Kucun Mustafa Kemal, Guler Eray Metin, Saracoglu Ayten, Yildirim Mehmet, Demirtas Cumaali, Serdogan Ferda, Beyaztas Hakan, Aktas Selman, Kacan Merve, Gaszynski Tomasz, Ratajczyk Pawel, Saracoglu Kemal Tolga
Department of Anesthesiology and Intensive Care, Bartin State Hospital, Bartin, Turkey.
Department of Medical Biochemistry, Hamidiye Faculty of Medicine, University of Health Sciences Turkey, Istanbul, Türkiye.
J Inflamm Res. 2025 Jan 10;18:431-443. doi: 10.2147/JIR.S493566. eCollection 2025.
The aim of this study was to compare the effects of dexmedetomidine, midazolam, propofol, and intralipid on lidocaine-induced cardiotoxicity and neurotoxicity.
Forty-eight male Sprague-Dawley rats were randomly divided into six groups (n = 8 per group): control (C), lidocaine (L), lidocaine + dexmedetomidine (LD), lidocaine + midazolam (LM), lidocaine + propofol (LP), and lidocaine + intralipid (LI). Dexmedetomidine (100 µg/kg), midazolam (4 mg/kg), propofol (40 mg/kg), and intralipid (10 mg/kg) were administered intraperitoneally as pretreatment. Lidocaine (90 mg/kg) was administered intraperitoneally to induce oxidative stress in all groups except the control. After 60 minutes of electrocardiography (ECG) recording, the rats were sacrificed, and heart and brain tissue samples were collected. Comparative measurements of total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and inflammatory parameters were conducted.
In heart tissue samples, TAS was significantly higher in LI and LD groups (p < 0.05). Additionally, oxidative stress was significantly higher in the LM group (p < 0.05). Despite an increase in oxidative stress in brain tissue samples across all groups, it was found that all groups exhibited antioxidant protective effects (p < 0.05). Inflammatory parameters in heart and brain tissues significantly decreased in all groups, especially in the LI group (p < 0.05).
It was observed that pretreatment with midazolam increased oxidative stress induced by lidocaine, while dexmedetomidine and intralipid exhibited greater antioxidant effects. Dexmedetomidine and intralipid used as pretreatment were shown to be more effective in protecting against oxidative stress and inflammation.
本研究旨在比较右美托咪定、咪达唑仑、丙泊酚和脂质乳剂对利多卡因诱导的心脏毒性和神经毒性的影响。
48只雄性Sprague-Dawley大鼠随机分为六组（每组n = 8）：对照组（C）、利多卡因组（L）、利多卡因+右美托咪定组（LD）、利多卡因+咪达唑仑组（LM）、利多卡因+丙泊酚组（LP）和利多卡因+脂质乳剂组（LI）。右美托咪定（100μg/kg）、咪达唑仑（4mg/kg）、丙泊酚（40mg/kg）和脂质乳剂（10mg/kg）作为预处理腹腔注射。除对照组外，所有组腹腔注射利多卡因（90mg/kg）以诱导氧化应激。记录心电图（ECG）60分钟后，处死大鼠，收集心脏和脑组织样本。进行总氧化剂状态（TOS）、总抗氧化剂状态（TAS）、氧化应激指数（OSI）和炎症参数的比较测量。
在心脏组织样本中，LI组和LD组的TAS显著更高（p < 0.05）。此外，LM组的氧化应激显著更高（p < 0.05）。尽管所有组脑组织样本中的氧化应激均增加，但发现所有组均表现出抗氧化保护作用（p < 0.05）。所有组心脏和脑组织中的炎症参数均显著降低，尤其是LI组（p < 0.05）。
观察到咪达唑仑预处理会增加利多卡因诱导的氧化应激，而右美托咪定和脂质乳剂表现出更大的抗氧化作用。右美托咪定和脂质乳剂作为预处理在预防氧化应激和炎症方面更有效。
