Ethanol alters the expression of ion channel genes in Daphnia pulex.

BACKGROUND: Heavy drinking can increase heart rate and blood glucose, induce hypoxic tolerance, impair brain cognitive functions, and alter gene expressions. These phenomena may occur even in response to small dose of ethanol exposure or during its withdrawal. OBJECTIVES: To evaluate whether persistent low concentrations of ethanol exposure affect organism function and the gene expressions of ion channels. METHODS: Daphnids were randomized to receive placebo 300 min, 2 mM ethanol 300 min, or 2 mM ethanol 240 min and then placebo 60 min. Heart rate, glucose levels, phototactic behavior, and hypoxic tolerance were recorded during experiment. At the end of the study, changes in the mRNA levels of ion channel genes were assessed in response to exposure to ethanol using quantitative polymerase chain reaction (PCR) techniques. RESULTS: Heart rate was reversibly increased by ethanol withdrawal and returned to basal levels upon re-exposure to ethanol. Fifteen of 120 ion channel transcripts were affected by persistent ethanol exposure. Neither ethanol withdrawal nor persistent exposures showed an effect on blood glucose, phototactic behavior, or hypoxic tolerance. CONCLUSIONS: Small doses of ethanol can increase heart rate and alter gene expression of multiple ion channels in Daphnia pulex. Affected ion channel genes may assist in understanding the mechanism of ethanol adaptation and tolerance.

Is there a role of TNFR1 in acute lung injury cases associated with extracorporeal circulation?

The signaling pathway for tumor necrosis factor-α (TNF-α) and its receptors is up-regulated during extracorporeal circulation (ECC), and recruits blood neutrophil into the lung tissue, which results in acute lung injury (ALI). In this study, we evaluated the role of tumor necrosis factor receptor 1 (TNFR1) in ECC-induced ALI by blocking TNF-α binding to TNFR1 with CAY10500. Anesthetized Sprague-Dawley (SD) rats were pretreated intravenously with phosphate buffered saline (PBS) or vehicle (0.3 ml ethanol IV) or CAY10500, and then underwent ECC for 2 h. The oxygenation index (OI) and pulmonary inflammation were assessed after ECC. OI was significantly decreased, while TNF-α and neutrophil in bronchoalveolar lavage fluid (BALF) and plasma TNF-α increased after ECC. Pretreatment of CAY10500 decreased plasma TNF-α level, but did not decrease TNF-α levels and neutrophil counts in BALF or improve OI. Lung histopathology showed significant alveolar congestion, infiltration of the leukocytes in the airspace, and increased thickness of the alveolar wall in all ECC-treated groups. CAY10500 pretreatment slightly reduced leukocyte infiltration in lungs, but did not change the wet/dry ratio in the lung tissue. Blocking TNF-α binding to TNFR1 by CAY10500 intravenously slightly mitigates pulmonary inflammation, but cannot improve the pulmonary function, indicating the limited role of TNFR1 pathway in circulating inflammatory cell in ECC-induced ALI.

The common anesthetic, sevoflurane, induces apoptosis in A549 lung alveolar epithelial cells.

Lung alveolar epithelial cells are the first barrier exposed to volatile anesthetics, such as sevoflurane, prior to reaching the targeted neuronal cells. Previously, the effects of volatile anesthetics on lung surfactant were studied primarily with physicochemical models and there has been little experimental data from cell cultures. Therefore it was investigated whether sevoflurane induces apoptosis of A549 lung epithelial cells. A549 cells were exposed to sevoflurane via a calibrated vaporizer with a 2 l/min flow in a gas­tight chamber at 37˚C. The concentration of sevoflurane in Dulbecco's modified Eagle's medium was detected with gas chromatography. Untreated cells and cells treated with 2 µM daunorubicin hydrochloride (DRB) were used as negative and positive controls, respectively. Apoptosis factors, including the level of ATP, apoptotic­bodies by terminal deoxynucleotidyl transferase­mediated dUTP nick end labeling (TUNEL) assay, DNA damage and the level of caspase 3/7 were analyzed. Cells treated with sevoflurane showed a significant reduction in ATP compared with untreated cells. Effects in the DRB group were greater than in the sevoflurane group. The difference of TUNEL staining between the sevoflurane and untreated groups was statistically significant. DNA degradation was observed in the sevoflurane and DRB groups, however this was not observed in the untreated group. The sevoflurane and DRB groups induced increased caspase 3/7 activation compared with untreated cells. These results suggest that sevoflurane induces apoptosis in A549 cells. In conclusion, 5% sevoflurane induced apoptosis of A549 lung alveolar epithelial cells, which resulted in decreased cell viability, increased apoptotic bodies, impaired DNA integrality and increased levels of caspase 3/7.

Minimum infusion rates and recovery times from different durations of continuous infusion of fospropofol, a prodrug of propofol, in rabbits: a comparison with propofol emulsion.

OBJECTIVE: To explore, in rabbits, the minimum infusion rates (MIR) required and recovery time from long duration (≤ 8 hours) continuous infusion of fospropofol disodium, a novel water-soluble prodrug of propofol, and compare it with propofol. STUDY DESIGN: Prospective, randomized, blinded experimental trial. ANIMALS: Ninety-six adult laboratory rabbits, mean ± SD weight 2.20 ± 0.15 kg. METHODS: Stage 1. 16 rabbits were assigned to receive fospropofol disodium or propofol to measure MIR, using an up-and-down method with response to tail-clamping stimulus (TCS). Stage 2. Eighty rabbits were allocated to group F (fospropofol disodium) or group P (propofol), and further subdivided (n = 10 in each subgroup) according to infusion time (2, 4, 6 or 8 hours), to groups F(2h), F(4h), F(6h), F(8h) and P(2h), P(4h), P(6h), P(8h). Fospropofol or propofol were infused, and tail clamping applied to maintain the same depth of anaesthesia until infusion was completed. Times to recover righting reflex (RR), to respond to TCS, and total recovery to different durations of continuous infusion of two anaesthetic drugs were noted. Respiratory and pulse rates and oxygen saturation were analyzed. The plasma concentrations of fospropofol disodium, the active metabolite propofol (propofol(F) ) and propofol emulsion were measured with respect to loss and recovery of RR and TCS. RESULTS: MIR of fospropofol disodium was 2.0 mg kg(-1) minute(-1) , and MIR of propofol was 0.9 mg kg(-1) minute(-1) . Times in minutes to total recovery from anaesthesia in groups F and P were as follows, F(2h) 15 ± 3; F(4h) 26 ± 4; F(6h) 52 ± 6; F(8h) 84 ± 10; and P(2h) 10 ± 1; P(4h) 19 ± 7; P(6h) 36 ± 7; P(8h) 48 ± 5. CONCLUSIONS AND CLINICAL RELEVANCE: After continuous intravenous infusion in rabbits (≤ 8 hours), fospropofol disodium and propofol both show an extension of recovery time with increasing infusion time, fospropofol disodium showing a significantly greater prolongation compared to propofol emulsion when infusion time increases to 6 and 8 hours.

[Apoptosis inhibition of capsaicin on myocardial ischemia-reperfusion injury in rats].

OBJECTIVE: To determine apoptosis inhibition effect of capsaicin on myocardial ischemia-reperfusion injury in rats and its underlying mechanisms. METHODS: The rat model of myocardial ischemia-reperfusion injury was established by ligating the left anterior descending coronary artery for 45 min and then loosing the ligation (reperfusion) for 120 min. Twenty healthy male rats were randomly divided into sham group, control group (I/R), capsaicin group (CAP+I/R), capsazepine group (CAPZ+CAP+I/R), and S-3144 group (S-3144+CAP+I/R). All drugs were delivered bolusly into left ventricle (LV)via right carotid artery at 10 min and 5 min before ischemia. Rats in I/R group and sham group only received vehicle injection. Myocardial protection was assessed by measurements of heart rate (HR) and left ventricular developed pressure (LVDP). The pathologic changes of myocardial tissue in each group were observed under light microscopy. TUNEL-positive nuclei were tested by immunofluorescent method. RESULTS: At 120 min after reperfusion, there were significant increases of HR and LVDP in CAP+I/R group when compared with control group, capsazepine group, and S-3144 group (P < 0.05). The apoptotic index in the sham group was lower than that in the groups with ischemia/reperfusion injury (P < 0.05). Among the groups with ischemia/reperfusion injury, CAP+I/R group had the lowest apoptotic index (P < 0.05). CONCLUSION: CAP could generate cardioprotection associated with cardiomyocyte apoptosis inhibition in vivo, likely by stimulating TRPV1 and further activating NK1 receptor.

A model for the preferential delivery of isoflurane to the spinal cord of the goat.

To identify the blood supply of the caprine central nervous system, six anaesthetised goats were perfused with coloured suspension into the brachiocephalic artery, the aorta, the iliac artery and the femoral artery. The subsequent distribution indicated that the brain and the main segments of the spinal cord were supplied by the brachiocephalic artery and aorta, respectively. Ten similarly anaesthetised goats then received emulsified isoflurane randomly via either the proximal part of the descending aorta (arterial group) or an ear vein (venous group). In the arterial group, the isoflurane partial pressure (P(iso)) in femoral arterial blood was almost double the P(iso) in jugular venous blood. The model showed that preferential delivery of isoflurane to the goat spinal cord in situ was possible and could be used for further research into the mechanisms of anaesthetic action, particularly factors affecting immobility.

[Preferential delivery of emulsified isoflurane to peripheral nerves in goats].

OBJECTIVE: To develop a new model for preferential delivery of isoflurane to peripheral nerves in goats, and to identify preliminarily volatile anesthetic action sites. METHODS: Eighteen goats were randomly and equally divided into arterial group, control group and venous group. In the arterial group, emulsified isoflurane was infused into the femoral artery of the goats to deliver isoflurane to the peripheral nerves. In the control group, 30% Intralipid which used as a solvent of emulsified isoflurane was infused via the femoral artery of the goats with the same infusing speed as that of the arterial group. In the venous group, emulsified isoflurane was infused via an ear peripheral vein. Minimum partial pressure (MPP), the partial pressure (Piso) of isoflurane in blood producing immobility in 50% of the goats exposed to noxious stimuli, was determined with an up-and-down method and a noxious stimulus by clamping the dew-claw of the hindlimbs of the goats in the arterial group and the control group, or the dew-claw of the hindlimb of the goats in the venous group. RESULTS: No isoflurane was found in the jugular and femoral veins of the goats in the control group, and normal nociceptive reflexeswere maintained. The MPP of the femoral vein of the goats from the control group did not differ from the MPP of the jugular vein of the goats from the arterial and venous groups. The MPP of femoral vein p was 7 times of that of jugular vein ](38.45 +/- 17. 01) mmHg vs. (5.82 +/- 2.32) mmHg, 1 mmHg = 0.1333 kPa, P < 0.05] in the goats from the arterial group, and 4 times of that of jugular vein in the goats from the venous group [(9.41 +/- 1.61) mmHg, P < 0.05]. The MPP of jugular vein in the goats from the arterial group was about half of that of the goats in the venous group. CONCLUSION: A new model of preferential delivery of isoflurane to the peripheral nerves in goats has been developed. Only Piso higher than that used in clinical anesthetic range has a significant anesthetic effect on peripheral nerves.

[Effect of focal irrigation with mild hypothermic artificial cerebral spinal fluid on the spinal ischemia/reperfusion injury].

OBJECTIVE: To investigate the effect of focal irrigation with mild hypothermic artificial cerebral spinal fluid on the spinal ischemia/reperfusion injury. METHODS: Eighteen health male New Zealand white rabbits were randomly divided into three groups: normal control group (Group NC), spinal ischemia-reperfusion group (Group SIR) and focal irrigation with mild hypothermic artificial cerebral spinal fluid group (Group FI). The rabbits in Group SIR and Group FI were subjected to spinal ischemia/reperfusion injury by clamping the infrarenal abdominal aorta. The rabbits in Group FI received focal irrigation with 25 degrees C artificial cerebral spinal fluid during the spinal ischemia period. The mean arterial pressure (MAP) and cerebral spinal fluid pressure (CSFP) were continuously measured during the ischemic/reperfusion processes. The neurological conditions of the rabbits were assessed at 24 h, 48 h and 72 h after reperfusions. The spinal cords were harvested 72 h after reperfusions for histological analysis. RESULTS: The MAP and CSFP in Group NC remained stable. The MAP in Group SIR and Group FI decreased continuously in the first 30 min of spinal ischemia period and 30 min after reperfusion. The CSFP in Group SIR increased continuously in the first 10 min of spinal ischemia and was higher than the baseline and those in Group NC. The CSFP in Group FI decreased to 3.8 mmHg (1 mmHg = 0.1333 kPa) at the beginning of spinal ischemia, and remained at 3-5 mmHg until 20 min after reperfusions. Group FI had better neurological outcomes and less severe pathological changes than Group SIR measured at 72 h after ischemia/reperfusion. CONCLUSION: Focal irrigation with mild hypothermic artificial cerebral spinal fluid can decrease CSFP during spinal ischemia/reperfusion and protect spinal cords against ischemia/reperfusion injuries.

[The sedative and hypnotic effects and safety of oral emulsified isoflurane in rats].

OBJECTIVE: To investigate the sedative and hypnotic effects and safety of oral emulsified isoflurane in rats. METHODS: Thirty healthy Sprague-Dawley (SD) rats were randomly divided into three groups. The rats in the emulsified isoflurane group were orally administered with emulsified isoflurane with the sequential method, while the rats in the normal sodium group and the intralipid group were orally administered with sodium and intralipid respectively. The rats in the emulsified isoflurane group received 2.15 mL/100 g of 8% emulsified isoflurane, a dosage calculated with an increase of a common ratio (r = 0.8) on the basis of median effective dose (ED50). Similarly, 2.15 mL/100 g of normal sodium and 2.15 mL/100 g of 30% intralipid were given to the rats in the normal sodium group and the intralipid group, respectively. The neurobehaviors of the rats were assessed, and the interval of disappearance and recovery of the righting reflex were recorded. RESULTS: Oral emulsified isoflurane reduced the autonomic activity time and induced the loss of righting reflex. The ED50 of the loss of righting reflex was 1.72 mL/100 g. The rats orally administered with 2.15 mL/100 g of 8% emulsified isoflurane had 90% of loss of righting reflex, with a sleeping latency of 15-20 min and up to 60 min of sleeping duration. CONCLUSION: Oral emulsified isoflurane has obvious sedative and hypnotic effects.

Further proof that the spinal cord, and not the brain, mediates the immobility produced by inhaled anesthetics.

BACKGROUND: Previous investigations indicate that the spinal cord, perhaps with a minor cerebral contribution, mediates the capacity of inhaled anesthetics to produce immobility in the face of noxious stimulation. The implications of these investigations may be limited by the trauma associated with their experimental methods (e.g., cardiopulmonary bypass or transection of the spinal cord). The present study avoided such trauma. METHODS: Thirty goats received emulsified isoflurane via either the initial section of the aorta (arterial group; preferential isoflurane delivery to the spinal cord) or an ear vein (venous group; equal delivery of isoflurane to the cord and brain). The authors determined the minimum partial pressure of isoflurane (the isoflurane partial pressure in the blood required to produce immobility in 50% of the goats exposed to a noxious stimulus). RESULTS: For the venous group, the minimum partial pressure in carotid versus femoral arterial blood (9.56 +/- 1.86 mmHg vs. 9.68 +/- 1.90 mmHg) did not differ. For the arterial group, the minimum partial pressure in carotid arterial blood was half that in femoral arterial blood (5.35 +/- 1.45 mmHg vs. 10.97 +/- 3.04 mmHg, P < 0.05). As these data show, the minimum partial pressure in femoral arterial blood did not differ for the arterial group versus the venous group. CONCLUSIONS: In this novel and minimally traumatic model, the anesthetic partial pressure delivered to the spinal cord governed the suppression of movement in response to noxious stimulation. The results indicate that the spinal cord is the primary mediator of immobility and that the brain plays little or no role.

The protective effects of emulsified isoflurane on myocardial ischemia and reperfusion injury in rats.

PURPOSE: Pretreatment with volatile anesthetics has been demonstrated to exert cardioprotective effects. The purpose of this study was to examine the effect of emulsified isoflurane, a new formulation of isoflurane in lipid emulsion, administered intravenously in an ischemia and reperfusion model of myocardial injury. METHODS: Thirty-two Sprague Dawley rats of both sexes were subjected to 30 min of myocardial ischemia followed by 180 min of reperfusion. Each was assigned to one of four pretreatment groups to receive an isovolumetric intravenous infusion of saline: control group, 30% intralipid group, 8% emulsified isoflurane 2 ml kg(-1) group, and sham group (each group, n = 8). The vehicles were administered at a constant rate for 30 min and then discontinued 30 min before left anterior descending coronary artery occlusion. The cardioprotective effects were examined by determining hemodynamics, infarct size, enzyme activity, and cardiomyocytic apoptosis. RESULTS: Pretreatment with emulsified isoflurane 2 ml kg(-1) (P = 0.000) significantly reduced infarct size (22.6 +/- 2.2%) compared with control (34.8 +/- 2.3%) and 30% intralipid (31.1 +/- 2.9%). When compared with the control and intralipid groups, emulsified isoflurane increased Bcl-2 expression while decreasing Bax and Caspase-3 expression and enhancing Bcl-2/Bax ratios. The apoptotic index in the emulsified isoflurane treatment group showed a significant reduction compared with that in the control group (P = 0.000) and the intralipid group (P = 0.001). In addition, the serum levels of lactate dehydrogenase and creatine kinase were markedly reduced in the emulsified isoflurane treatment group compared with the control and intralipid groups (lactate dehydrogenase, P = 0.015 vs. control; creatine kinase, P = 0.000 vs. control and intralipid). CONCLUSION: These data support a cardioprotective effect of intravenous emulsified isoflurane against myocardial ischemia and reperfusion injury, which are mediated, at least in part, by the inhibition of apoptosis and cell damage.

[Model establishment for emulsified isoflurane delivered selectively to the goat spinal cord and preliminary research on the immobility mechanism of isoflurane].

OBJECTIVE: To develop a new model of preferentially delivering isoflurane to the goat spinal cord, and to explore preliminarily volatile anesthetic action sites. METHODS: Eighteen goats were randomly and equally divided into group artery and group vein. In group artery, emulsified isoflurane was infused into descending aorta for developing the model to deliver isoflurane to the goat spinal cord. In group vein, emulsified isoflurane was infused via the ear vein. After the end-tidal isoflurane concentration of 1 minimum alveolar concentration (MAC) was maintained for 20 min, the isoflurane partial pressures (P(iso)) in samples which were drawn from the femoral artery and the carotid artery were determined by a gas chromatography. RESULTS: In group vein, there was no statistical difference among all the P(iso). In group artery, the P(iso) of the femoral arterial blood was almost same as that in group vein, but the P(iso) of the carotid arterial blood was near half of that in group vein [(6.07 +/- 3.60) mmHg vs (10.21 +/- 2.41) mmHg, P < 0.05]. CONCLUSION: This new model permits preferentially to deliver the isoflurane to the in situ goat spinal cord, and the results support the importance of the spinal cord in suppressing nociceptive reflex under isoflurane anesthesia.

Comparison of minimum alveolar concentration between intravenous isoflurane lipid emulsion and inhaled isoflurane in dogs.

BACKGROUND: As in inhaled isoflurane anesthesia, when isoflurane lipid emulsion (ILE; 8%, vol/vol) is intravenously administered, the primary elimination route is through the lungs. This study was designed to determine the minimum alveolar concentration (MAC) and the time course of washout of isoflurane for intravenously infused ILE by monitoring end-tidal isoflurane concentration. METHODS: Twelve healthy adult mongrel dogs were assigned randomly to an intravenous anesthesia group with 8% ILE or to an inhalation anesthesia group with isoflurane vapor. An up-and-down method and stimulation of tail clamping were used to determine MAC of 8% ILE by intravenous injection in the intravenous anesthesia group and MAC by the inhaled approach in the inhalation anesthesia group, respectively. Isoflurane concentration and partial pressure in end-tidal gas, femoral arterial blood, and jugular venous blood were measured simultaneously just before each tail clamping and during washout. RESULTS: The induction time in the intravenous anesthesia group (105 +/- 24 s) was shorter than that in the inhalation anesthesia group (378 +/- 102 s; P < 0.01). MAC of 8% ILE by intravenous injection (1.12 +/- 0.18%) was significantly less than MAC by the inhaled approach (1.38 +/- 0.16%; P < 0.05). No significant difference was found between the two groups in the time course of washout of isoflurane. CONCLUSION: The MAC of intravenous anesthesia with 8% ILE was less than that of inhalation anesthesia with isoflurane vapor in dogs.

The efficacy and safety of intravenous emulsified isoflurane in rats.

Although direct IV injection of liquid volatile anesthetics is usually lethal, anesthesia using emulsified halothane and isoflurane without adverse effects has been safely induced in animals. We identified the safe concentration of emulsified volatile anesthetic preparations and determined the dose-response relationship of IV emulsified isoflurane and propofol in rats. Liquid/gas partition coefficients of desflurane, sevoflurane, isoflurane, enflurane, and halothane in 20% and 30% Intralipid were measured and used to calculate their saturated concentrations. Unsaturated emulsified isoflurane was prepared by adding liquid isoflurane to 30% Intralipid. The loss of forepaw righting reflex was taken as induction of anesthesia, and disappearance of electrocardiogram was taken as death. The median effective induction dose (ED50) and median lethal dose (LD50) of emulsified isoflurane were 0.072 and 0.216 mL/kg liquid isoflurane, respectively. The ED50 and LD50 of propofol were 5.89 mg/kg and 18.19 mg/kg, respectively. Time to return of forepaw righting reflex after injection of emulsified isoflurane (38 +/- 18 s) was significantly shorter than with propofol (101 +/- 62 s; P < 0.05). Anesthesia was successfully induced in rats by IV emulsified isoflurane with a comparable safety index and certain safety factor as propofol. Recovery of anesthesia after IV emulsified isoflurane was faster than with propofol.

[Acute isolation and identification of cerebral neurons from the late third instar larvae of Drosophila melanogaster].

OBJECTIVES: To develop a new method for acute isolation of the cerebral neurons from late third instar larvae of Drosophila melanogaster. METHODS: The dissociated cells were characterized by morphological observation and whole-cell voltage-clamp recording. The brains were dissected from late third instar larvae, torn into small fragments, and then were digested in the calcium-magnesium-free PBS solution endowed with collagenase for 45-60 minutes. Single cell was obtained by micro-shaking the digested fragments for 5 to 10 s until the clumps of the tissue were not invisible. Preparation of dispersed cells was incubated in the culture media of Drosophila for thirty minutes at room temperature (20 +/- 1) degrees C. RESULTS: All neurons studied were categorized into three types according to morphological observation: large (> 8 microm) round type I neuroblast-like cells (7%), small (2-5 microm) type II cells (77%). and intermediate-sized type II cells (16%). Neurogliocytes were not found. The electrophysiological properties of three types of neurons were investigated by whole-cell voltage-clamp recording technique. Five types of outward potassium currents were detected readily. CONCLUSION: Morphological and electrophysiological investigation showed that the method for acute isolation of Drosophila neurons is simple, available and stable.

[The in vitro model of inhalation anesthesia using rodent ventilator].

OBJECTIVE: To set up a method of applying inhalation anesthesia in rodent using rodent ventilator and to study the dynamic procedure of the in vitro model. METHODS: The output port of the anesthesia machine was connected to the input port of the rodent ventilator, which was connected to a syringe simulating the lung. After supply of anesthetic gas, the gas samples from the input port of the ventilator and the syringe in the end-expiratory phase were collected at 10, 20, 30, 40, 50, 60, 90, 120, 180, 300, 600 and 900 seconds respectively and were determined using the gas chromatography(GC). The ratios of the anesthetic concentrations of the syringe to that of the input port were calculated (CE/CI). In elimination phase, the gas samples from the syringe were collected at 0,10, 20, 30, 40, 50, 60, 90, 120, 180, 300, 600 and 900 seconds respectively and were determined by GC. The ratios of the anesthetic concentrations of the gas at 10, 20, 30, 40, 50, 60, 90, 120, 180, 300, 600 and 900 seconds to that at 0 second were calculated(C'E/C0). RESULTS: CE/CI increased in the inhalation phase, there was an inverse relationship between CE/CI and time, the correlation coefficients were 0.90, 0.95 and 0.93 respectively (P < 0.01). The mathematical fitting equations were y = -0.19 + 0.19x(-1), y = -7.75 + 0.99x(-1), and y = -7.21 + 0.97x(-1) respectively. C'E/C0 decreased in the elimination phase,the correlation coefficients were 0.90, 0.94 and 0.95 respectively (P < 0.01). The mathematic fitting eqations were y = 5.65-0.02x(-1), y = 7.82-0.01x(-1),and y = 8.20-0.01x(-1), respectively. CONCLUSION: The in vitro model of rodent inhalation anesthesia using the rodent ventilator was set up. The establishment of this model has provided a basis for studies on inhalation anesthesia in rodents.