EFFECTS OF THE TOXIN OF RED TIDE, PTYCHODISCUS-BREVIS, ON CANINE TRACHEAL SMOOTH-MUSCLE - A POSSIBLE NEW ASTHMA-TRIGGERING MECHANISM
EFFECTS OF THE TOXIN OF RED TIDE, PTYCHODISCUS-BREVIS, ON CANINE TRACHEAL SMOOTH-MUSCLE - A POSSIBLE NEW ASTHMA-TRIGGERING MECHANISM
复制标题
DOI:
10.1016/0091-6749(82)90116-6
复制
发表时间:
1982-01-01
影响因子:
14.2
通讯作者:
SZENTIVANYI, A
中科院分区:
文献类型:
--
作者:
ASAI, S;KRZANOWSKI, JJ;SZENTIVANYI, A
The red tide toxin produced by P. brevis becomes airborne by the thrashing action of the surf and wind and induces cough, rhinorrhea, watery eyes and sneezing in normal humans and wheezing in asthmatic patients. The mechanism of the contractile response induced by P. brevis toxin (PBTX) was investigated with isolated canine tracheal smooth muscle. Tetrodotoxin and atropine blocked the contractile effect of PBTX, and neostigmine potentiated the contraction. Mepyramine, phentolamine, methysergide and chlorisondamine did not inhibit the effect of PBTX. This was the 1st description of a naturally occurring airborne substance that caused smooth muscle contraction by stimulating the axon Na channels, resulting in the release of acetylcholine at postganglionic parasympathetic efferent nerve endings. The in vitro effect of PBTX on canine tracheal smooth muscle indicated that PBTX was capable of causing respiratory irritation and may precipitate an asthmatic attack. It was possible that the mechanism in vivo may also include stimulation of a cough receptor reflex and/or stimulation of Na channels of afferent vagus nerve fibers. Isoproterenol, atropine and verapamil may be used to eliminate or prevent the respiratory symptoms that follow exposure to airborne red tide toxin. The use of high-pressure liquid chromatography-separated fractions indicated that the neurotoxic component, not the hemolytic component, was responsible for contractions.