美蓝对电刺激毁脑脊髓大鼠交感神经诱发的后肢缩血管反应的影响

用含10/μmol·L~(-1)的美蓝及同浓度的血红蛋白营养液恒速灌流,使高频(16Hz)电刺激毁脑脊髓大鼠交感神经诱发的后肢血管灌流压升高作用明显增强,但对低频电刺激作用无明显影响.1μmol·L~(-1)乙酰胆碱显著抑制各频率电刺激引起的灌流压增高,提示血管内皮可能通过释放血管内皮舒张国子来缓解过度刺激肾上腺素能神经引起的缩血管反应。

Influence of methylene blue on vasoconstrictor response to spinal sympathetic nerve stimulation in pithed rat hind limb

It has recently been proposed that alpha 2 adrenergic receptor is also located at the vascular endothelial cells and the stimulation of thereceptor leads to the release of endothelium derived relaxing factor(EDRF).Therefore,the removal of the endothelium markedly enhanced the vasoconstrictor re- spouse to norepinephrine(NE)and other alpha-agonists.However,the influence of the endothelium on the vasoconstrictor response to endogenous NE from adrenergic nerves remains unclear.In this work,the influence of methylene blue(MB),hemoglobin(Hb)and acetylcholine(ACh)on the vasoconstrictor response to electrical stimulation of the spinal sympathetic nerve in the perfused hind limb of the pithed rats has been observed.The spinal stimulation induced the frequency-dependent increase of the hind limb perfused pressure(HPP).During the infusion of MB(10μmol·L-1)and Hb(10μmol·L-1),the special inhibitors of EDRF,HPP to spinal stimulation at 16 Hz for 20 s were significantly enhanced,whereas the responses at 1 and 4 Hz were unaffected.ACh(1μmol·L-1)markedly inhibited the response to spinal stimulation at 1,4 and 16 Hz.It is concluded thatEDRF inhibits the vascular response to the sympathetic stimulation and released NE by high frequency stimulation from adrenergic nerve terminal,located almost exclusively at adventitial-medial border,would diffuse through smooth muscle cells prior to reaching and stimulating alpha-2 receptor at the endothelial cells.However,NE level by low frequency stimulation is so low that it would not reach the endothelium.As a physiological role,the endothelium will modulate the vascular response to severe stimulation by releasing EDRF.