Preconditioning of isofl urane on spinal cord ischemia can increase the number of inducible nitric oxide synthaseexpressing motor neurons in rat

• Published in: Korean journal of anesthesiology pp. 70 - 75
• Main Authors: 성윤희, 이상학, 성준경, 한진희, 김홍, 김창주, 강종만
• Format: Journal Article
• Language: English
• Published: 대한마취통증의학회 01.01.2010
• Subjects: 마취과학
• ISSN: 2005-6419; 2005-7563

Background: Spinal cord ischemia with resulting paraplegia remains one of the most common complications after repair of thoracoabdominal aortic aneurysms or dissection. Inducible nitric oxide synthase (iNOS) is known to have both neuroprotective and neurotoxic effects in the central nervous system. We investigated the possible relationship between the eff ect of pre-ischemic isofl urane exposure on mild spinal cord ischemia and the inducible nitric oxide synthase (iNOS) expression by using iNOS-specific antibody and pyrrolidinedithio carbamate (PDTC), NF-κB inhibitor, in the ventral horn of spinal cord in rats. Methods: The animals were divided into five groups (n = 6 in each group): sham group, control group, PDTC-treated group, isoflurane-treated group, and PDTC/ isofl urane-treated group. In the PDTC-treated groups, 2% 100 mg/kg PDTC was administered intraperitoneally at 1 h before operation and at 24 h and 48 h after reperfusion. The rats in the isofl urane-treated groups received 30 min inhalation of 2.8% isofl urane at 24 h before spinal cord ischemia. Immunohistochemistry was performed to detect iNOS expression in the motor neuron of the ventral horn in spinal cord. Results:Preconditioning with isofl urane increased the iNOS expression when compared to the control group (P < 0.05),whereas pre-treatment with both PDTC and isoflurane significantly decreased the iNOS expression compared to isofl urane-treated group (P < 0.05). Conclusions: Pre-ischemic isofl urane exposure was related with increase of the iNOS expression via a pathway modulated by NF-κB. iNOS may act as an important mediator of delayed preconditioning with isofl urane for the protective eff ect against spinal cord ischemia. KCI Citation Count: 1