K Takemori1, K Kobayashi, A Sakamoto. 1. Department of Anaesthesiology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan. kt2ndnmsmeb@hotmail.com
Abstract
BACKGROUND: Sevoflurane is a fluorinated volatile anaesthetic agent that lowers arterial pressure, in part by vasodilation. We previously showed, in rat lungs, that sevoflurane affected the expression of endothelin-1 (ET-1), a potent vasoconstrictor peptide. Therefore, we hypothesized that the vasodilation induced by sevoflurane involved vasodilatory and vasoconstrictor components. METHODS: Rats were anaesthetized with sevoflurane 4% for 0, 2, and 6 h (n=9 each group) before death. In addition, a further group (n=9) were anaesthetized for 6 h then awoken for 2 h before death (n=9). We measured expression of mRNA encoding ET-1, nitric oxide synthase-1, 2, 3 (NOS1, 2, 3), haeme oxygenase-1, 2 (HO-1, 2), adrenomedullin (ADM), calcitonin gene-related peptide, vasoactive intestinal peptide, and prostacyclin synthase in whole lung using real-time reverse transcriptase-polymerase chain reaction. RESULTS: Expressions of ET-1 and ADM were significantly increased by inhalation of sevoflurane for 2 and 6 h (P<0.05). Expression of NOS3 was significantly increased at 6 h (P<0.05). After awaking from anaesthesia, the expressions of NOS3, ET-1, and ADM returned to baseline levels. CONCLUSIONS: Sevoflurane increased the expressions of ET-1, NOS3, and ADM. Our results suggest that the increased expressions of NOS3 and ADM may counteract that of ET-1 and so regulate pulmonary circulation under sevoflurane anaesthesia.
BACKGROUND:Sevoflurane is a fluorinated volatile anaesthetic agent that lowers arterial pressure, in part by vasodilation. We previously showed, in rat lungs, that sevoflurane affected the expression of endothelin-1 (ET-1), a potent vasoconstrictor peptide. Therefore, we hypothesized that the vasodilation induced by sevoflurane involved vasodilatory and vasoconstrictor components. METHODS:Rats were anaesthetized with sevoflurane 4% for 0, 2, and 6 h (n=9 each group) before death. In addition, a further group (n=9) were anaesthetized for 6 h then awoken for 2 h before death (n=9). We measured expression of mRNA encoding ET-1, nitric oxide synthase-1, 2, 3 (NOS1, 2, 3), haeme oxygenase-1, 2 (HO-1, 2), adrenomedullin (ADM), calcitonin gene-related peptide, vasoactive intestinal peptide, and prostacyclin synthase in whole lung using real-time reverse transcriptase-polymerase chain reaction. RESULTS: Expressions of ET-1 and ADM were significantly increased by inhalation of sevoflurane for 2 and 6 h (P<0.05). Expression of NOS3 was significantly increased at 6 h (P<0.05). After awaking from anaesthesia, the expressions of NOS3, ET-1, and ADM returned to baseline levels. CONCLUSIONS:Sevoflurane increased the expressions of ET-1, NOS3, and ADM. Our results suggest that the increased expressions of NOS3 and ADM may counteract that of ET-1 and so regulate pulmonary circulation under sevoflurane anaesthesia.
Authors: Deborah De Geyter; Wendy Stoop; Tine Zgavc; Sophie Sarre; Yvette Michotte; Jacques De Keyser; Ron Kooijman Journal: J Neuroinflammation Date: 2012-05-30 Impact factor: 8.322