Penurunan Kadar Glutamat pada Cedera Otak Traumatik Pascapemberian Agonis Adrenoseptor Alpha-2 Dexmedetomidin sebagai Indikator Proteksi Otak

MM Rudi Prihatno, M. Sofyan Harahap, Ieva B Akbar, Tatang Bisri

Abstract


Latar Belakang dan Tujuan: Dexmedetomidin untuk kasus-kasus neurotrauma masih kontroversi, antara yang setuju dan menolak. Dexmedetomidin sebagai agonis adrenoseptor α2 memiliki beberapa keuntungan dalam kaitannya dengan kemampuannya sebagai neuroprotektan. Penelitian ini bertujuan untuk mengkaji efek neuroproteksi dari dexmedetomidin yang dilihat dari pengaruhnya terhadap penurunan kadar glutamat.

Subjek dan Metode Penelitian single blind randomized controlled trial dilakukan pada 16 orang yang datang ke IGD RSUD Prof. Dr. Margono Soekarjo dengan cedera otak traumatik dengan GCS ≤8 pada Mei–Desember 2013. Subjek dibagi dalam 2 kelompok yaitu kelompok dexmedetomidin dan NaCl 0,9%. Pembedahan dilakukan dalam rentang waktu 9 jam pascatrauma. Pemeriksaan kadar glutamat dengan menggunakan metode ELISA. Analisis data menggunakan uji-t dan uji Mann-Whitney.

Hasil: Kelompok yang mendapatkan dexmedetomidin menunjukkan bahwa pemberian dexmedetomidin 0,4 μg/kgBB/jam secara kontinyu, menunjukkan penurunan kadar glutamat yang diukur mulai dari awal perlakuan hingga jam ke-24 sebanyak 27,9% (p=0,025), dari jam ke-24 hingga jam-72 sebanyak 9,6% (p=0,208), serta dari awal perlakuan hingga jam ke-72 sebanyak 57,1% (p=0,036). Kelompok yang tidak mendapatkan dexmedetomidin mengalami peningkatan kadar glutamat.

Simpulan: Pemberian dexmedetomidin 0,4 μg/kgBB/jam dapat menurunkan kadar glutamat pada pasien cedera otak traumatik dengan GCS ≤ 8.

 

Decreased Level of Glutamate after Administration of Dexmedetomidine (Alpha-2 Adrenoreceptor Agonist) as Neuroprotective Indicator in Traumatic Brain Injury

Background and Objective: The usage of Dexmedetomidine in neurotrauma cases is still controversial, between the pros and cons. Dexmedetomidine as α2-adrenoceptor agonist has several benefits in concomitant with its properties as neuroprotector. This study aims to evaluate the neuroprotection effect of dexmedetomidine based on the decline in glutamate level.

Subject and Method: This single blind randomized controlled trial was done in 16 TBI patients with GCS ≤ 8, recruited from May-December 2013. Subjects were equally divided into 2 groups: dexmedetomidine and 0.9% NaCl group. Surgery was performed within 9 hours post TBI. Glutamate level was examined using ELISA method. Data were analyzed using t-test and Mann-Whitney test.

Result: This study showed that glutamate levels in patient who received continuous intravenous dexmedetomidine 0.4 mcg / kg / h were decreased, starting from baseline to 24 h (27.9%, p=0.025), 24 to 72 h (9.6%, p= 0.208) and baseline to 72 h (57.1%, p= 0.036). All patients in NaCl 0.9% group experienced an increase in glutamate level.

Conclusion: Administration of dexmedetomidine 0.4 mcg/kg/h in TBI patient with GCS ≤ 8 could decrease glutamate level.


Keywords


Dexmedetomidin; glutamat; neuroproteksi; cedera otak traumatik; dexmedetomidine; glutamate; neuroprotective; traumatic brain injury

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DOI: https://doi.org/10.24244/jni.vol3i2.138

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