Goldie P, Hellström S, Idahl L A
Department of Anatomy, University of Umeá, Sweden.
Acta Otolaryngol. 1989 Sep-Oct;108(3-4):246-52. doi: 10.3109/00016488909125524.
Vascular leakage in the middle ear cavity was studied after i.v. administration of various substances in rats and determined by the Evans blue technique. Bradykinin, histamine, serotonin, acetylcholine, substance P (SP) and vasoactive intestinal polypeptide (VIP) resulted in extravasation of Evans blue. In the case of bradykinin and histamine, the leakage was dose dependent. Calcitonin gene-related peptide (CGRP) did not affect vessel permeability. In other experiments the effect of histamine antagonists was tested on production of middle ear effusion, caused by blowing air at 14 degrees C into the external auditory canal (EAC). The increase in vessel permeability in this otitis media model was inhibited by the H2-receptor antagonist cimetidine, at doses 0.1 and 1.0 mg/ml. Diphenhydramine, an H1-receptor antagonist, arrested only partly middle ear fluid accumulation. Our study demonstrated that various inflammatory mediators and neuropeptides are capable of inducing vascular leakage in the middle ear cavity. It was also concluded that H2-receptors are involved in the regulation of middle ear vascular permeability.
通过静脉注射不同物质后，采用伊文思蓝技术对大鼠中耳腔血管渗漏情况进行了研究。缓激肽、组胺、5-羟色胺、乙酰胆碱、P物质（SP）和血管活性肠肽（VIP）均导致伊文思蓝外渗。就缓激肽和组胺而言，渗漏呈剂量依赖性。降钙素基因相关肽（CGRP）不影响血管通透性。在其他实验中，检测了组胺拮抗剂对因在14℃向外耳道（EAC）吹气引起的中耳积液产生的影响。在该中耳炎模型中，血管通透性的增加受到H2受体拮抗剂西咪替丁的抑制，剂量分别为0.1和1.0mg/ml。H1受体拮抗剂苯海拉明仅部分抑制了中耳积液的积聚。我们的研究表明，多种炎症介质和神经肽能够诱导中耳腔血管渗漏。还得出结论，H2受体参与中耳血管通透性的调节。
