Saito Y, Eraslan A, Lockard V, Hester R L
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.
Am J Physiol. 1994 Sep;267(3 Pt 2):H1227-31. doi: 10.1152/ajpheart.1994.267.3.H1227.
This study was designed to determine the importance of the venular endothelium in the vasodilation of adjacent arterioles during functional hyperemia. The hamster cremaster muscle was prepared for in vivo microscopy. Two silver-silver chloride electrodes were placed across the pedicle of the cremaster muscle, and a square-wave pulse (10 V amplitude, 1 ms duration, and 1 Hz frequency) was used to elicit muscle contraction. Muscle stimulation for 1 min resulted in a vasodilation of the first-order arterioles from 74 +/- 2 to 91 +/- 2 microns (n = 9, P < 0.05). After perfusion of the venule with air to disrupt the venular endothelium, there was no significant effect on the resting diameter, 73 +/- 3 microns, but the vasodilation associated with the muscle stimulation was significantly attenuated to 82 +/- 3 microns (P < 0.01). After completion of these experiments, the disruption of venular endothelium was confirmed by electron microscopy. The functional vasodilation of arterioles adjacent to venules with an intact endothelium (venules in which air did not enter) was retained after air perfusion (n = 6). These results suggest that the presence of the venular endothelium is important for the arteriolar vasodilation during functional hyperemia. We propose that the venular endothelium releases a relaxing factor responsible for a portion of the functional arteriolar vasodilation.
本研究旨在确定在功能性充血期间，微静脉内皮在相邻小动脉血管舒张中的重要性。制备仓鼠提睾肌用于体内显微镜观察。将两个银 - 氯化银电极置于提睾肌蒂上，使用方波脉冲（幅度10 V，持续时间1 ms，频率1 Hz）引发肌肉收缩。肌肉刺激1分钟导致一级小动脉血管舒张，直径从74±2微米增至91±2微米（n = 9，P < 0.05）。用空气灌注微静脉以破坏微静脉内皮后，对静息直径（73±3微米）无显著影响，但与肌肉刺激相关的血管舒张显著减弱至82±3微米（P < 0.）。这些实验完成后，通过电子显微镜证实了微静脉内皮的破坏。空气灌注后，与完整内皮微静脉（空气未进入的微静脉）相邻的小动脉的功能性血管舒张得以保留（n = 6）。这些结果表明，微静脉内皮的存在对功能性充血期间小动脉血管舒张很重要。我们提出，微静脉内皮释放一种舒张因子，该因子负责部分功能性小动脉血管舒张。
