Protective Effect Of Dexmedetomidine On Patients Undergoing Craniocerebral Surgery

BackgroundThere are pathophysiological changes such as brain cell and tissue edema,ischemia and anoxia,inflammatory response,tissue necrosis and so on in patients undergoing craniocerebral operation.There are different degrees of hypoxic-ischemic brain injury,and the mechanical injury during operation will further aggravate the brain injury.Therefore,the use of drug intervention to protect the brain to reduce brain damage,improve the state of brain hypoxia and ischemia,maintain normal brain function,has become an urgent clinical problem.ObjectiveTo explore the brain protective effect and mechanism of dexmedetomidine in craniocerebral surgery,and to provide reference for the establishment of clinical midbrain protection program.MethodsSelect 100 patients with craniocerebral injury who underwent emergency craniotomy and hematoma removal in our hospital from December 2019 to December 2020 as the research objects.The research objects were divided into a control group and a study group by a random number table.50 cases each.Both groups of patients used the same anesthesia induction and anesthesia maintenance methods.The study group was pumped with 1μg/kg dexmedetomidine 10 minutes before tracheal intubation,and 0.5μg/kg/h was continuously infused to the suture skin.the control group received the same dose of 0.9%sodium chloride injection.Before monitoring the serum levels of the two groups of patients induction of anesthesia（T₁）,after tracheal intubation（T₂）,before craniotomy（T₃）,before meningotomy（T₄）,at the end of surgery（T₅）,and 24 hours after surgery（T₆）Norepinephrine（NE）,epinephrine（E）,S100β,internal carotid artery oxygen saturation（SaO₂）,jugular blood oxygen saturation（SjvO₂）concentration and inducible nitric oxide synthase（iNOS）,Phosphatidylinositol 3-kinase（PI3K）concentration,and count the extubation time of the two groups for comparative.Results1.At T₁,the NE and E levels of the study group and the control group had no significant difference（P>0.05）;T₂～T₆,the NE and E levels of the study group were significantly lower than those of the control group,and the difference was statistically significant（P<0.05）.2.At T₁,the S100β of the study group and control group difference was not statistically significant（P>0.05）;at T₂～T₆,the S100β level of the study group was significant Lower than the control group,and the difference was statistically significant（P<0.05）.3.At T₁,the SaO₂ level of the study group and the control group had no significant difference（P>0.05）;at T₂～T₆,the SaO₂ level of the study group was significantly higher than Control group,and the difference was statistically significant（P<0.05）.At T₁,there was no obviously different in SjvO₂ levels between the two groups of patients（P>0.05）;at T₂ to T₆,there was an increase in SjvO₂ levels,but the differences were not statistically significant（P>0.05）.4.At T₁ and T₂,there was no significant difference in the levels of iNOS and PI3K between group（P>0.05）;at T₃～T₆,the levels of iNOS and PI3K in the study group were significantly lower than control group,and the difference was statistically significant（P<0.05）.5.The extubation time of the study group was significantly shorter than that of the control group,and the difference was statistically significant（P<0.05）.ConclusionThe application of medetomidine in brain surgery anesthesia can reduce the patient’s NE,E,S100βprotein levels,improve cerebral oxygenation,and reduce brain injury.The mechanism of action may be to inhibit the activation of PI3K/iNOS pathway.Moreover,brain protection with this program can effectively shorten the extubation time and promote the recovery of postoperative cognitive function.