Biochemical and physiological effects of compound 48/80 on canine trachea in vivo.

Biochemical and physiological effects of compound 48/80 on canine trachea in vivo.
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化合物48/80对体内犬气管的生化和生理作用。

DOI:
10.1152/jappl.1983.54.3.720
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发表时间:
1983
期刊:
Journal of applied physiology: respiratory, environmental and exercise physiology
影响因子:
--
通讯作者:
Gold,WM
Gold,WM
中科院分区:
--
文献类型:
--
作者:
Leff,AR;Brown,JK;Frey,M;Reed,B;Gold,WM

文献摘要

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在32只麻醉犬中,观察了化合物48/80对气管肥大细胞脱颗粒后气管组织胺含量和气管肌张力的变化。在4只犬中,化合物48/80导致气管张力增加[13 +/- 5(SD)g/cm],而股动脉血压仅降低14 +/-11%。动脉内给予化合物48/80(5 × 10 - 3至10 - 1 mg/kg)的5只犬的气管组织组胺降低17 +/- 6%。H1受体拮抗剂扑尔敏选择性地抑制化合物48/80和组胺引起的气管收缩。西咪替丁,一个H2-拮抗剂,并没有改变动脉内组胺的反应。在11只狗中,比较了产生8 g/cm气管张力阈值增加所需的动脉内组胺和乙酰胆碱的剂量。在这些狗中,乙酰胆碱的阈值剂量变化了10倍,而组胺的阈值剂量变化了100倍。化合物48/80引起的气管张力增加与组胺有显著相关性(r = 0.62)。我们的结论是,化合物48/80导致可变的增加,在体内气管张力,因为显着的变化,在气管平滑肌组胺的H1-受体反应,并因为可变的介质从呼吸道肥大细胞释放的化合物48/80。
We studied changes in tracheal histamine content and tracheal muscle tension after degranulation of tracheal mast cells by compound 48/80 in 32 anesthetized dogs. In four dogs compound 48/80 caused an increase in tracheal tension [13 +/- 5 (SD) g/cm], while femoral arterial blood pressure decreased only 14 +/- 11%. Tracheal tissue histamine decreased 17 +/- 6% in five dogs receiving intra-arterial compound 48/80 (5 X 10(-3) to 10(-1) mg/kg). Chlorpheniramine, an H1-antagonist, selectively inhibited tracheal contraction to compound 48/80 and histamine. Cimetidine, an H2-antagonist, did not alter the response to intra-arterial histamine. In 11 dogs, the doses of both intra-arterial histamine and acetylcholine required to produce a threshold increase in tracheal tension of 8 g/cm were compared. Threshold doses for acetylcholine varied 10-fold, compared with 100-fold variation for histamine among these dogs. There was a significant correlation between increased tracheal tension produced by compound 48/80 and histamine (r = 0.62). We conclude that compound 48/80 causes a variable increase in tracheal tension in vivo because of marked variability in the H1-receptor response of tracheal smooth muscle to histamine and because of variability in the release of mediator from respiratory mast cells by compound 48/80.