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一氧化碳对血管紧张度的作用。

The contribution of carbon monoxide to vascular tonus.

作者信息

Koçer Günnur, Nasircilar Ülker Seher, Şentürk Ümit Kemal

机构信息

Department of Physiology, Medical Faculty, Near East University, Nicosia, Cyprus.

Department of Physiology, Medical Faculty, Akdeniz University, Antalya, Turkey.

出版信息

Microcirculation. 2018 Oct;25(7):e12495. doi: 10.1111/micc.12495. Epub 2018 Aug 27.

DOI:10.1111/micc.12495
PMID:30040171
Abstract

OBJECTIVE

The aim of this descriptive study was to examine the contribution of CO in the maintenance of vascular tonus in different organs and different vessel segments; the underlying mechanism of CO-induced vasodilation was investigated.

METHODS

Sixty Wistar albino rats, aged 6-8 months, were used in this study. Response to CO by isolated arteries from the thoracic and abdominal aorta and mesenteric, renal, gastrocnemius, and gracilis muscles as well as heart, lung, and brain vascular beds was endogenously and exogenously studied using organ baths or myograph. In addition, HO-2 protein expression was assessed using Western blot analysis in isolated vessel segments.

RESULTS

Although CO was shown to contribute to the regulation of vascular tonus in all feed arteries except those of the gracilis vascular bed, no effect was observed in the resistance arteries, with the sole exception of the pial artery. No relationship between HO-2 protein level and CO contribution to endogenous vascular tonus was observed.

CONCLUSIONS

While the vasodilator effect of CO in vessels smaller than 600 μm in diameter was found to be mediated via potassium channels, in vessels larger than 600 μm in diameter, the effect was through both the potassium channels and the cGMP pathway.

摘要

目的

本描述性研究旨在探讨一氧化碳(CO)在维持不同器官和不同血管段血管张力中的作用;研究CO诱导血管舒张的潜在机制。

方法

本研究使用了60只6 - 8个月大的Wistar白化大鼠。采用器官浴或肌动描记器对内源性和外源性给予CO后,胸主动脉、腹主动脉、肠系膜、肾、腓肠肌和股薄肌的离体动脉以及心脏、肺和脑血管床的反应进行研究。此外,采用蛋白质免疫印迹分析法评估离体血管段中血红素加氧酶-2(HO-2)蛋白的表达。

结果

尽管已证明CO有助于调节除股薄肌血管床以外的所有供血动脉的血管张力,但在阻力动脉中未观察到影响,唯一的例外是软脑膜动脉。未观察到HO-2蛋白水平与CO对内源性血管张力的作用之间存在关联。

结论

虽然发现直径小于600μm的血管中CO的血管舒张作用是通过钾通道介导的,但在直径大于600μm的血管中,其作用是通过钾通道和环磷酸鸟苷(cGMP)途径实现的。

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