Efek Anestesia Aliran Rendah Sevofluran terhadap Respon Inflamasi pada Susunan Saraf Pusat
Abstract
Anestesi aliran rendah adalah teknik anestesi yang menggunakan aliran gas <1L/menit. Oleh karena adanya rebreathing, maka pada anestesi aliran rendah yang menggunakan sevofluran akan terjadi produk degradasi dengan CO2 absorber sehingga terbentuk senyawa A dan senyawa B. Senyawa A bersifat neprotoksik pada ginjal tikus, karena enzim β liase 30 kali lebih aktif pada tikus dari pada manusia, sedangkan pada manusia tidak terbukti senyawa A berefek neprotoksik. Anestesia sevofluran dapat menimbulkan respons inflamasi yang diawali dengan pelepasan interleukin (IL)–1 dan TNF–α, kemudian menstimulasi IL–6 yang sangat berperan pada respons fase akut. Akan terjadi interaksi antara sistem imun dengan sistem neuroendokrin, yang mana IL–1 dan IL–6 dapat menstimulasi adrenocorticotrophic hormone (ACTH) sehingga terjadi peningkatan pelepasan kortisol. Metabolit sevofluran dan senyawa A tidak dapat menembus sawar darah otak sehingga pengaruh negatif dari metabolit dan produk degradasi sevofluran terhadap otak tidak ada. Bahkan, melalui penelitian lebih lanjut, sevofluran diketahui mempunyai efek neuroproteksi.
The Effect of Sevoflurane Low Flow Anesthesia to Inflammatory Response on Central Nervous System
Low flow anesthetic is an anesthesia technique using gas flow less than 1 L/ min. Due to the rebreathing system, a low flow anaesthesia using sevoflurane will produce degradation products through reaction with the CO2 absorber which will form compound A and compound B. Compound A is nephrotoxic to rat kidney because the β -lyase enzyme in rat is 30-fold more active than in human, and this compound has been proven to be not nephrotoxic in human. Sevoflurane can cause inflammatory response which started with the release of interleukin (IL)-1 and TNF-α followed by stimulation of IL-6, which plays important part in the acute phase. Interaction between the neuroendocrine and immune systems will occur where IL-1 and IL-6 cytokines will stimulate the production of adrenocorticotrophic hormone (ACTH), which in turn will increase the production of cortisol. Sevoflurane metabolites and compound A can not penetrate blood brain barrier, therefore, the negative effects of sevoflurane metabolites and degradation products to the brain does not happen. Further advanced studies even showed that sevoflurane has a neuroprotective effect.
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DOI: https://doi.org/10.24244/jni.vol3i2.140
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