Journal List > Tuberc Respir Dis > v.54(1) > 1062245

Kim, Kim, Yoon, Kim, Choi, Oh, Shim, Lim, Lee, Kim, Kim, Kim, and Koh: Role of Endogenous Histamine on the Pathogenesis in the Endotoxin-Induced Acute Lung Injury

Abstract

Background

Histamine is widely distributed in the lung. It increases capillary permeability and the P-selectin expression on vascular endothelial cell surfaces. We studied the role of endogenous histamine on the pathogenesis of endotoxin-induced acute lung injury (ALI) in rats.

Methods

We instilled either normal saline (control group) or lipopolysaccharide (3 mg/Kg, LPS group) to tracheas of Sprague-Dawley rats. H1-receptor blocker (mepyramine, 10 mg/Kg, H1RB group), H2-receptor blocker (ranitidine, 10 mg/Kg, H2RB group), and H3-receptor blocker (thioperamide, 2 mg/Kg, H3RB group) were administered through vein or peritoneum along with intratracheal LPS administration. Statistical significance was accepted at p<0.05.

Results

LPS increases the histamine level in BAL fluid significantly at 2 h after the treatment compared with control group. LPS significantly increases protein concentration, PMN cell count in bronchoalveolar lavage (BAL) fluid, and myeloperoxidase (MPO) activity in the lung tissue at 6 h compared to control group. PMN cell count in BAL fluid and MPO activity in lung tissue were significantly lower in H2RB-group compared to LPS-group. However, protein concentration in BAL fluid showed no significant differences between the LPS alone and LPS with histamine receptor blockade.

Conclusions

Endogenous histamine might be involved in the recruitment of PMNs in LPS-induced ALI via H2 receptor. However, its role in ALI would not be significant in this model.

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