• Lili Zhang, Jin Jin, Jianyu Yao, Ziyong Yue, Yuting Wei, Wanchao Yang, Songbin Fu, and Wenzhi Li.
• Department of Anesthesiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin, 150081, China.
• Neurocrit Care. 2016 Jun 1; 24 (3): 459-71.

IntroductionPropofol exhibits neuroprotective effects mediated by the inhibition of excitatory amino acid (EAA) neurotransmitter release and potentiation of inhibitory amino acid (IAA) neurotransmitters. To our knowledge, this is the first study to investigate the effects of propofol on the EAA and IAA balance in neurogenic pulmonary edema (NPE).MethodsSixty male Wistar rats were randomized to Sham, NPE, Low-dose propofol, and High-dose propofol groups. NPE was induced via rapid injection of autologous blood (0.5 ml) into the cisterna magna. The Low- and High-dose propofol groups were pretreated with boluses of 2 and 5 mg kg(-1), respectively, prior to blood injection, followed by continuous propofol infusion at 6 and 15 mg kg(-1) h(-1), respectively. The mean arterial pressure (MAP), heart rate, intracranial pressure (ICP), peak inspiratory pressure (PIP), and arterial blood gases were continuously recorded. After 2 h, the lung wet-to-dry weight ratio, total protein concentration in the bronchoalveolar lavage fluid (BALF), brain water content, cortical EAA and IAA levels, chest X-ray, and histological staining of lung sections were evaluated.ResultsBlood injections into the cisterna magna induced NPE and hemodynamic changes. Propofol alleviated the increases in the MAP, ICP, and PIP, improved oxygenation and histopathological changes, ameliorated pulmonary and cerebral edema, increased the IAA brain levels, and decreased the ratio of Glu to γ-aminobutyric acid.ConclusionsThe current findings suggest that propofol improves NPE likely via IAA accumulation and the regulation of EAA and IAA balance, which may represent an effective treatment for NPE.

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