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OBJECTIVE To reveal the role of the basal forebrain(BF)GABAergic neurons in the regulation of isoflurane anesthesia and to elucidate the underlying neural pathways.METHODS The activity of BF GABAer-gic neurons was monitored during isoflurane anesthesia using a genetically encoded calcium indicator in Vgat-Cre mice of both sexes.The activity of BF GABAer-gic neurons was manipulated by chemogenetic and opto-genetic approaches.Sensitivity,induction time and emer-gence time of isoflurane anesthesia were estimated by righting reflex.The electroencephalogram(EEG)power and burst-suppression were monitored by EEG recording.The effects of activation of GABAergic BF-thalamic reticu-lar nucleus(TRN)pathway on isoflurane anesthesia were investigated with optogenetics.RESULTS The activity of BF GABAergic neurons was generally inhibited during isoflurane anesthesia,obviously decreased during the induction of anesthesia and gradually restored during the emergence from anesthesia.Activation of BF GABAergic neurons with chemogenetics and optogenetics promoted behavioral emergence from isoflurane anesthesia,with decreased sensitivity to isoflurane,delayed induction and accelerated emergence from isoflurane anesthesia.Optogenetic activation of BF GABAergic neurons prom-oted cortical activity during isoflurane anesthesia,with decreased EEG delta power and burst suppression ratio during 0.8%and 1.4%isoflurane anesthesia,respectively.Similar to the effects of activating BF GABAergic cell bod-ies,photostimulation of BF GABAergic terminals in the TRN also strongly promoted cortical activation and behav-ioral emergence from isoflurane anesthesia.CONCLU-SION The GABAergic neurons in the BF is a key neural substrate for general anesthesia regulation that facilitates behavioral and cortical emergence from general anesthe-sia via the BF-TRN pathway.
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Objective:To investigate the changes of autonomic nervous active substances in myocardium of rats with acute high-level spinal cord injury.Methods:Twenty-four clean-level healthy adult male SD rats weighting 250-300 g for 8-10 weeks old were divided into control group ( n=6) and spinal cord injury group ( n=18) according to the random number table. The spinal cord injury group was subdivided at 4, 12 and 24 hours, with 6 rats at each time point. The high-level spinal cord injury model was established by the modified Allen′s weight-drop method, and the spinal cord was only exposed in control group. The postoperative performance and BBB score for limb movement were observed in each group. The myocardium of each group was resected and used to observe ultrastructure of myocardial cells under transmission electron microscope and detect protein and mRNA levels of tyrosine hydroxylase (TH), noradrenaline transporter (NET), acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) by Western blot and RT-PCR analysis. Results:Rats of control group showed normal limb motion after operation without significant change from the preoperation level, and mean BBB score was 21 points. Rats of spinal cord injury group showed significantly reduced activities and feeding, with flaccid paralysis of both lower limbs as well as no spontaneous excretion, and showed BBB score of 0 point at 4 hours and 12 hours after injury, which was increased slightly at 24 hours after injury, with the highest score for 1 point. The ultrastructure of myocardial cells showed no obvious abnormalities in control group, while different degrees of changes in spinal cord injury group. Compared with control group, Western blot analysis showed that protein levels of TH and NET were decreased, while AChE and ChAT were increased in spinal cord injury group ( P<0.05 or 0.01). Compared with control group, RT-PCR analysis showed that mRNA levels of TH and NET were decreased, while AChE and ChAT were increased in spinal cord injury group ( P<0.05 or 0.01). mRNA levels of TH and NET in spinal cord injury group at 24 hours after injury were significantly different from those at 4 hours and 12 hours after injury (all P<0.05). mRNA levels of ChAT in spinal cord injury group were statistically significant at 12 hours and 24 hours after injury from those at 4 hours after injury, with significant difference at 12 hours and 24 hours after injury (all P<0.05). Conclusion:Sympathetic nerve active substances TH and NET are down-regulated but vagal nerve active substances AChE and ChAT up-regulated in myocardium of rats with acute high-level spinal cord injury, which may be related to the relative excitation of the parasympathetic nerve blocking the sympathetic innervation of the higher center to the heart following high-level spinal cord injury.
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Objective To evaluate the effect of low-flow sevoflurane anesthesia on the early postoperative renal function in patients.Methods Sixty patients of both sexes,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,aged 18-64 yr,scheduled for elective non-urological surgery with general anesthesia,with an expected surgical duration＞4 h,were divided into 2 groups (n =30 each) using a random number table method:middle-flow anesthesia group (group Ⅰ) and low-flow anesthesia group (group Ⅱ).Anesthesia was induced with Ⅳ midazolam,sufentanil,propofol and cisatracurium besylate.Mechanical ventilation was performed after tracheal intubation.Pure oxygen served as carrier,the fresh gas flow of oxygen was set at 4-5 L/min,sevoflurane was inhaled for 10-15 min,and then fresh gas flow was decreased to 2 L/min (group Ⅰ) and 0.5 L/min (group Ⅱ).End-tidal pressure of carbon dioxide was maintained at 35-45 mmHg.The end-tidal concentration of sevoflurane was set at 2.0％-2.4％,remifentanil and cisatracurium besylate were infused intravenously,and sufentanill or propofol was injected intermittently to maintain anesthesia.Bispectral index value was maintained at 40-60 during operation.Before anesthesia induction (T0),at 1,2,3 and 4 h after anesthesia induction (T1-4),immediately after operation (T5) and at 24 h after operation (T6),peripheral venous blood samples were collected for determination of serum fluoride ion concentrations.Peripheral venous blood samples and urine specimens were collected at T0,T5,T6,48 h after operation (T7) and 72 h after operation (T8) for determination of creatinine (Cr),blood urea nitrogen (BUN) and cystatin C (Cys C) and serum and urine β2-microglobulin (β2-MG) concentrations.Results Compared with the baseline at T0,serum fluoride ion concentrations were significantly increased at T1-6 in two groups,the serum Cys C concentration was increased at T5,and serum and urine β2-MG concentrations were increased at T5 and T6 in group Ⅰ,serum Cr and BUN concentrations and serum and urine β2-MG concentrations were increased at T5 and T6,and the serum Cys C concentration was increased at T5-T7 in group Ⅱ (P＜0.05).Compared with group Ⅰ,serum fluoride concentrations were significantly increased at T1-6,serum Cr and BUN concentrations and serum and urine β2-MG concentrations were increased at T5,and serum Cys C concentrations at T5-T7 and urine β2-MG concentrations at T5 and T6 were increased in group Ⅱ (P＜0.05).Conclusion Low-flow sevoflurane anesthesia produces no marked effect on early postoperative renal function in patients.
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Objective To evaluate the effect of dexmedetomidine on phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3 beta (GSK-3β) signaling pathway during apoptosis in cardiomyocytes of rats with severe scald.Methods Twenty-four healthy adult male SpragueDawley rats,weighing 220-280 g,were divided into 3 groups (n=8 each) using a random number table method:control group (group C),severe scald group (group S) and dexmedetomidine group (group D).Thirty percent of the total body surface area was shaved on the back and then exposed to 94 ℃ water (with 37 ℃ warm water in group C) for 12 s to establish the model of third degree scald in pentobarbital sodium-anesthetized rats.Dexmedetomidine 30 μg/kg (2 μg/ml) was intraperitoneally injected immediately after scald in group D.Rats received anti-shock treatment by intraperitoneal injection of isotonic saline according to Parkland formula,and group C received no injection.Rats were anesthetized using the method previously mentioned at 12 h after treatment,and myocardial specimens of the left ventricle were rapidly excised and stored at-80 ℃ for determination of cell apoptosis (by TUNEL) and expression of P13K,phosphorylated Akt (p-Akt) and phosphorylated GSK-3β (p-GSK-3β) (by Western blot).Apoptosis index (AI) was calculated.Results Compared with group C,AI was significantly increased,and the expression of P13K,p-Akt and p-GSK-3β was up-regulated in S and D groups (P＜0.05).Compared with group S,AI was significantly decreased,and the expression of P13K,p-Akt and p-GSK-3β was up-regulated in group D (P＜0.05).Conclusion Dexmedetomidine inhibits apoptosis in cardiomyocytes through activating PI3K/Akt/GSK-3β signaling pathway in the rats with severe scald.
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Objective To evaluate the changes in the expression of spinal aquaporin-4 (AQP4) during remifentanil-induced hyperalgesia in a mouse model of incisional pain.Methods Seventy-two pathogen-free healthy adult male CD1 mice,weighing 25-30 g,were divided into 4 groups (n=18 each) using a random number table:control group (group C),incisional pain (group I),remifentanil group (group R) and remifentanil plus incisional pain group (group R+I).Normal saline was infused subcutaneously in group C.An incision was made in the left hind paw in group I.Remifentanil 80 μg/kg was subcutaneously infused for 30 min at a rate of 0.8 ml/h in group R.Remifentanil was infused subcutaneously before establishment of the model in group R+I.The thermal paw withdrawal latency (TWL) and mechanical paw withdrawal threshold (MWT) were measured at 1 day before establishment of the model (T0) and 6 h and 1,2 and 7 days after establishment of the model (T1-4).After measurement of the pain threshold at T3,12 animals were sacrificed randomly,and the lumbar segment of the spinal cord was removed for determination of the distribution and expression of AQP4 by Western blot.Results Compared with group C,the TWL was significantly shortened at T1-3,and the MWT was decreased at T2-4 in R and R + I groups,and the expression of AQP4 was significantly up-regulated at T3 in I,R and R+I groups (P＜0.05).Compared with group I,the TWL was significantly shortened at T2,3,and the MWT was decreased at T2.4 in group R,and the TWL was significantly shortened at T1-3,the MWT was decreased at T2.4,and the expression of AQP4 was up-regulated at T3 in group R+I (P＜0.05).Conclusion The mechanism by which remifentanil induces hyperalgesia is related to up-regulation of AQP4 expression in the spinal cord in a mouse model of incisional pain.
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Objective To investigate the effect of dexmedetomidine on protein kinase RNA-like endoplasmic reticulum kinase (PERK) signaling pathway in cardiomyocytes of the rats with severe scald.Methods Twenty-four healthy adult male Sprague-Dawley rats,weighing 220-280 g,were randomly divided into 3 groups (n =8 each) using a random number table:control group (group C),severe scald group (group S),and scald + dexmedetomidine group (group D).Thirty percent of the total body surface area was shaved on the back and then exposed to 94 ℃ water for 12 s to establish the model of 3rd degree scald.Dexmedetomidine 30 μg/kg (2 μg/ml) was intraperitoneally injected immediately after scald in group D.Myocardial specimens were obtained at 12 h after scald for examination of the pathological changes and for determination of cell apoptosis and expression of C/EBP-homologous protein (CHOP),PERK,and phosphorylated PERK (p-PERK) by Western blot.The apoptosis index and p-PERK/PERK ratio were calculated.Results Compared with group C,the apoptosis index was significantly increased,the expression of CHOP,PERK and p-PERK was significantly up-regulated,and the p-PERK/PERK ratio was significantly increased in S and D groups (P＜0.05).Compared with group S,the apoptosis index was significantly decreased,the expression of CHOP,PERK and p-PERK was significantly down-regulated,and the p-PERK/PERK ratio was significantly decreased (P＜0.05),and the pathological changes of myocardium were significantly attenuated in group D.Conclusion The mechanism by which dexmedetomidine inhibits apoptosis in cardiomyocytes is related to inhibition of PERK signaling pathway in the rats with severe scald.
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Objective To evaluate the effect of acute hypervolemic hemodilution (AHH) on myocardial damage in severely burned rabbits.Methods Eighteen healthy adult rabbits,weighing 2.0-2.5 kg,were randomly divided into 3 groups (n =6 each) using a random number table:control group (group C),burn group (B group) and AHH group.Rabbits were subjected to 3rd degree burn covering 40％ of the total body surface area.After the model was established,6％ hydroxyethyl starch 130/0.4 was infused intravenously,and the target Hct was 25％ in AHH group.Before AHH (To) and at 2,4 and 8 h after AHH (T1-3),left ventricular systolic pressure (LVSP),left ventricular end-diastolic pressure (LVEDP),+dp/dtmax and-dp/dtmax were recorded,and blood samples from femoral veins were taken to determine the concentration of serum cardiac troponin I (cTnI) by ELISA.The rabbits were sacrificed at T3,and myocardial specimens were removed for microscopic examination of pathological changes with light microscope.Results Compared with group C,the serum cTnI concentration and LVEDP were significantly increased,LVSP and +dp/dtmaxwere decreased at T1-3 in B and AHH groups,and-dp/dtmax at T1-3 in group B and-dp/dtmax at T3 in group AHH were decreased.Compared with group B,LVSP,+dp/dtmax and-dp/dtm,x were significantly increased at T1-3,and no significant change was found in serum cTnI concentration and LVEDP in group AHH.There was no significant difference in the pathological changes between group B and group AHH.Conclusion AHH can not aggravate the early myocardial damage in severely burned rabbits.
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<p><b>OBJECTIVE</b>To observe the effects of preconditioning with different concentrations of sevoflurane on cariomyocyte apoptosis and myocardial inflammation in rats with sepsis and explore the possible mechanism of sevoflurane for myocardial protection.</p><p><b>METHODS</b>Forty adult male Sprague-Dawley rats were randomly divided into 4 groups (n=10), namely the control group, LPS group, low-concentration sevoflurane group and high-concentration sevoflurane group. Following sevoflurane pretreatment for 30 min and a washout period for 10 min, all the rats received intraperitoneal injection of LPS or normal saline (NS) and were sacrificed 12 h later to observe the myocardial histopathology. Apoptosis of the ardiomyocytes was detected with TUNEL assay, and enzyme-linked immunosorbent assay was used to detect serum cTnI level and myocardial TNF-α level.</p><p><b>RESULTS</b>Compared with the control group, the rats in the other 3 groups showed significantly increased serum cTnI level, myocardial TNF-α content, and apoptotic index of the cardiomyocytes (P<0.05). Compared with those in LPS group, serum cTnI level, myocardial TNF-α content, and apoptotic index of the cardiomyocytes were significantly decreased in the two sevoflurane preconditioning groups (P<0.05), and the effect was more obvious with a high dose of sevoflurane (P<0.05 CONCLUSION: Sevoflurane preconditioning can concentration-dependently reduce LPS-induced myocardial injury in rats possibly by decreasing cardiomyocyte apoptosis and alleviating myocardial inflammations.</p>
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Animals , Male , Rats , Apoptosis , Methyl Ethers , Pharmacology , Myocarditis , Drug Therapy , Myocardium , Pathology , Myocytes, Cardiac , Cell Biology , Rats, Sprague-Dawley , Sepsis , Troponin I , Blood , Tumor Necrosis Factor-alpha , MetabolismABSTRACT
Objective To evaluate the effects of remifentanil post-conditioning on aquaporin-1 (AQP-1) expression during myocardial ischemia-reperfusion (I/R) injury in rats.Methods Twenty-four male.SpragueDawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =8 each) using a random number table:sham operation group (group S),group I/R,and remifentanil post-conditioning group (group RP).Myocardial I/R was induced by 45 min occlusion of left anterior descending branch of coronary artery followed by 24 h reperfusion.Remifentanil 10 μg· kg-1· min-1 was infused over 10 min starting from 10 min before reperfusion in group RP,while the equal volume of normal saline was given instead in S and I/R groups.At the end of reperfusion,all the rats were sacrificed and their myocardial specimens from left ventricles were obtained for microscopic examination of thepathological changes and for determination of AQP-1 mRNA (using real-time fluorescent quantitative PC R) and AQP-1 protein (by Western blot) expression in the ischemic area and myocardial water content.Results Compared with S group,myocardial water content was significantly increased in the other two groups,AQP-1 mRNA and protein expression was up-regulated in group I/R,and no significant change was found in AQP-1 mRNA and protein expression in RP group.Compared with I/R group,myocardial water content was significantly reduced,and AQP-1 mRNA and protein expression was down-regulated in RP group.Conclusion Remifentanil post-conditioning reduces myocardial I/R injury possibly through down-regulating AQP-1 expression in myocardial tissues of rats.
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Objective To evaluate the effect of dexmedetomidine on the intraocular pressure during laparoscopic gastrectomy.Methods Forty ASA physical status Ⅰ or Ⅱ patients of both sexes,aged 34-64 yr,weighing 45-81 kg,scheduled for elective laparoscopic gastrectomy,were randomly divided into 2 groups with 20 patients in each group using a random number table:control group (group C) and dexmedetomidine group (group D).In group D,a loading dose of dexmedetomidine 1.0 μg/kg was infused intravenously over 15 min,followed by continuous infusion of dexmedetomidine at 0.4 μg·kg-1 · h-1 until the end of surgery.In group C,normal saline 0.25 ml/kg was infused intravenously over 15 min,followed by continuous infusion of normal saline at 0.1 ml·kg-1 · h-1 until the end of surgery.Anesthesia was induced with propofol,sufentanil and rocuronium.After tracheal intubation,intermittent positive pressure ventilation was carried out.PET CO2 was maintained at 33-36 mmHg.Anesthesia was maintained with sevoflurane,propofol,cisatracurium and sufentanil.The pressure of carbon dioxide insufflation was maintained at 9-14 mmHg and airway pressure was maintained at 11-23 cmH2O.Intraocular pressure was measured at 5 min after intubation (T1),at 5,30 and 60 min of pneumoperitoneum (T2-4),and at 5,30 and 60 min after pneumoperitoneum (T5-6).Results Compared with the value at T1,intraocular pressure was significantly increased at T2-6 in group C,and intraocular pressure was increased at T3-5 in group D.Intraocular pressure was significantly lower at T3-5 in group D than in group C.Conclusion Dexmedetomidine can decrease the intraocular pressure during laparoscopic gastrectomy.
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Objective To evaluate the effect of dexmedetomidine on apoptosis in myocardial cells in rats with severe scald.Methods Eighteen healthy male Sprague-Dawley rats,weighing 220-280 g,were randomly divided into 3 groups (n =6 each) using a random number table:control group (group C),scald group (group B)and scald + dexmedetomidine 30 μg/kg group (group D).Thirty percent of the total body surface was shaved and then exposed to 94 ℃ water for 12 s.Rats were resuscitated with isotonic saline according to Parkland formula immediately after burn.Sham burn was produced in C group.In group D,the rats received inraperitoneal injection of dexmedetomidine 30 μg/kg immediately after burn,and the equal volume of normal saline was injected in group B.The left ventricle was removed at 12 h after burn to observe the pathological changes of myocardial tissues with light microscope and to detect the apoptosis in myocardial cells (TUNEL assay) and expression of glucose-regulated protein 78 (GRP78) and C/EBP-homologous protein (CHOP) (using Western blot).The apoptosis index was calculated.Results Compared with group C,the apoptosis index was significantly increased and the expression of GRP78 and CHOP was up-regulated in B and D groups (P ＜ 0.05).Compared with group B,the apoptosis index was significantly decreased and the expression of GRP78 and CHOP was down-regulated in group D (P ＜ 0.05).The pathological changes were obvious in group B and were significantly attenuated in group D.Conclusion Dexmedetomidine can protect myocardium through inhibiting endoplasmic reticulum stress-mediated apoptosis in myocardial cells in rats with severe scald.
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@#Objective To investigate the changes of morphology of injured nerve after pulsed radiofrequency (PRF) and radiofrequency thermocoagulation (RFTC) on rats. Methods 55 male Wistar rats were selected, in which 5 were allocated to control group (group C) and the other 50 were randomly divided into group PRF (n=25) and group RFTC (n=25). The specimens were analyzed both with light microscopy and electron microscopy at immediate, and 1, 7, 14 and 28 d after operation. Results In group PRF, the nerve function of rats maintained after operation. The edema among nerve fibers was found under light microscope, while myelin lamellar structure disorder and myelin balls shaped, and compensatory hyperplasia of ultrastructure under electron microscopic level. Those effects were more pronounced 1 d after operation. In group RFTC, the nerve function of rats disappeared and autophagy behaviors happened, meanwhile Waller's degeneration and nerve regeneration appeared under both light microscopy and electron microscopy. Conclusion PRF and RFTC can produce destruction of nerve, but PRF was minor and recoverable.
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ObjectiveTo investigate the effects of sevoflurane anesthesia on aquaporin-9 (AQP-9) expression in brain tissue after focal cerebral ischemia-reperfusion (I/R) in rats.MethodsSeventy-five male SD rats weighing 230-270 g were randomly divided into 3 groups ( n =25 each):group sham operation (group S) ; group I/R and group sevoflurane anesthesia (group SE).All the animals were tracheally intubated under 2.0％ sevoflurane and mechanically ventilated.Anesthesia was maintained with fentanyl infusion at 25 μg· kg-1 · h-1 after a bolus of fentanyl 10 μg/kg and inhalation of 65％ N2O in O2 in groups S and I/R and with inhalation of 2％ sevoflurane in 35％ O2 in group SE.Focal cerebral ischemin was induced by occlusion of middle cerebral artery for 2 h using a nylon thread with rounded tip which was inserted into the right internal carotid artery and advanced cranially until resistance was met.The neurologic function was assessed and scored (0=no deficit,4 =unable to move,unconscious) and brain edema rate (volume of ischemic hemisphere-volume of contralateral hemisphere ÷volume of contralateral hemisphere × 100％ ) and expression of AQP-9 were determined at 6 h,1,2,3 and 5 d of reperfusion.ResultsFocal cerebral I/R significantly increased neurologic deficit scores,brain edema rate and AQP-9 expression in brain tissue in group I/R as compared with group S.Sevoflurane anesthesia significantly attenuated the I/R-induced increase in neurologic deficit scores and brain edema rate and further increased I/R-induced increase in AQP-9 expression in brain tissue.ConclusionSevoflurane anesthesia can reduce focal cerebral I/R injury by up-regulating the expression of AQP-9 in brain tissue.
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Objective To investigate the changes in cerebral hemodynamics in different body positions in healthy volunteers.Methods Sixty right-handed healthy male volunteers,aged 22-26,height 167-178 cm,weighing 51-67 kg,were randomly divided into 4 groups ( n =15 each): 15 degrees head-down tilt group (group Ⅰ ),30 degrees head-down tilt group (group Ⅱ ),15 degrees head-up tilt group (group Ⅲ) and 30 degrees head-up tilt group (group Ⅳ ).Blood flow signals of right middle cerebral artery (MCA) and extracranial internal carotid artery (EICA) were detected by transcranial Doppler and systolic blood flow velocity (Vs),diastolic blood flow velocity (Vd ),mean blood flow velocity (Vm),pulsatility index (PI) and resistance index (RI) were recorded at supine position (baseline),immediately,10 and 30 min after body position change(T1-3 ).Lindegaard index was calculated.Results Compared with the baseline,in group [Ⅱ Lindegaard index was increased at T2,while Vs and Vm of MCA were decreased at T2,3,in group Ⅳ Vs of MCA and PI of EICA at T2,Vd and Vm of MCA at T2,3 were decreased ( P ＜ 0.05),while there was no significant difference in the variables mentioned above in the other two groups ( P ＞ 0.05 ).Conclusion In healthy adults,cerebral blood flow velocity decreases in 30 degrees headdown and head-up tilt positions,however there is no change in cerebral blood flow velocity in 15 degrees headdown and head-up tilt positions.
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Objeetlve To avoid inserting the tip of the central venous catheter into internal jugular vein (IJV) through subclavian vein under ultrasound guidance.Methods sixty breast cancel patients aged 28-63 yr weighing 41-70 kg who needed long-term intravenous infusion and chemotherapy through central venous catheter were randomly divided into 2 groups (n=30 each):control group (group C) and ultrasound group (group U).In group C the insertion of central venous catheter through subclavian vein was guided by pulsatile injection of ice-cold saline.In group U ultrasound detector (type HFL 38/13-6 MH,Sonosite Co,USA) was used to guide the insertion of tbe central vesons catheter.The position of the catheter tip was verified by X-ray radiography.The rate of successful placement at 1st attempt was calculated.Results The tip of the central venous catheter was correctly placed in the vena cava and right atrium in all patients in group U (success rate 100%),while in group C the tip was misplaced in IJV in 6 patients (success rate 80%) and had to be replaced.Conclusion Ultrasound guidance is effective for correct placement of the tip of central venous catheter in the vema cava and right atrium through subclavian vein.
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Objective To assess the association between the gene of complement C4A, C4B deficiency and schizophrenia. Methods 192 patients with schizophrenia and 142 healthy controls were tested with the amplification restriction fragment length polymorphism (Amp-RFLP) technique.Results The frequency of C4AQ0/C4AQ0 homozygote was higher in the patient group than in the control group (χ2=8.54, P＜0.01). The relative risk (RR) of C4AQ0/C4AQ0 homozygote for schizophrenia was 6.8. There was no increased frequency of C4B deficiency in patients with schizophrenia (χ2=0.11, P＞0.05, RR=0.73).Conclusions These results indicate that there is a positive association between complement C4A dificiency and schizophrenia. Moreover, our study did not support a widespread association between a deficiency in complement component C4B and schizophrenia.