| Objective:To study the effect of propofol on the serum contents ofendothelin (ET) and calcitonin gene-related peptide (CGRP) in the patientswith craniocerebral space-occupying lesions during neurosurgery.Methods: Forty healthy medical examnationers were selected as controlgroup. Forty patients with CSOL undergoing elective surgery under generalanesthesia were considered as test group. The patients in test group weredivided randomly into two groups :propofol group(n=20)andisoflurane(n=20).The patients of propofol group were administeredintravenously with propofol (4-12mg.kg -1.h -1).The patients of groupisoflurane were administrated inhalantly with isoflurance (1.0%-2.0%).SerumET and CGRP contents were determined before anesthesia,1 ,4 hours and 24hours following anesthesia by radioimmunoassay.We monitored ECG ,heartrate ,blood pressure and SPO2 to ensure the same anesthetic level accordingto Evans PRST clinical mark .Results: ET level and ET/CGRP were significantly increased beforeanesthesia in patients with CSOL compared to control group (P<0.05).Onehours after propofol administration ET level significantly decreased in patientswith CSOL than before anesthsia,four hours following anesthesia,ET andET/CGRP decreased more than before anesthesia,meanwhile,plasma CGRPlevel was markedly increased (P < 0.05).In isoflurane group ET wassignificantly increased 1 and 4 hours during anesthesia than before anesthesia(P<0.05).Twenty four hours following anesthesia , the contents CGRP inpropofol group were still higher than before anesthesia .Discussion: Propofol is a new intravenous anesthetic which has manyadvantages such as quick react, high blood clearance rate ,quick analepsia andso on. Now it has been used widely in clinical anesthesia. ET and CGRP arebioactive polypeptide which have close relevance with cerebral diseases.They have physiological balance. This balance is out of controlpathologically .The changes of this balance are relevant to the mechanism ofcerebral diseases. From the research, we can see that ET level is higher thanthat of patients in control group and draw a conclusion that ET is a innerpathogenic factor. Latest research finds that the high level of ET is related tothe level of cerebral damage. There are many reseasons for this but the mainreasons are as follows: the craniocerebral space-occupying lesions makeneurogliocyts release the high level of ET. Meanwhile, research indicatesthat compared to situation before anesthesia, the level of ET in propofolgroup has downtrend while that of ET in isoflurane group has no this trend.This result indicates that propofol can inhibit perioperative stress reactionand degrade the level of oxygen-derived free radicals .Propofol can alsoprotect vascular endothelial cells.Four hours following anesthesia plasmaCGRP level was markedly increased in propofol group (P<0.05).Thisshows that propofol can inhibit the release of ET and promote the delivery ofCGRP.CGRP is an inner protective factor .The protective mechanism ofCGRP is related to the adjustment of concentration of calcium in the cell.CGRP can also take part in function of Bcl-2 and c-fos. The joint action ofother neurotrophic agents play a vital role in the protection of CGRP.Twenty four hours following anesthesia, the contents CGRP in propofol groupwere still higher than before anesthesia in spite of complete metabolism ofpropofol in the body. This result shows that the mechanism of propofolprotective function is a complicated multi-factor process. So far it has notbeen made clear. Research about the mechanisms of propofol to protectcerebral neuron needs to be done more.Conclusion: Therapeutic doses of propofol may play a vital role incerebral protection through inhibiting the release of ET and promoting thedelivery of CGRP.
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