Abstract
This study aimed to explore the effect and mechanism of lidocaine pretreatment combined with dexmedetomidine on oxidative stress in patients with intracranial aneurysm clipping. Many studies have used various drugs such as lidocaine to explore the effect and mechanism of lidocaine pretreatment. A total of 80 patients with intracranial aneurysm clipping surgery were randomly divided into 4 groups: the single lidocaine group, single dexmedetomidine group, lidocaine combined with dexmedetomidine group, and control group. The thread embolism method was used to establish a stable intracranial aneurysm model of Hashimoto rats. Fifty adult rats were randomly divided into a sham operation group, ligation of the left common carotid artery and bilateral posterior branch of renal artery, lidocaine group, dexmedetomidine group, and lidocaine combined with dexmedetomidine group. The colorimetric method was used to determine the oxidative stress indicators in brain tissue: MDA content, SOD activity, and T-AOC content. The western blot method characterized the protein levels related to oxidative stress: nNOS, iNOS, and NADPH oxidase subunits p22phox, gp91phox, and p47phox. The differences in each index between the groups were statistically significant (P < 0.05). Animal experiment results revealed that the content of MDA in the brain tissue of rats in the LD group was significantly lower than that in the single-drug group and sham group. The T-AOC and SOD concentrations in the LD group were significantly higher than those in the single-drug group and sham group, and the differences between the groups were statistically significant (P < 0.05). The protein expression of the LD group was significantly lower than that of the drug-alone group and model group, and the difference between groups was statistically significant (P < 0.05). To sum up, lidocaine pretreatment combined with dexmedetomidine can effectively maintain the hemodynamic stability of patients with intracranial aneurysm clipping and reduce postoperative oxidative stress response. Its mechanism of action may be related to the inhibition of oxidative stress damage mediated by nNOS, iNOS, and p22phox, gp91phox, and p47phox in the hippocampus. Our study has significant and applicable medical aspects in lidocaine pretreatment combined with dexmedetomidine on oxidative stress in patients.
Highlights
Intracranial aneurysm clipping is one of the common surgical procedures for the treatment of cerebral aneurysms
Oxidative stress injury is an important cause of cerebral ischemia injury [4] and plays a vital role in each link in the acute stage of ischemic cerebrovascular disease. erefore, it is crucial to select pharmacologically effective cerebral protective drugs during craniocerebral surgery to improve the stability of intraoperative cerebral blood supply dynamics and oxidative stress levels in patients and to reduce the damage caused by cerebral ischemia
Liver or kidney injury, abnormal coagulation function, respiratory or circulatory diseases, or with allergy to drugs applied in this study were excluded. All patients and their families were informed and signed informed consent forms. is study was approved by the Ethics Committee. e abovementioned patients were randomly divided into four groups (20 cases in each group): the lidocaine group (L group), dexmedetomidine group (D group), lidocaine combined with dexmedetomidine group (LD group), and control group (A group)
Summary
Intracranial aneurysm clipping is one of the common surgical procedures for the treatment of cerebral aneurysms. Studies have shown that dexmedetomidine can alleviate the harmful stimulation caused by surgery, maintain cardiovascular stability, and reduce cerebral blood flow during the operation of craniocerebral patients [11]. Dexmedetomidine can reduce the level of inflammatory factors in patients with craniocerebral injury It improves cerebral oxygen metabolism, reduces oxidative stress reaction, and effectively improves the stability of central blood vessels in craniocerebral operation. It reduces brain edema caused by craniocerebral injury [12], improving the ischemic and hypoxic injury of brain tissue with effect [13]. The mechanism of lidocaine and dexmedetomidine affecting oxidative stress response is the key issue of this paper
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