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缺血大鼠心脏再灌注期间内源性去甲肾上腺素溢出的起源

Origins of endogenous noradrenaline overflow during reperfusion of the ischaemic rat heart.

作者信息

Dart A M, Riemersma R A

机构信息

Department of Medicine, University of Edinburgh, U.K.

出版信息

Clin Sci (Lond). 1988 Mar;74(3):269-74. doi: 10.1042/cs0740269.

Abstract
  1. Reperfusion of the globally ischaemic isolated rat heart is associated with an enhanced overflow of endogenous noradrenaline (NA) after ischaemic periods of 20, 40 or 60 min but not of 10 min. 2. Reperfusion NA overflow, after 40 min of ischaemia, is suppressed by desipramine and increased when ischaemia follows a period of substrate deprivation. 3. Reperfusion after 40 min of ischaemia is associated with a significant rise in NA concentration despite a simultaneous 20-fold increase in flow. This increase in concentration is abolished by treatment with desipramine or if ischaemia follows a period of substrate deprivation. 4. Reperfusion NA overflow correlates with the reperfusion overflow of an extracellular space marker infused before the ischaemic episode. 5. These results suggest that ischaemia is heterogeneous and that NA is released into regions of particularly profound ischaemia from which it is subsequently eluted during reperfusion.
摘要
  1. 对整体缺血的离体大鼠心脏进行再灌注时,在缺血20、40或60分钟(而非10分钟)后,内源性去甲肾上腺素(NA)的溢出会增强。2. 缺血40分钟后的再灌注NA溢出,会被地昔帕明抑制,而当缺血发生在底物剥夺期之后时,溢出会增加。3. 缺血40分钟后的再灌注与NA浓度的显著升高相关,尽管血流量同时增加了20倍。这种浓度的增加会被地昔帕明治疗消除,或者如果缺血发生在底物剥夺期之后也会消除。4. 再灌注NA溢出与缺血发作前注入的细胞外空间标记物的再灌注溢出相关。5. 这些结果表明缺血是异质性的,并且NA会释放到缺血特别严重的区域,随后在再灌注期间从这些区域洗脱。

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