| Objective: On brain tissue distraction, compression, electrocoagulationand other factors can cause the surgical field surrounding or its supply areadifferent scope and degree of brain ischemia hypoxia injury in surgicaloperation. Mechanical ventilation and controlled hypotension may also affectthe balance of cerebral oxygen supply and demand. With the development ofintracranial aneurysm, intracranial mass resection, cardiopulmonary bypasssurgery technology swift and violent, cerebral ischemia hypoxia injuries inclinical are more and more prevalent. And intracranial tumor patients oftenlead to intracranial hypertension, cerebral ischemia, hypoxia, edema, necrosisand pathological changes. Intraoperative electrical cutting, coagulation,suction, automatic retractor oppression and pulling operation could inevitablylead to the surrounding normal brain tissue ischemia hypoxia injury. Theneurosurgeries are relatively elaborate and time consuming than the averageoperation, may affect neural cell metabolism and even damage the brain tissue.Therefore, how to reduce and eliminate this injury and to illustrate themechanism of this injury are very important in the clinical application andalso are one of the important and hot spots in recent years.Hypoxic-ischemic brain injury mechanisms may be related to oxygenfree radicals and excitatory amino acid produced in great quantities and theresult of the role of calcium overload and apoptosis factors. Underphysiological conditions, EAA and inhibitory amino acid level maintainhomeostasis. Non-physiological perfusion can lead to cerebral hypoxia andEAA abnormal release of neurotoxicity, damage the nerve cells.As a widely used intravenous anesthetics, propofol can enhance centralinhibition of neurotransmitter, but also through inhibition of central excitatoryneurotransmission play a narcotic effect. The main role of propofol is the central inhibitory GABAa receptors. Propofol can reduce cerebral blood flow,intracranial pressure and cerebral metabolic rate and maintain a good match ofthe cerebral blood flow and cerebral metabolism, can also inhibit the releaseof EAA, and reduce the concentration of cerebral ischemia glutamate (Glu),thereby reducing the EAA receptor-mediated neurotoxicity. Propofol canreduce cerebral blood flow, intracranial pressure and cerebral metabolic rateand maintain a good match of the cerebral blood flow and cerebralmetabolism, can also inhibit the release of EAA. So that the cerebralischemia glutamate (Glu) concentration is reduced, thereby reducing theEAA receptor mediated neurotoxicity. Animal experiments show that theprotective effect of propofol on ischemic injury of the animal brain. But itsexact mechanism remains to be studied.At present, the evaluation of cerebral hypoxic-ischemic injuryindicators include monitoring of cerebral oxygen supply and demand balance,detection of excitatory amino acid concentrations, superoxide dismutase(SOD), malondialdehyde (MDA) and other methods. Each represents adifferent aspect: Monitor the balance of cerebral oxygen and energymetabolism reflects not only the brain tissue oxygen uptake and utilization,but also indirectly reflect changes in cerebral blood flow and intracranialpressure. Detection of excitatory amino acid concentrations calculatedexcitatory toxicity index can reflect the degree of brain injury and prognosis;detection of SOD, MDA in brain tissue reflect the degree of brain tissue thecontent of free radicals and lipid peroxidation. In view of this, the brain EAA,MDA, SOD and SjvO2combined with testing can be a good reflection of brainmetabolism. At present, clinical studies have also reported the effects ofpropofol on acute brain injury patients with cerebral protection effect, but insurgical operation by monitoring the EAA and SOD indexes to measure thecerebral protective effect of propofol are rarely reported. Patients underanesthesia in a benefit, there is some clinical value, has a broad applicationprospect. Methods:1. We selected28patients for resection of intracranial meningioma,ASA I~II, age20~55.They were randomly divided into propofol group (groupP) and midazolam group (group M),14cases in each. All patients were firstelective intracranial tumor surgery patients with preoperative non-obviousintracranial pressure, coronary heart disease, diabetes, kidney disease andother complications.2. Patient before surgery by the provisions of regulation forbidden todrink, fasting for8~12h. They must in both groups inject intramuscularatropine0.5mg, the radial artery catheterization in local anesthesia, the jugularvein puncture and retrograde catheter to the internal jugular venous bulbdepartment. Induction of general anesthesia：group P sequential intravenouspropofol1.5~2.0mg/kg, fentanyl4.0ug/kg atracurium0.8mg/kg induction ofgeneral anesthesia, the oxygen nitrogen removal3min after tracheal intubation,and5minutes after using propofol-remifentanil-atracurium compoundintravenous anesthesia; group M sequential intravenous midazolam0.1~0.2mg/kg fentanyl4.0ug/kg atracurium0.8mg/kg, anesthesia was maintainedwith midazolam-remifentanil-atracurium compound intravenous anesthesia.Intraoperative input liquid as lactated Ringer's solution, hydroxyethyl starchinjection. The ratio of crystal colloidalis1:1. GE Aespire-7100anesthesiamachine control of breathing, tidal volume8~10ml/kg respiratory rate of10to12times per minute, according to blood gas analysis to adjust the tidalvolume. Should not be used inhaled anesthetics, transfusion volume of morethan2unit cases culling; Should not be used of sugar containing liquid, inorder to avoid the impact on the experiment.3. Respectively before general anesthesia induced by intubationimmmediate(T1), began operation (T2), open dural instantly(T3), end ofoperation (T4),1h after of anesthesia (T5) five times synchronous acquisitionof the internal jugular vein and the radial artery for blood gas analysis and5mlblood samples from the test tube to be centrifugal.4. Specimens2000r/min,10min, pipette plasma0.4ml,1.2ml anhydrousethanol, after mixing,12000centrifuge30min,the supernatant from pipettes, frozen in-80℃to avoid repeated freezing and thawing.5. Detection:Serum EAA was measured with HPLC, plasma SOD, MDAcontent was measured using visible light.Result:1. There were no significant differences by age, body weight, operationtime, anesthesia time and the dosage of remifentanil infusion amount betweentwo groups of patients (P>0.05).There were no significant differences withMAP and HR in surgical procedures (P>0.05).2.2.1two groups of patients with Saturation of internal jugular venousbulb blood oxygen (SjvO2)T4and T5were significantly higher thanT1(P<0.05)；there were no significant differences with SjvO2at different timepoint between two groups of patients (P>0.05).2.2two groups of patientswith Content of internal jugular venous bulb blood oxygen (CjvO2) T4and T5were significantly higher than T1(P<0.05)； there were no significantdifferences with CjvO2at different time point between two groups of patients(P>0.05).2.3two groups of patients with Atrerial venous contentdifference(Ca-jvO2) T2,T3,T4and T5were significantly lower than T1(P<0.05)；there were no significant differences with Ca-jvO2at different time pointbetween two groups of patients (P>0.05).2.4two groups of patients withCerebral extraction of oxygen(CERO2) T2,T3,T4and T5were significantlylower than T1(P<0.05)；there were no significant differences with CERO2atdifferent time point between two groups of patients (P>0.05).3.3.1Two group of patients with Glu concentration in T4,T5have asignificantly increased than T1(P <0.05), of which P group was significantlylower than that in group M in T4and T5(P <0.05).3.2Two group of patientswith Gly concentration in T4,T5have a significantly increased than T1(P<0.05); there were no significant differences with Gly at different time pointbetween two groups of patients (P>0.05).3.3Two patients with GABAconcentration within the group comparison, T5were significantly lower thanT1in P group (P<0.05), T4and T5were significantly lower than T1in M group(P<0.05); T4and T5points between the two groups were significantly different, P group was significantly higher than group M(P<0.05).3.4Twopatients with ETI concentration within the group comparison, T5wassignificantly higher than T1in P group (P<0.05), T4and T5were significantlyhigher than T1in M group (P<0.05);T4and T5points between the two groupswere significantly different, P group was significantly lower than group M(P<0.05).4.4.1Two group of patients with SOD activity T4,T5were significantly lowerthan T1(P <0.05), T4and T5points between the two groups were significantlydifferent, P group was significantly higher than group M(P<0.05). Two groupof patients with MDA content T4,T5were significantly higher than T1(P<0.05), T4and T5points between the two groups were significantly different,P group was significantly lower than group M(P<0.05).Conclusion:1. Intracranial tumor resection with propofol total intravenous anesthesia,can play a significant neuroprotective effect by reducing the concentration ofthe intracranial surgery in patients with EAA, increase of GABAconcentration and reduce excitotoxicity index.2. Propofol intravenous anesthesia can increase the serum SOD activity,reduce the content of MDA, has significant neuroprotective effect.3. Propofol total intravenous anesthesia with midazolam total intravenousanesthesia in patients compared to improve cerebral oxygen supply anddemand balance advantage is not clear, too few number of cases may beobserved with this study is related to further study. |
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