Rubanyi G M
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota 55905.
Am J Physiol. 1988 Oct;255(4 Pt 2):H783-8. doi: 10.1152/ajpheart.1988.255.4.H783.
Experiments were conducted in a bioassay system, where a canine coronary artery ring without endothelium (bioassay tissue) was superfused by the effluent from a perfused canine carotid artery segment with endothelium (donor segment). A rapid increase in transmural pressure (from near 0 to 32-38 mmHg) triggered active contraction of the donor segment and simultaneously of the bioassay tissue. These contractions were prevented by removal of the endothelium from the donor segment but not by treatment of the segment with indomethacin. Exposure to elevated pressure depressed basal, acetylcholine-, and flow-induced release of endothelium-derived relaxing factor(s). Methylene blue prevented the pressure-induced contraction of the bioassay ring. These data show that pressure-induced contraction of isolated carotid arteries is endothelium dependent and is mediated by the depression of the synthesis and/or release of endothelium-derived relaxing factor(s).
实验在一个生物测定系统中进行，在该系统中，无内皮的犬冠状动脉环（生物测定组织）被来自有内皮的灌注犬颈动脉段（供体段）的流出液灌流。跨壁压力的快速升高（从接近0至32 - 38 mmHg）引发供体段以及同时生物测定组织的主动收缩。这些收缩可通过去除供体段的内皮来防止，但用吲哚美辛处理该段则不能防止。暴露于升高的压力会抑制基础的、乙酰胆碱诱导的以及血流诱导的内皮衍生舒张因子的释放。亚甲蓝可防止生物测定环的压力诱导收缩。这些数据表明，离体颈动脉的压力诱导收缩是内皮依赖性的，并且是由内皮衍生舒张因子的合成和/或释放受抑制所介导的。
