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NEUROSURGICAL ANESTHESIOLOGY AND NEUROSCIENCE

The Effects of β-Adrenoceptor Antagonists on Proinflammatory Cytokine Concentrations After Subarachnoid Hemorrhage in Rats

From the Department of Anesthesiology, Nara Medical University, Kashihara City, Nara, Japan.

Address correspondence and reprint requests to Haruto Kato, MD, Department of Anesthesiology, Nara Medical University, 840 Shijo-cho, Kashihara City, Nara 634-8522, Japan. Address e-mail to hkato{at}naramed-u.ac.jp.

Abstract

BACKGROUND: Proinflammatory cytokines increase in cerebrospinal fluid (CSF) after subarachnoid hemorrhage (SAH). Recent evidence suggested that β-adrenoceptor antagonist could reduce proinflammatory cytokines. We conducted the present study to examine whether β-adrenoceptor antagonists would reduce proinflammatory cytokine concentrations after SAH in rats.

METHODS: In Experiment 1, to investigate the time course of interleukin-6 (IL-6) and tumor necrosis factor- (TNF-), rats were randomized into groups: 1, 3, 6, and 12 h after SAH or sham operation. CSF and blood samples were obtained at each time point. In Experiment 2, to investigate the effects of β-adrenoceptor antagonists on the IL-6 and TNF- concentrations, rats were randomized into groups: 1) control group: SAH + normal saline, 2) propranolol group: SAH + propranolol, 3) metoprolol group: SAH + metoprolol, and 4) butoxamine group: SAH + butoxamine (β₂-adrenoceptor antagonist). CSF and blood samples were obtained 6 h after SAH. IL-6 and TNF- concentrations in samples were measured.

RESULTS: In Experiment 1, CSF IL-6 concentrations in the SAH groups increased markedly and peaked at 6 h after SAH, whereas CSF TNF- concentrations in the SAH groups were consistently low. In Experiment 2, CSF IL-6 concentrations in the propranolol and butoxamine groups were significantly lower compared with those in the control group (P < 0.01 and P < 0.05 for each group). Plasma IL-6, CSF TNF-, and plasma TNF- concentrations were comparable in all four groups.

CONCLUSIONS: CSF IL-6 concentrations increased in the acute stage of SAH and β-adrenoceptor antagonists with a β₂-adrenoceptor blocking action suppressed this elevation of IL-6 concentrations after SAH in rats.

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