1968
DOI: 10.1007/978-3-662-25618-3_5
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Durchblutung und Sauerstoffaufnahme des Gehirns

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Cited by 4 publications
(1 citation statement)
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“…Summary: In search of factors influencing the outcome of an ischemic insult, we induced 10 min of forebrain ischemia in rats and assessed neuronal necrosis by quan titative histopathology after I week of recovery, Proce dures for inducing ischemia included bilateral carotid ar tery clamping and reduction of blood pressure to 40-50 mm Hg by bleeding, To facilitate rapid lowering of blood pressure, a ganglionic blocker, trimethaphan (TMP), was administered at the onset of ischemia, Omission of the ganglionic blocker proved to markedly ameliorate neu-Although the problem is of considerable theoret ical and practical importance, controversy still re volves around the question of the true revival times of neurons in the brain, i,e" the longest period of anoxia-ischemia that can be sustained without causing neuronal damage, In the clinical setting de finitive brain damage is usually incurred if cardiac arrest lasts longer than 4-5 min (Cole and Corday, 1956;Hirsch and Schneider, 1968), However, clin ical revival times may be that short because post ischemic conditions do not favor prompt resump tion of an adequate recirculation, Experimentally these problems can be circum vented and long-term recovery can be instituted, allowing assessment of the final behavioral-neuro logical deficit and/or histological damage, In spite of this, reported revival times are surprisingly vari able (see Hirsch and Schneider, 1968;Siesjo, 1978;Hossmann, 1985). On the one hand, some experi ments have revealed moderate but unequivocal ronal damage, Similarly favorable effects were obtained when a mixture of adrenaline and noradrenaline (I fLg kg -[ min -[ each) was infused during the early recircula tion period in animals previously given TMP Infusion of noradrenaline alone also ameliorated the damage, though the efficacy was somewhat less, The results suggest that catecholamines, released as a response to stress, ame liorate ischemic brain damage, Key Words: Circulating catecholamines-Ischemic neuronal necrosis-Revival times, neuronal necrosis, localized to selective vulnerable areas, following 4-6 min of ischemia (Ito et al, 1975;Kirino, 1982;Kirino and Sano, 1984;Smith et al, 1984a;Bl omqvist and Wieloch, 1985).…”
mentioning
confidence: 99%
“…Summary: In search of factors influencing the outcome of an ischemic insult, we induced 10 min of forebrain ischemia in rats and assessed neuronal necrosis by quan titative histopathology after I week of recovery, Proce dures for inducing ischemia included bilateral carotid ar tery clamping and reduction of blood pressure to 40-50 mm Hg by bleeding, To facilitate rapid lowering of blood pressure, a ganglionic blocker, trimethaphan (TMP), was administered at the onset of ischemia, Omission of the ganglionic blocker proved to markedly ameliorate neu-Although the problem is of considerable theoret ical and practical importance, controversy still re volves around the question of the true revival times of neurons in the brain, i,e" the longest period of anoxia-ischemia that can be sustained without causing neuronal damage, In the clinical setting de finitive brain damage is usually incurred if cardiac arrest lasts longer than 4-5 min (Cole and Corday, 1956;Hirsch and Schneider, 1968), However, clin ical revival times may be that short because post ischemic conditions do not favor prompt resump tion of an adequate recirculation, Experimentally these problems can be circum vented and long-term recovery can be instituted, allowing assessment of the final behavioral-neuro logical deficit and/or histological damage, In spite of this, reported revival times are surprisingly vari able (see Hirsch and Schneider, 1968;Siesjo, 1978;Hossmann, 1985). On the one hand, some experi ments have revealed moderate but unequivocal ronal damage, Similarly favorable effects were obtained when a mixture of adrenaline and noradrenaline (I fLg kg -[ min -[ each) was infused during the early recircula tion period in animals previously given TMP Infusion of noradrenaline alone also ameliorated the damage, though the efficacy was somewhat less, The results suggest that catecholamines, released as a response to stress, ame liorate ischemic brain damage, Key Words: Circulating catecholamines-Ischemic neuronal necrosis-Revival times, neuronal necrosis, localized to selective vulnerable areas, following 4-6 min of ischemia (Ito et al, 1975;Kirino, 1982;Kirino and Sano, 1984;Smith et al, 1984a;Bl omqvist and Wieloch, 1985).…”
mentioning
confidence: 99%