SUBSTANCE-P AS NEUROGENIC MEDIATOR OF ANTIDROMIC VASODILATION AND NEUROGENIC PLASMA EXTRAVASATION

SUBSTANCE-P AS NEUROGENIC MEDIATOR OF ANTIDROMIC VASODILATION AND NEUROGENIC PLASMA EXTRAVASATION
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DOI:
10.1007/bf00500282
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发表时间:
1979-01-01
影响因子:
3.6
通讯作者:
HOLZER, P
HOLZER, P
中科院分区:
医学4区
文献类型:
--
作者:
LEMBECK, F;HOLZER, P

文献摘要

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在胍乙啶处理的大鼠中,通过逆向刺激隐神经诱导逆向血管舒张和神经源性血浆外渗。通过股静脉流出量的变化来测量血管舒张,通过伊文思蓝渗出来确定血浆外渗。在出生第二天接受辣椒素预处理的成年大鼠中,逆向血管舒张减少了 85%。西咪替丁加美吡拉敏预处理后,逆向血管舒张作用被抑制46%,化合物48/80[对甲氧基苯乙基甲胺-甲醛产品]预处理后,逆向血管舒张作用被抑制64%,但西咪替丁、阿托品、美西麦角或吲哚美辛预处理则不影响逆向血管舒张作用。神经源性血浆外渗在用西咪替丁加美吡拉敏预处理后减少了50%,在用化合物48/80预处理后减少了88%,但在用吲哚美辛预处理后没有改变。将 P 物质输注到股动脉中会产生剂量依赖性的血管舒张(阈值:0.1 pmol/min-)和血浆外渗(阈值:0.5 pmol/min)。在用西咪替丁加美吡拉敏预处理后,由P物质诱导的血管舒张被抑制47%,在用化合物48/80预处理后被抑制58%。在用西咪替丁加美吡拉敏预处理后,由P物质引起的血浆外渗减少了61%,在用化合物48/80预处理后减少了81%。吲哚美辛预处理对 P 物质诱导的血管舒张和血浆外渗没有影响。显然,感觉神经的逆向刺激后的血管舒张和血浆外渗是由化学敏感性疼痛纤维的外周释放 P 物质引发的。 P物质的作用除了直接作用外还包括肥大细胞释放组胺。
Antidromic vasodilation and neurogenic plasma extravasation were induced by antidromic stimulation of the saphenous nerve in guanethidine-treated rats. Vasodilation was measured by the change of outflow from the femoral vein and plasma extravasation was determined by Evans blue exudation. Antidromic vasodilation was reduced by 85% in adult rats which were pretreated with capsaicin on the 2nd day of life. Antidromic vasodilation was inhibited by 46% after pretreatment with cimetidine plus mepyramine and by 64% after pretreatment with compound 48/80 [p-methoxyphenethyl methyl amine-formaldehyde product], but was not affected by pretreatment with cimetidine, atropine, methysergide or indomethacin. Neurogenic plasma extravasation was reduced by 50% after pretreatment with cimetidine plus mepyramine, and by 88% after pretreatment with compound 48/80, but was not altered after pretreatment with indomethacin. Infusion of substance P into the femoral artery dose-dependently produced vasodilation (threshold: 0.1 pmol/min-) and plasma extravasation (threshold: 0.5 pmol/min). Vasodilation induced by substance P was inhibited by 47% after pretreatment with cimetidine plus mepyramine and by 58% after pretreatment with compound 48/80. Plasma extravasation induced by substance P was reduced by 61% after pretreatment with cimetidine plus mepyramine and by 81% after pretreatment with compound 48/80. Pretreatment with indomethacin had no influence on substance P-induced vasodilation and plasma extravasation. Apparently vasodilation and plasma extravasation after antidromic stimulation of sensory nerves are initiated by peripheral release of substance P from chemosensitive pain fibers. The actions of substance P include, besides direct effects, release of histamine from mast cells.