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大鼠固定应激期间儿茶酚胺介导的脑氧摄取增加。

A catecholamine-mediated increase in cerebral oxygen uptake during immobilisation stress in rats.

作者信息

Carlsson C, Hägerdal M, Kaasik A E, Siesjö B K

出版信息

Brain Res. 1977 Jan 1;119(1):223-31. doi: 10.1016/0006-8993(77)90102-0.

DOI:10.1016/0006-8993(77)90102-0
PMID:830383
Abstract

Anxiety and grave apprehension have been supposed to increase cerebral metabolism, and it has earlier been suggested that intravenous infusion of adrenaline may increase cerebral blood flow (CBF) and cerebral oxygen consumption (CMR02). In an experimental model on rats, it could be shown that immobilisation stress increased CBF and CMR02 after 5 min (about 150% of control values) and 30 min (about 190% of control values). By previous adrenalectomy or by administration of a beta-receptor blocker (propranolol, 1.4 mg/kg) the changes in CBF and CMR02 could be prevented. It is concluded that the excessive increase in CBF and CMR02 was mediated via release of catecholamines from the adrenal glands.

摘要

焦虑和严重忧虑被认为会增加大脑代谢,并且早些时候有人提出静脉注射肾上腺素可能会增加脑血流量(CBF)和脑氧耗量(CMR02)。在大鼠实验模型中,可以证明固定应激在5分钟(约为对照值的150%)和30分钟(约为对照值的190%)后会增加CBF和CMR02。通过先前的肾上腺切除术或给予β受体阻滞剂(普萘洛尔,1.4mg/kg),可以防止CBF和CMR02的变化。得出的结论是,CBF和CMR02的过度增加是通过肾上腺释放儿茶酚胺介导的。

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