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Objective To investigate the effects of epidural ropivacaine block combined with propofol intravenous anesthesia on CaMKⅡ and ERK1/2 total protein (T-CaMKⅡ and T-ERK1/2) and phosphorylation(p-CaMKⅡ and p-ERK1/2) levels in the hippocampus and cortex of rats.Methods Rats were randomly assigned to three groups: group P(control,propofol intravenous anesthesia),group PS(propofol and epidural normal saline) and group PR(propofol and epidural 0.5% ropivacaine).Anesthesia were performed in 72 h after epidural catheter placement.The rats in group PR received 70 μL of 0.5% ropivacaine to achieve epidural block.1% propofol was infused through rats caudal vein.Propofol dosage for anesthesia induction was 12 mg/kg,for anesthesia maintenance was 40 mg/(kg·h).Before the rats were decapitated,the depth of anaesthesia was assessed as either light anesthesia or deep anesthesia by checking of pinch withdrawalreflex,eyelid reflex and spontaneous rapid whisking of the vibrissae after propofol continuous infusion for 1 h.T-CaMKⅡ/T-ERK1/2 and p-CaMKⅡ/p-ERK1/2 in hippocampus and frontal cortex were examined by Western blot.Results 7 rats were assessed as light anesthesia and one rat as deep anesthesia in group P;6 rats were assessed as light anesthesia and 2 rats as deep anesthesia in group PS;in group PR,1 rat was assessed as light anesthesia and 7 rats as deep anesthesia.Significant differences were seen among three groups (P<0.05).In hippocampus of rats,p-CaMKⅡ(Thr286)43.7%±8.8% and p-ERK1/2 32.4%±7.9% in group PR were significantly lower than those in group P (100%,P<0.05).Conclusions Epidural ropivacaine block may strengthen the depth of anesthesia achieved with propofol intravenous anesthesia.The decrease of p-CaMKⅡ(Thr286) and p-ERK1/2 in hippocampus of rats may explain the effects of epidural block.
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Objective To evaluate the effects of controlled heart rate (HR) on the nasal mucosa blood flow (NMBF) during nitroglycerin (NTG)-induced controlled hypotension in the patients undergoing endoscopic sinus surgery.Methods Seventy-two ASA physical status Ⅰ or Ⅱ patients of both sexes,weighing 49-85 kg,with body mass index ＜ 30 kg/m2 and Lund-Mackay score between 7 and 15,scheduled for elective endoscopic sinus surgery,were randomly divided into 2 groups (n =36 each) using a random number table:NTG group (group N) and NTG-induced controlled hypotension combined with esmolol group (group E).Controlled hypotension was induced with continuous iv infusion of NTG at 1-3 μg· kg-1 · min-1 before surgery,and MAP was maintained at 70％ of baseline value until the end of surgery.In group E,when MAP was decreased to 70％ of baseline value,esmolol was infused intravenously at 20-100 μg· kg-1 · min-1,the consumption was adjusted according to the HR,and the HR was maintained at 60-70 beats/min until termination of controlled hypotension.Before induction of anesthesia (T0),after topical anesthesia (T1),at 15,30 and 45 min of controlled hypotention (T2-4),and at packing hemostasis at the end of surgery (T5),HR,stroke volume (SV) and cardiac output (CO) were recorded.NMBF was monitored at T1-T4.Blood samples were drawn from the radial artery and jugular blub at T1-T5 for blood gas analysis.Arteriovenous blood O2 difference (Da-jvO2) and cerebral O2 extraction rate (CERO2) were calculated.The quality of the surgical field in terms of blood loss was rated by the same attending surgeon.Results Compared with group N,HR,SV and CO at T2-T5,NMBF at T2-T4 and the volume of blood loss in the surgical field was significantly decreased in group E (P ＜ 0.01).There was no significant difference in Da-jvO2 and CERO2 between the two groups (P ＞ 0.05).Conclusion Controlled HR (60-70 beats/min) can reduce the NMBF during nitroglycerin-induced controlled hypotension in the patients undergoing endoscopic sinus surgery without causing tissue hypoperfusion.
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Objective To investigate the characteristics of upper airway collapse in patients with obstructive slcep apnea hypopnea syndrome (OSAHS) when muscle is fully relaxed.Methods Thirty male ASA Ⅱ or Ⅲ patients with OSAHS aged 20-59 yr with body mass index 21-36 kg/m2 and apnea-hypopnea index (AHI) of 28-102times/h were studied.The patients were sedated with iv midazolam 1 mg and sufentanil 5 μg.Nasotracheal intubation was then performed under topical anesthesia with 1％ dicaine.After confirmation of correct position of nasotracheal tube,anesthesia was induced with propofol 0.5 mg/kg and vecuronium 0.08 mg/kg and maintained with target-controlled infusion of propofol and remifentanil.BIS was maintained at 40-60.Fiberopticnasopharyngoscope and pressure transducer were inserted via contralateral nasal cavity and connected with imaging workstation.The site and length of the obstruction were measured and calibrated.Positive pressure was applied to the pharyngeal cavity and gradually increased in increments of 1 cm H2O until 20 cm H2O.The change in cross-section area and critical opening pressure at different planes in pharyngeal cavity were recorded.Results Complete obstruction occurred at the plane of hard palate in one patient (3％).The soft palate and uvula completely collapsed in all 30 patients (100 ％).The collapse occurred at tongue level in 23 patients (77 ％).Every 1 cm H2O increase in pressure produced increase in cross-section area by (10 ± 4)mm2 at the level of hard palate and by(28 ± 18) mm2 at the level of soft palate and uvula.The critical opening pressure ranged from 3 to 18 cm H2O and was≤ 15 cm H2O in 90％ patients.Conclusion Soft palate and uvula collapse in all patients with OSAHS when muscle is fully relaxed.The critical opening pressure is ≤ 15 cm H2O in 90％ patients.
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Objective To investigate the factors affecting the protective effects of morphine preconditioning on murine hippocampal neurons against anoxia/reoxygenation (A/R) injury and the underlying mechanisms.Methods Hippocampal slices (400 μm thick) were prepared using hippocampi isolated from decapitated mice. A/R injury was simulated in vitro using artificial cerebral spinal fluid (ACSF) deprived of O_2 and glucose for 20 min followed by reoxygenation and glucose supply for 2 h. The experiment was performed in 4 parts: I .The slices were incubated with 5 different concentrations of morphine (0.1, 0.3, 0.5, 1.0, 3.0, 10.0 /μmol/L) for 30 min at 30 min before A/R; Ⅱ. The slices were incubated with morphine 3.0 /μmol/L for 5 different periods of time (5, 15, 30, 45, 60 min) at 30 min before A/R; Ⅲ. The slices were incubated with morphine 3.0 μmol/L for 30 min followed by A/R at 6 different intervals (0, 5, 15,30,60, 120 min); Ⅳ. The slices were incubated with (a) chelerythrine (a non-selective PKC antagonist) 10 /μmol/L or (b) εVl-2 (a selective nPKCe isoform antagonist) 2 μmol/L or (c) AIP 2 μmol/L (a selective CaMK Ⅱ antagonist) or (d) MK-801 10 μmol/L (a non-competitive NMDA receptor blocker) for 30 min and then for another 30 min together with morphine 3.0 μmol/L before A/R at 30 min interval. The survival rates of the hippocampal neurons were assessed by TTC staining. Results Neuronal survival rates were significantly higher in morphine preconditioning groups which preconditioned with morphine (0.5-10.0 μmol/L) for 15-60 min at an interval of 0-60 min before A/R than in A/R group. Increase in neuronal survival rate induced by morphine preconditioning was partially blocked by chelerythrine or εV1-2 or AIP or MK-801. Conclusion Preconditioning with appropriate concentrations of morphine (0.5-10.0 μmol/L) for appropriate period of time (15-60 min) at appropriate interval (within 60 min) before A/R can protect hippocampal neurons against A/R injury through activation of nPKCε, NMDA receptor and CaMKⅡ.
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Objective To determine whether morphine postconditioning (MP) could protect the heart against ischemia reperfusion (I/R) injury and which specific type(s) of the opioid receptor is involved in the cardioprotective effect produced by hiP. Methods Male SD rots weighing 180-200 g were killed after intraperitoneal heparin 500 U/kg. The hearts were immediately removed and passively perfused in a Langendorff apparatus with K-H solution gassed with 95% O2-5% CO2. HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. The experiment was performed in 3 parts. In Part Ⅰ 32 isolated rat hearts were randomly divided into 4 groups (n = 8 each): group Ⅰ control received no treatment; group Ⅱ ,Ⅲ,Ⅳ were first perfused with K-H solution containing morphine 0.3, 3.0 and 30 μmol/L respectively for 10 min immediately after the end of ischemia followed by 50 min normal K-H solution perfusion. In part Ⅱ,the concentration of morphine in K-H solution which provided the best cardio-protective effects was chosen according to the result of Part Ⅰ , 32 isolated rat hearts were randomly divided into 4 groups ( n = 8 each) : group Ⅰ received no treatment; gvoup Ⅱ,ⅢⅣ were first perfused with K-H solution containing morphine for 5, 10, 20 min respectively immediately after ischemia followed by 50 min peffusion with normal K-H solution. In part Ⅲ,the MP method which provided the best cardio-protective effects was chosen according to the result of Part Ⅱ , 37 isolated rat hearts were randomly divided into 5 groups: group Ⅰ control (n=8);group Ⅱ-Ⅴ were first perfused for 10 min with K-H solution containing morphine (Ⅱ,n = 8)/morphine + naloxone 10 μmol/L(Ⅲ, n = 7)/morphine + nor-binaltorphimine 5 μmol/L (specific κ receptor antagonist, n = 7)/morphine + nalu'indole 5 μmol/L (specific δ receptor antagonist, n = 7) followed by 50 min reperfusion with normal K-H solution. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) determined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion.Results The postconditioning with morphine 3.0 μmol/L perfusion for 10 min provided the best cardio-protective effects in terms of IS/AAR and myocardial release of CK-MB. Nuloxone completely abolished the cardio-protective effects of MP. Nor-binaltorphimine partly reversed the protective effect of MP, while naltrindole had no effects on MP. Conclusion MP protects the heart against I/R injury via activating κ receptor.
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Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .
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Objective To evaluate the effect of remifentanil on heart rate variability,to discuss the optimal does of remifentanil for tracheal intubation.Methods Thirty six ASA Ⅰ～Ⅱ patients were randomly assigned to one of three groups(n=12/group)according to the remifentanil target plasma concentration(2、4、6ng/mL).No premedication was given.The target-controlled infusion(TCI)of renifentanil was initiated 5 minutes after the TCI of propofol given at the target plasma concentration of 3.5?g/mL.Mean arterial pressure(MAP),heart rate(HR),HF,LF,HF/LF were measured from baseline values to 5 minutes after the operation began every minutes.MAP,HR,HF,LF and HF/LF were obtained on the time point as follows:before the induction(T0),before the start of remifentanil TCI(T1),before laryngoscopy(T2),and maximum values after intubation(T3),before operation(T4),maximum values after operation.All the data obtained were analyzed used ANOVA with SPSS 11.5 statistical software.P
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OBJECTIVE To observe the effect of clonidine on the proinflammtory cytokine and haemodynamics in hypoxia and trauma rats. METHODS Forty male SD rats were randomly divided into 5 groups: (A) hypoxia control group (n=8), (B) trauma control group (n=8), (C) hypoxia and trauma group(n=8), (D) hypoxia trauma clonidine precondition group (n=8), (E) hypoxia trauma colindine postcondition group (n=8). Except B group, the rats of each hypoxia group were placed in a sealed hypoxia chamber which O2 concentrate were maintained at (10 ?0.5)% for 6 days, 7h per day. Except A group, the rats of each trauma group received pharyngeal trauma after anesthesia. The rats in D and E group received clonidine 30 ?g/kg before 10 minutes or right after the pharyngeal trauma respectively. The mean artery pressure (MAP) and heart rate (HR) on the several moment around the trauma were recorded. The serum level of TNF-?, IL-6 was measured 1h after trauma. The tissues from lung and kidneys were taken to study the pathologic changes through microscope. RESULTS The MAP and HR raised obviously in each trauma group except D group on the trauma moment (P
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OBJECTIVE To study the influenceof clonidine on the hemadynamics and plasma catecholamine of the postoperative patients in PACU. METHODS Twenty eight patients suffered from severe OSAHS who underwent modified UPPP and monitored in the PACU after operation were divided randomly into two groups:clonidine group and control group. Both group received the same protocol of sedation and analgesia. Patients in clonidine group received clonidine 3ug/kg injected slowly when entered the PACU,and patients in control group received same volume of NS. Esmolol and Nitroglycerin were used to adjust the hemadynamics. The changing of hemadynamics was recorded,blood samples were taken before operation,2 hours after entering PACU,before discharge from PACU to determine the changing of plasma catecholamine. RESULTS The hemadynamics was more stable in clonidine group than that in control group and less vasoactive agents were needed. The plasma catecholamine was much lower in clonidine group 2 hours after entering PACU and before discharge from PACU than that in control group. CONCLUSION Clonidine could be administered to stabilize the hemadinamics,to lower the level of stress hormone and could improve the recovery of the patients.
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OBJECTIVE To observe the controlled hypotensive effect of remifentanil in patients of different age groups undergoing FESS. METHODS Forty-seven ASAI-II patients were divided into two groups: young-middle aged group(18～55yr,n=24)and elderly group(60～72yr,n=23). Both groups received remifentanil by continuous infusion. Their systolic blood pressures (SBP) were reduced to 30～35 % of the base values and sustained throughout surgery. SBP,diastolic blood pressure (DBP) and heart rate (HR) were monitored throughout surgery. The surgical field quality score, total dose of remifentanil and postoperative complications of each patient were recorded after the operation. RESULTS The SBP and DBP of two group were reduced to the target pressure at the beginning of the operation(P0.05). CONCLUSION Remifentanil enabled controlled hypertensions and offer superior surgical field conditions for FESS in patients of different age groups. Moreover,it was a more suitable alternative for elderly patients because HR did not increase during controlled hypotension.
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Objective To evaluate the effects of different concentration of propofol on the anoxic response of primary cultured hippocampal neurons Methods Newborn (
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Objective To investigate the effect of ketamine on the delayed rectifier outward potassium currents (IK) using whole-cell patch clamp technique. Methods Pyramidal neurons were enzymatically isolated from Wistar rat hippocampus. The effect of ketamine on the IK was assessed using whole-cell patch clamp technique. We measured the amplitude of the delayed outward rectifier IK by activating depolarizing pulse from -50 mV to 40 mV. Different concentrations of ketamine were added and potassium currents were measured. Results IK was inhibited by ketamine in a concentration-dependent manner. The five concentrations of ketamine (10, 30, 100, 300, 1000 ?mol/L) reduced peak IK currents by (10 ? 4)% , (19?4)%, (31 ?5)%, (50?7)%, (54?8) % respectively, with a mean IC50 of (100?18)?mol/L and Hill coefficient of 1.33?0.48. The V1/2 of activation curve was shifted from (1.82 ? 0.20) mV to (9.30 ? 1.03) mV (n = 8, P
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Objective The purpose of this study was to determine and compare the effect of patient controlled analgesia(PCA) with tramadol and fentanyl on postoperative sleep pattern in patients with severe obstructive sleep apnea syndrome(OSAS) Methods Forty five ASA Ⅱ patients with severe OSAS undergoing uvula palate pharyngoplasty(UPPP) were randomly divided into 3 groups of 15 patients each according to the postoperative PCA the patients received: 1) tramadol group; 2) fentanyl group and 3) control group The patients were premedicated with intramuscular atropine 0 01mg?kg -1 .The patients were adequately sedated (Ramsay Ⅱ Ⅲ) with midazolam 0 03 mg?kg -1 and fentanyl 2?g?kg -1 Awake intubation was performed under topical anesthesia Anesthesia was then induced with propofol 1 5 2 0 mg?kg -1 and maintained with inhalation of 1 0% 1 5% isoflurane and 60% N 2O and intermittent intravenous boluses of vecuronium PCA was started when the patients were awake Tramadol 500mg (tramadol group) and fentanyl 500?g (fentanyl group) were diluted to 100ml(tramadol 5mg?ml -1 , fentanyl 5?g?ml -1 ) A loading does of 10ml was given followed by continuous intravenous infusion at a rate of 3ml?h -1 PCA bolus does was 1 5ml and lock out time 10 min Polysomnography(PSG) was continuously monitored and recorded the first night after operation from 10 pm to 6 am next morning According to Rechtschaffen standard sleep was divided into 6 stages: stage Ⅰ, stage Ⅱ, slow wave sleep(SWS)(stageⅢ+Ⅳ), stageV (rapid eye movement REM) and stage Ⅳ(awake) Results During the 480 min of PSP monitoring, SWS was (13 06?7 56) min in tramadol group, (9 2?7 26) min in fentanyl group and (6 33?4 68)min in control group and the total sleep time (TST) was (197 4?84 48) min in tramadol group, (148 33?72 73)min in fentanyl group and (124 13?61 38)min in control group SWS and TST were significantly longer in tramadol group than those in control group(P
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Objective Propofol has been found to have anti-lipid peroxidation effect. We aimed to evaluate the effects of propofol on primarily cultured hippocampal neurons injured by glutamic acid. Methods Hippocampal neurons were obtained from newborn Wistar rats (within 24 h after birth) and cultured for 12 days. The 12 d cultured hippocampal neurons were randomly divided into three groups : (1) control group; (2) glutamate group in which cells were incubated with glutamate 100 ?mol?L-1 for 24 h; (3) propofol-glutamate group in which cells were incubated with propofol 500 ?mol?L-1 and glutamate 100 ?mol?L-1 for 24 h. Cell survival rate (MTT), apoptosis (flow cytometry) and C-fos protein (immuno-histochemistry) production were determined in each group. Results C-fos protein and apoptosis were significantly increased and survival rate was decreased in glutamate group compared with those in control group ( P
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Objective Propofol has profound influence on respiration. The purpose of this study was to evaluate the effect of propofol on respiratory mechanics during painless induced abortion. Methods Forty ASA Ⅰ women in early pregnancy (45-60 days) aged 17-52 yrs, weighing 42-80 kg undergoing induced abortion were enrolled in this study. Anesthesia was induced with intravenous 2.5 mg?kg-1 and maintained with intermittent i.v. boluses of propofol 30-50 mg. SpO2 and HR were monitored with Nellcor N-180 pulse oximeter. Respiratory mechanics was monitored with IFA-300 anemometer (TSI Co. USA) . The parameters measured included inspiratory / expiratory maximal air-flow velocity, inspiratory / expiratory mean air flow velocity, mean inspiratory and expiratory time, respiratory rate, inspiratory / expiratory air flow volume, dynamic inspiratory and expiraory airway pressure and indidence of apnea.Results SpO2 decreased significantly during maintenance of anesthesia with propofol. The mean and maximal inspiratory / expiratory airflow velocity and the inspiratory / expiratory airflow volume all decreased significantly during propofol anesthesia. The dynamic inspiratory / expiratory airway pressure significantly decreased during propofol anesthesia. The respiratory rate was significantly higher during propofol anesthesia while the mean inspiratory /expiratory time became shorter. Three patients developed apnea during induction of anesthesia with propofol (7.5%) . Spontaneous breathing returned within 1 min. Conclusion Spontaneous breathing is significantly depressed during propofol anesthesia in terms of respiratory mechanics. Care should be taken to maintain oxygenation and ventilation of the patient.
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Objective To investigate the effects of lidocaine and ketamine on resting membrane potentials of primary cultured anoxic hippocampal neurons using patch-clamp technique. Methods Hippocampal neurons were isolated from newborn Wistar rats (
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Objective To study the role of NMDA-R system in the differential reaction of pain sense between peripheral inflamed local portion and distal portion Methods One hundred and forty-one adults Wistar rats were randomly divided into 6 groups The pain thresholds (PT) of bilateral feet were measured by paw-pressure technique NMDA receptor antagonist CGP378495mg?kg -1, NMDA receptor agonist NMDA 5mg?kg -1 or NS 1ml was injected intraperitonealy in the first three groups, respectively after one hindpaw was inflamed In the later three groups the same drugs were injected before one hindpaw was inflamed PT of bilateral feet in all groups were measured at virous times Results In the first three groups, PT of inflamed paw decreased ,and of non-inflamed paw increasedmarkedly after inflammation (P0 05), decreased significantly(P0 05), decreased significantly (P
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Objective To observe the effects of isoflurane on ocular hemodynamics .Methods Fifteen patients without eye diseases undergoing non-head and non-neck surgical procedures ,were enrolled in this study. Anesthesia was induced with intravenous propofol and atracuronium, followed by laryngeal mask insertion, and was maintained with isoflurane. Peak systolic velocity(PSV),end diastolic velocity(EDV),Tmax and resistant index(RI) of double ophthalmic arteries, central retinal artery and posterior ciliary arteries were determined by coloured Doppler imaging before anesthesia, 30 min following inhalation of isoflurane 1.0MAC or 1.5MAC respectively . Blood pressure, heart rate and SpO 2 were also measured at above time points.Results As compared with those before anesthesia ,no significant changes were found in all above parameters of double ocular arteries in all time points; PSV and EDV of central retinal artery decreased significantly with increase of isoflurane level(P005); all above parameters of posterior ciliary artery decreased significantly ,with increase of isoflurane level(P005). The diastolic pressure was positively correlated with PSV and EDV of central retinal artery and posterior ciliary arteries ,and negatively with RI , but no correlation to all above parameters of double ophthalmic arteries.Conclusions It may be dangerous for the patients with potential ischemia of eyes undergoing isoflurane anesthesia. Decreasing its concentration and improving blood pressure can increase ocular blood supply to prevent ophthalmic ischemic complications from occurrence.
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Objective To investigate the effects of ketamine on the voltage-gated sodium channels in hippocampal pyramidal neurons, trying to elucidate the possible mechanism of general anesthesia with ketamine.Methods Hippocampal pyramidal neurons were isolated from Wistar rats of 2 weeks old. Whole-cell patch-clamp recordings were made from cultured hippocampal pyramidal neurons before and after the application of ketamine The effect of ketamine on the sodium current amplitude and the kinetics of the channel were studied. Results The sodium channels were reversibly inhibited by ketamine in a dose-dependent manner. IC50 of ketamine was (794?21) ?mol/L.The hyperpolarizing shift of both steady-activation and steady-inactivation was observed.Conclusion Ketamine inhibits the voltage-gated sodium channels to some degree. Sodium channel inhibition may be involved in the mechanism of general anesthesia induced with ketamine.
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Objective To research and develop the model of external reciprocating sports intermittent hypoxia box for rats. Methods Two animal cabins (28 cm?20 cm?15 cm) and one hypoxia chamber (80 cm?80 cm?60 cm) which covered each cabin in turn were developed. 4 male SD rats were placed in each animal cabin. The hypoxia chamber in which low O2 concentration was maintained with filling high-pure Nitrogen continuously, moved to and fro between two animal cabins, and driven by a servomotors. Two animal cabins were covered in turn by the hypoxia chamber and get the same low O2 concentration as in the hypoxia chamber. The goal volume fraction of oxygen in hypoxia chamber was (10?0.5)% and the time of unilateral movement from one animal cabin to another was 4 s, the cycle time of intermittent hypoxia was 180 s, the retention time was 86 s (including the hypoxia and normoxia time was 90 s respectively). The hypoxia chamber runs 8 h per day. The numerical value on artery blood gas of rats in which hypoxia chamber inside and outside was measured Results The reciprocating sports intermittent hypoxia chamber can be operated safely and reliably. The lowest PaO2 is (4.766? 0.536) kPa(or (35.75 ?4.02) mmHg) and the lowest SaO2 is 0.69 ?0.08 when the animal cabin in hypoxia chamber. Conclusion The chronic intermittent hypoxia model for rats is established by self-developed external reciprocating sports intermittent hypoxia chamber.