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Updated: Mar 29, 2026
A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
Published on: January 17, 2013
Erythropoietin Inhibits the Increase of Pulmonary Labile Zinc and the Expression of Inflammatory Mediators Following
Yiting Zhou1, Xudong Zhao2, Yanna Tang2
1Department of Radiology, Wuxi Integrated Traditional Chinese and Western Medicine Hospital, 585 North Xingyuan Road, Wuxi, 214041, Jiangsu, People's Republic of China.
Background:
Aneurysmal subarachnoid hemorrhage (SAH) is a common condition with relatively poor clinical outcome. Pulmonary complication after SAH is an important contributor to poor outcome. Previous studies have shown that labile zinc and inflammatory mediators participate in many pathophysiological processes. The present study investigated the effects of SAH on the levels of labile zinc and certain proinflammatory factors in rat lung and determined the effect of erythropoietin (EPO) on the pulmonary labile zinc and the inflammatory factor after SAH in rats.
Methods:
Experiment 1 aimed to investigate the time course of increase of pulmonary labile zinc, wet/dry weight ratio, and the expression of inflammatory mediators after SAH. In Experiment 2, we chose the maximum time point which lung injury was maximally severity and assessed the effect of EPO on regulation of the pulmonary labile zinc, inflammatory reaction, and wet/dry weight ratio after SAH.
Results:
SAH caused a gradual increase of pulmonary labile zinc as demonstrated by fluorescence staining with Zinpyr-4. The levels of TNF-α and IL-8 and the lung wet/dry weight ratios were higher in the SAH groups compared to the control group and peaked on 3 days following SAH (p < 0.05). EPO significantly reduced the pulmonary labile zinc, the inflammatory mediators, and the lung wet/dry weight ratio compared with SAH group (p < 0.05).
Conclusions:
EPO can protect lung from SAH-induced injury by attenuating pulmonary inflammation and labile zinc accumulation in vivo.
