Department of Anesthesia, McMaster University, Hamilton, Ontario, Canada.
Anesth Analg. 2011 Jun;112(6):1339-45. doi: 10.1213/ANE.0b013e318215e094. Epub 2011 May 5.
Propofol causes hypotension due to relaxation of vascular smooth muscle cells through its direct or indirect vasodilator effects. Perivascular adipose tissue (PVAT) and endothelium attenuate vascular contraction, and the function of PVAT is altered in hypertension and diabetes. Whether PVAT affects the action of anesthetics on vascular function is unknown. We studied the mechanisms of propofol-induced relaxation in relation to the involvement of PVAT and endothelium.
Thoracic aortic rings from Wistar rats were prepared with or without PVAT (PVAT+ and PVAT-), intact endothelium (E+), or both, or with the endothelium removed (E-) for functional studies.
In phenylephrine precontracted vessels, propofol-induced relaxation was highest with both PVAT and E+ and lowest in vessels denuded of both PVAT and endothelium. Propofol-induced relaxation occurred via both endothelium-dependent and -independent mechanisms. The relaxation response induced by propofol was significantly reduced by nitric oxide synthase inhibitor (l-NNA), K(+) channel blockers (tetraethylammonium and glibenclamide) in E+ and E- vessels, and by soluble guanylyl cyclase inhibitor 1H-(1,2,4) oxadiazolo (4,3-A) quinazoline-1-one and hydrogen peroxide scavenger (catalase) in E- vessels. The presence of PVAT significantly enhanced the relaxation response induced by propofol. In contrast to phenylephrine precontracted vessels in which the presence of PVAT or endothelium had an effect, in vessels precontracted with KCl, propofol-induced relaxation was similar among the 4 types of vessel preparation.
PVAT enhances the relaxation effect induced by propofol in rat aorta through both endothelium-dependent and endothelium-independent pathways thus highlighting the clinical importance of PVAT.
丙泊酚通过其直接或间接的血管扩张作用引起血管平滑肌松弛，导致低血压。血管周围脂肪组织 (PVAT) 和内皮细胞可减轻血管收缩，PVAT 的功能在高血压和糖尿病中发生改变。PVAT 是否影响麻醉剂对血管功能的作用尚不清楚。我们研究了与 PVAT 和内皮细胞参与相关的丙泊酚诱导松弛的机制。
用或不用血管周围脂肪组织 (PVAT+) 和/或完整内皮细胞 (E+) 或两者均无 (E-) 从 Wistar 大鼠胸主动脉环中制备，用于功能研究。
在去氧肾上腺素预收缩的血管中，同时存在 PVAT 和 E+时丙泊酚诱导的松弛作用最强，而两者均不存在时最低。丙泊酚诱导的松弛作用通过内皮细胞依赖和非依赖机制发生。一氧化氮合酶抑制剂 (l-NNA)、K(+) 通道阻滞剂 (四乙铵和格列本脲) 在 E+和 E-血管中显著降低丙泊酚诱导的松弛反应，而在 E-血管中可溶性鸟苷酸环化酶抑制剂 1H-(1,2,4) 恶二唑 (4,3-A) 喹唑啉-1-酮和过氧化氢清除剂 (过氧化氢酶) 也降低了丙泊酚诱导的松弛反应。存在 PVAT 可显著增强丙泊酚诱导的松弛反应。与存在 PVAT 或内皮细胞对去氧肾上腺素预收缩血管松弛反应有影响不同，在 KCl 预收缩的血管中，4 种血管制备类型的丙泊酚诱导的松弛反应相似。
PVAT 通过内皮细胞依赖和非依赖途径增强大鼠主动脉中丙泊酚诱导的松弛作用，从而凸显了 PVAT 的临床重要性。
