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在颈动脉内膜切除术期间缺血再灌注过程中脂质过氧化的生理反应。

Physiological response to lipid peroxidation in ischemia and reperfusion during carotid endarterectomy.

机构信息

Università degli Studi di Cagliari - Dipartimento di Biologia Sperimentale - Cittadella, Universitaria - 09042 Monserrato, Cagliari, Italy.

出版信息

Lipids Health Dis. 2010 Apr 21;9:41. doi: 10.1186/1476-511X-9-41.

DOI:10.1186/1476-511X-9-41
PMID:20409338
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2874547/
Abstract

BACKGROUND

In this study we aimed to assess lipid peroxidation during carotid endarterectomy by the formation of PUFA hydroperoxides (PUFAHP) and isoprostanes (IP) and concomitant peroxisomal beta-oxidation as a physiological mechanism to limit their concentration. Two markers of peroxisomal beta oxidation have been evaluated, formation of 2,3 dinor from IP and conjugated esadecadienoic acid (CD 16:2) from peroxisomal beta-oxidation of conjugated linoleic acid (CLA), an unusual fatty acid present in small concentration in our diet and preferentially beta-oxidised in peroxisomes.The study was conducted on 30 patients undergoing carotid endarterectomy. Blood samplings were performed before, during endarterectomy in the "ischemic phase", and 30 seconds, 30 minutes and 2 hours after reperfusion.

RESULTS

The results showed that PUFAHP increased significantly after 30 min of reperfusion in patients with controlateral stenosis > 50%, and steeply decreased after 2 hour of reperfusion. Interestingly, IP increased in a similar fashion of PUFAHP but never significantly. Both ratios CD16:2/CLA and DIN/IP also increased significantly after 30 min of reperfusion to decrease thereafter.

CONCLUSIONS

Our data show that lipid peroxidation takes place only in patients with high controlateral stenosis and within 2 hours occurs a physiological response aimed to decrease IP and PUFAHP by increasing their catabolism in peroxisomes.

摘要

背景

在这项研究中，我们旨在通过多不饱和脂肪酸（PUFA）过氧化物（PUFAHP）和异前列腺素（IP）的形成以及伴随的过氧化物体β-氧化来评估颈动脉内膜切除术过程中的脂质过氧化作用，这是一种限制其浓度的生理机制。评估了过氧化物体β氧化的两个标志物，即 IP 从 2,3 二诺到形成和共轭亚油酸（CLA）的过氧化物体β-氧化共轭的 esadecadienoic 酸（CD16：2），CLA 是一种在我们饮食中浓度较低的不寻常脂肪酸，并且优先在过氧化物体中β-氧化。该研究在 30 名接受颈动脉内膜切除术的患者中进行。在术前、内膜切除术期间的“缺血期”以及再灌注后 30 秒、30 分钟和 2 小时进行血液采样。

结果

结果显示，在对侧狭窄> 50%的患者中，再灌注 30 分钟后 PUFAHP 显著增加，并在再灌注 2 小时后急剧下降。有趣的是，IP 以与 PUFAHP 相似的方式增加，但从未显著增加。CD16：2/CLA 和 DIN/IP 比值在再灌注 30 分钟后也显著增加，随后降低。

结论

我们的数据表明，脂质过氧化作用仅发生在对侧狭窄程度较高的患者中，并且在 2 小时内发生了一种生理反应，旨在通过增加其在过氧化物体中的分解代谢来降低 IP 和 PUFAHP。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff6/2874547/2ab7bdc7f3f5/1476-511X-9-41-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff6/2874547/b8bbe0df07a4/1476-511X-9-41-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff6/2874547/7085244fe9a9/1476-511X-9-41-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff6/2874547/2ab7bdc7f3f5/1476-511X-9-41-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff6/2874547/b8bbe0df07a4/1476-511X-9-41-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff6/2874547/7085244fe9a9/1476-511X-9-41-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff6/2874547/2ab7bdc7f3f5/1476-511X-9-41-3.jpg

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