増加が末梢血管抵抗低下の原因となっている。われわれは敗血症性ショック患... |
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Title | メチレンブルーが敗血症性ショックの呼吸・循環に及ぼす影響 |
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