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水浸应激诱导的大鼠血浆组胺双相升高及其来源

Biphasic elevation of plasma histamine induced by water immersion stress, and their sources in rats.

作者信息

Huang Z L, Mochizuki T, Watanabe H, Kagoshima M, Maeyama K

机构信息

Department of Pharmacology, Ehime University School of Medicine, Japan.

出版信息

Eur J Pharmacol. 1998 Nov 6;360(2-3):139-46. doi: 10.1016/s0014-2999(98)00670-0.

DOI:10.1016/s0014-2999(98)00670-0
PMID:9851580
Abstract

The effect of water immersion stress on the plasma concentration of histamine, in Wistar and mast cell-deficient (Ws/Ws) rats, was investigated. The histamine content of the plasma, skin and gastric mucosa, as well as the level of activity of histidine decarboxylase in the gastric mucosa, were determined by high performance liquid chromatography (HPLC)-fluorometry. In Wistar rats exposed to water immersion stress for a total of 6 h, an initial, acute, four-fold, transient increase in the plasma histamine level, followed by a sustained, though lower, elevation of the plasma histamine level, was observed. The initial acute increase in plasma histamine level was also seen in gastrectomized Wistar rats exposed to water immersion stress, but not in Ws/Ws rats exposed to stress. The sustained elevation of the plasma histamine level was observed in the Ws/Ws rats. However, in both the gastrectomized Wistar rats and gastrectomized Ws/Ws rats, the sustained elevation in plasma histamine level was not observed. The histamine content of the skin of Wistar rats after 15 min or more exposure to water immersion stress, was 20% lower than that of control rats. The mucosal histamine content of both Wistar rats and Ws/Ws rats, was 20% lower, whereas histidine decarboxylase activity in the gastric mucosa was enhanced by two-fold, during exposure to stress for 4 h. These findings indicate that water immersion stress causes a biphasic increase in plasma histamine concentration in Wistar rats; the initial acute increase in plasma histamine level originates from mast cells, and the second, sustained increase is attributed to enterochromaffin-like cells.

摘要

研究了水浸应激对Wistar大鼠和肥大细胞缺陷型(Ws/Ws)大鼠血浆组胺浓度的影响。采用高效液相色谱(HPLC)-荧光法测定血浆、皮肤和胃黏膜中的组胺含量,以及胃黏膜中组氨酸脱羧酶的活性水平。在总共暴露于水浸应激6小时的Wistar大鼠中,观察到血浆组胺水平最初出现急性、四倍的短暂升高,随后血浆组胺水平持续升高,尽管升高幅度较小。在接受水浸应激的胃切除Wistar大鼠中也观察到血浆组胺水平最初的急性升高,但在接受应激的Ws/Ws大鼠中未观察到。在Ws/Ws大鼠中观察到血浆组胺水平的持续升高。然而,在胃切除的Wistar大鼠和胃切除的Ws/Ws大鼠中,均未观察到血浆组胺水平的持续升高。暴露于水浸应激15分钟或更长时间后,Wistar大鼠皮肤中的组胺含量比对照大鼠低20%。在应激4小时期间,Wistar大鼠和Ws/Ws大鼠的黏膜组胺含量均降低20%,而胃黏膜中的组氨酸脱羧酶活性增强了两倍。这些发现表明,水浸应激导致Wistar大鼠血浆组胺浓度出现双相升高;血浆组胺水平最初的急性升高源于肥大细胞,而第二次持续升高则归因于肠嗜铬样细胞。

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