• Shouping Wang, Kelly Peretich, Yifan Zhao, Ge Liang, Qingcheng Meng, and Huafeng Wei.
• Department of Anesthesiology and Critical Care, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
• Pediatr. Res. 2009 Oct 1; 66 (4): 435-40.

AbstractWe investigated the extent of isoflurane-induced neurodegeneration on the fetuses of pregnant rats exposed in utero. Pregnant rats at gestational d 21 were divided into three experimental groups. Rats in the control group spontaneously breathed 100% oxygen for 1 h. Rats in the treatment groups breathed either 1.3 or 3% isoflurane in 100% oxygen through an endotracheal tube, with mechanical ventilation for 1 h. Rat pups were delivered by cesarian section 6 h after treatment, and fetal blood was sampled from the left ventricle of each fetal heart and evaluated for S100beta. Fetal brains were then evaluated for apoptosis, using caspase-3 immunohistochemistry in the CA1 region of the hippocampus and the retrosplenial cortex (RS). The 3% isoflurane treatment group showed significantly higher levels of S100beta levels and significantly increased average densities of total caspase-3-positive cells in the CA1 hippocampus and RS cortex compared with the control and the 1.3% isoflurane groups. There were no differences in S100beta levels or densities of caspase-3-positive cells between the control and 1.3% isoflurane groups. Isoflurane at a concentration of 3% for 1 h increased neurodegeneration in the hippocampal CA1 area and the retrosplenial cortex in the developing brain of fetal rats.

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