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血管周围脂肪组织对大鼠主动脉冷却所致抗收缩效应的减弱作用。

Attenuation of the anti-contractile effect of cooling in the rat aorta by perivascular adipose tissue.

作者信息

Rafique Y, AlBader M, Oriowo M

机构信息

Pharmacology & Toxicology Department, Health Sciences Centre, Kuwait University, Kuwait, Kuwait.

出版信息

Auton Autacoid Pharmacol. 2017 Sep;37(4):52-60. doi: 10.1111/aap.12058. Epub 2017 Sep 4.

Abstract

In addition to providing mechanical support for blood vessels, the perivascular adipose tissue (PVAT) secretes a number of vasoactive substances and exerts an anticontractile effect. The main objective of this study was to find out whether the anticontractile effect of cooling in the rat aorta is affected by PVAT. Our hypothesis was that PVAT would enhance the anticontractile effect of cooling in the rat aorta. Aorta segments, with or without PVAT, were used in this investigation. Cumulative concentration-response curves were established for phenylephrine at 37°C or 24°C. Phenylephrine (10 M - 10 M) induced concentration-dependent contractions of aorta segments with or without PVAT at 37°C. The maximum response, but not pD value, was reduced in aorta segments with PVAT. Cooling the tissues to 24 °C resulted in a significant reduction in the maximum response in aorta segments without PVAT with no change in pD values. However, the anticontractile effect of cooling was attenuated in the presence of PVAT with no significant (p > 0.05) change in either the maximum response or pD value. L-NAME potentiated PE-induced contractions and this was greater in aorta segments without PVAT at both temperatures. The expression of eNOS protein and basal tissue level of nitric oxide (NO) were greater in aorta segments with PVAT at both temperatures. However, PE significantly increased tissue levels of NO only in aorta segments without PVAT. We concluded that PVAT-induced loss of anticontractile effect of cooling against PE-induced contractions could be due to impaired generation of NO in aorta segments with PVAT.

摘要

除了为血管提供机械支持外,血管周围脂肪组织(PVAT)还分泌多种血管活性物质并发挥抗收缩作用。本研究的主要目的是探究大鼠主动脉冷却的抗收缩作用是否受PVAT影响。我们的假设是PVAT会增强大鼠主动脉冷却的抗收缩作用。本研究使用了带或不带PVAT的主动脉段。分别在37°C或24°C下建立去氧肾上腺素的累积浓度-反应曲线。在37°C时,去氧肾上腺素(10⁻⁹ M - 10⁻⁵ M)可诱导带或不带PVAT的主动脉段产生浓度依赖性收缩。带PVAT的主动脉段的最大反应降低,但pD值未降低。将组织冷却至24°C会导致不带PVAT的主动脉段的最大反应显著降低,而pD值无变化。然而,在存在PVAT的情况下,冷却的抗收缩作用减弱,最大反应或pD值均无显著变化(p > 0.05)。L-NAME增强了PE诱导的收缩,且在两个温度下,不带PVAT的主动脉段这种增强作用更大。在两个温度下,带PVAT的主动脉段中eNOS蛋白的表达和一氧化氮(NO)的基础组织水平均更高。然而,PE仅在不带PVAT的主动脉段中显著增加了组织中的NO水平。我们得出结论,PVAT导致冷却对PE诱导收缩的抗收缩作用丧失可能是由于带PVAT的主动脉段中NO生成受损。

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