RESUMEN

Reactive oxygen species (ROS) in the paraventricular nucleus (PVN) play a pivotal role in the pathogenesis of hypertension. Nuclear factor E2-related factor-2 (Nrf2) is an important transcription factor that modulates cell antioxidant defense response against oxidative stress. The present study aimed to explore the efficacy of PVN administration of tert-butylhydroquinone (tBHQ), a selective Nrf2 activator, in hypertensive rats. 16-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were used in this study. These rats were chronic bilateral PVN infusion of tBHQ (0.8µg/day), or oxygen free radical scavenger tempol (20µg/h), or vehicle for 2weeks. SHR rats had higher mean arterial pressure (MAP), plasma norepinephrine (NE) levels, and sympathetic nerve activity (RSNA) and lower PVN levels of Nrf2, hemeoxygenase-1 (HO-1), superoxide dismutase-1 (SOD1) and catalase (CAT) as compared with those in the WKY group. Bilateral PVN infusion of tBHQ or tempol significantly reduced MAP, RSNA, plasma NE levels in SHR rats. In addition, tBHQ treatment enhanced the nuclear accumulation of Nrf2 and increased the expression of HO-1, CAT and SOD1 in SHR rats. Furthermore, tBHQ attenuated PVN levels of ROS, the expression of proinflammatory cytokines and restored the imbalance of neurotransmitters in PVN. Knockdown of Nrf2 in the PVN by adeno-associated virus mediated small interfering RNA abrogated the protective effects of tBHQ on hypertension. These findings suggest that PVN administration of tBHQ can attenuate hypertension by activation of the Nrf2-mediated signaling pathway.

Asunto(s)

Antihipertensivos/farmacología , Hidroquinonas/farmacología , Hipertensión/metabolismo , Factor 2 Relacionado con NF-E2/metabolismo , Núcleo Hipotalámico Paraventricular/efectos de los fármacos , Adenoviridae/genética , Animales , Antihipertensivos/uso terapéutico , Presión Arterial/efectos de los fármacos , Hidroquinonas/uso terapéutico , Hipertensión/tratamiento farmacológico , Hipertensión/fisiopatología , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Interleucina-6/genética , Interleucina-6/metabolismo , Masculino , Factor 2 Relacionado con NF-E2/genética , Estrés Oxidativo/efectos de los fármacos , Núcleo Hipotalámico Paraventricular/metabolismo , ARN Interferente Pequeño/genética , Ratas Endogámicas SHR , Ratas Endogámicas WKY , Transducción de Señal/efectos de los fármacos , Sistema Nervioso Simpático/efectos de los fármacos

RESUMEN

PURPOSE: Iatrogenic noise produced by mastoid or craniotomy drills may cause hearing damage, which is induced by the generation of reactive oxygen species (ROS) and the reduction of cochlear blood flow (CoBF). This study investigated whether propofol could reduce noise-induced hearing loss (NIHL) in a guinea pig model. METHODS: Sixty-four male pigmented guinea pigs were randomly and equally divided into 4 groups: control, noise, propofol and propofol+noise. Propofol was infused intravenously for 20min prior to noise exposure with a loading dose of 5mg·kg-1 for 5min and a maintenance infusion of 20mg·kg-1·h-1 for 135min. For noise exposure, an octave band noise at a 124dB sound pressure level (SPL) was administered to animals for 2h. The mean arterial pressure (MAP) and CoBF were monitored continuously. Auditory function was measured by the level of distortion product otoacoustic emission (DPOAE) before and at 1h, 72h and 240h after noise exposure. Cochlear levels of 8-iso-Prostaglandin F2alpha (8-iso-PGF2α) were measured immediately after the termination of noise exposure. Cochlear silver nitrate staining and outer hair cell (OHC) counting were performed after the final functional test. RESULTS: Noise exposure caused decreases in the CoBF and DPOAE amplitudes, over-generation of 8-iso-PGF2α and the loss of OHCs. Pre-treatment with propofol significantly increased the CoBF and DPOAE amplitudes, decreased 8-iso-PGF2α and the loss of OHCs. CONCLUSIONS: Propofol exerted protective effects against NIHL in this animal model by suppressing a lipid peroxidation reaction and improving CoBF.

Asunto(s)

Pérdida Auditiva Provocada por Ruido/tratamiento farmacológico , Fármacos Neuroprotectores/farmacología , Propofol/farmacología , Animales , Presión Sanguínea/efectos de los fármacos , Recuento de Células , Cóclea/irrigación sanguínea , Cóclea/efectos de los fármacos , Cóclea/patología , Dinoprost/análogos & derivados , Dinoprost/metabolismo , Modelos Animales de Enfermedad , Ensayo de Inmunoadsorción Enzimática , Cobayas , Células Ciliadas Auditivas Externas/efectos de los fármacos , Células Ciliadas Auditivas Externas/patología , Pérdida Auditiva Provocada por Ruido/patología , Pérdida Auditiva Provocada por Ruido/fisiopatología , Infusiones Intravenosas , Masculino , Ruido , Distribución Aleatoria , Flujo Sanguíneo Regional/efectos de los fármacos , Nitrato de Plata

RESUMEN

A novel strategy of rapid transport across the blood-brain barrier (BBB) via phosphatidylethanolamine-triggered release is developed through both molecular dynamics (MD) simulation and experiments. Hydrophobic drugs, namely, propofol, iodine, and 1,1'-dioctadecyltetramethyl indotricarbocyanine iodide, were loaded with propionylated amylose helix (HLPAH) nanoclusters to form PLPAH, ILPAH, and DLPAH nanoclusters, respectively. These clusters were subjected to MD simulation, structure measurement, in vitro triggered study, in vivo DLPAH imaging, and analysis of PLPAH sedative effects on rabbits. Results indicated that HLPAH nanoclusters were initially located on the BBB, and the helix was unfolded to release the loaded hydrophobic drugs. The released drugs crossed the BBB and performed their functions in the central nervous system (CNS) through concentration gradient and hydrophobicity. This mechanism of HLPAH across the BBB featured high membrane permeability and specificity, rapid onset, short maintenance, rapid recovery, and lower dosage of drugs. Hence, this novel strategy is very meaningful for the development of CNS drug carriers and the proposed system could be used to improve the therapeutic effects of CNS diseases.

Asunto(s)

Amilosa/química , Barrera Hematoencefálica/metabolismo , Portadores de Fármacos/química , Hipnóticos y Sedantes/administración & dosificación , Nanopartículas/química , Propofol/administración & dosificación , Animales , Barrera Hematoencefálica/efectos de los fármacos , Sistemas de Liberación de Medicamentos , Interacciones Hidrofóbicas e Hidrofílicas , Hipnóticos y Sedantes/farmacocinética , Masculino , Simulación de Dinámica Molecular , Nanopartículas/ultraestructura , Propofol/farmacocinética , Conejos

RESUMEN

Generally accepted, inflammation and neuron apoptosis are two characterized pathological features of cerebral ischemia-reperfusion (IR) injury. Ginsenoside Rg1 was reported showing distinct neuroprotective effect in cerebral IR injury but the underlying mechanisms are still unclear. PPARγ/Heme oxygenase-1 (HO-1) signaling was proved effective in suppressing both apoptosis and inflammation. This study was aimed to investigate whether PPARγ/HO-1 signaling was involved in cerebral IR injury and ginsenoside Rg1's neuroprotective effect in cerebral IR injury. Cerebral IR injury was induced by middle cerebral artery occlusion in rats. The PPARγ agonist rosiglitazone (ROZ) and the HO-1 inhibitor zinc protoporphyrin-IX (ZnPP) and ginsenoside Rg1 at various concentrations were used to treat the modeled rats. Neurological deficits, apoptosis and inflammation in hippocampus were evaluated. Furthermore, HO-1 enzymatic activity, expression levels of apoptosis-related and inflammation-related proteins, concentrations of inflammatory cytokines were also determined. The results showed that PPARγ activation by ROZ significantly attenuated neurological deficits, apoptosis and inflammation in hippocampus in cerebral IR rats. However, the neuroprotective effect of ROZ was then impaired by HO-1 inhibitor ZnPP. This effect was evidenced by changes of expression levels of PPARγ, bcl-2, cleaved caspase-3, cleaved caspase-9, IL-1ß, TNF-α, HMGB1, and RAGE in hippocampus of modeled animals. Ginsenoside Rg1 showed similar effect to ROZ in activating PPARγ/HO-1 in protecting against apoptosis and inflammation but also impaired by ZnPP administration. In conclusion, PPARγ/HO-1 signaling was critical in mediating apoptosis and inflammation, which was also the therapeutic target of ginsenoside Rg1 in cerebral IR injury.

Asunto(s)

Apoptosis/efectos de los fármacos , Ginsenósidos/farmacología , Hipocampo/efectos de los fármacos , Neuronas/efectos de los fármacos , Fármacos Neuroprotectores/farmacología , Daño por Reperfusión/metabolismo , Animales , Western Blotting , Isquemia Encefálica/metabolismo , Isquemia Encefálica/patología , Modelos Animales de Enfermedad , Ensayo de Inmunoadsorción Enzimática , Hemo-Oxigenasa 1/metabolismo , Inflamación/metabolismo , Inflamación/patología , Masculino , Proteínas de la Membrana/metabolismo , PPAR gamma/metabolismo , Ratas , Ratas Sprague-Dawley , Daño por Reperfusión/patología , Transducción de Señal/efectos de los fármacos

RESUMEN

Though starch has been a common material used for drug delivery, it has not been used as an encapsulation material for hemoglobin-based oxygen carriers. In this study, cationic amylose (CA) was synthesized by an etherification reaction. The interaction behaviors between CA and hemoglobin (Hb) were measured by zeta potential, size, and UV-Vis absorption spectra at different pH values. Cationic starch encapsulated Hb by electrostatic adhesion, reverse micelles, and cross-linking, and showed a core shell structure with a size of around 100 nm, when measured immediately after dispersing in PBS solution. However, we found that it was prone to swell, aggregate, and leak Hb with a longer duration of dispersal in PBS.

Asunto(s)

Amilosa/química , Sustitutos Sanguíneos/química , Hemoglobinas/química , Proteínas Inmovilizadas/química , Animales , Bovinos

RESUMEN

OBJECTIVE: To study the protective effect of sufentanil preconditioning against myocardial ischemia-reperfusion (I/R) injury and the role of PI3K/Akt signaling pathway. METHODS: Sixty male SD rats weighing 250-350 g were randomly divided into 5 equal groups, namely the sham-operated group, I/R group, sufentanil preconditioning group (Spc group), sufentanil preconditioning +PI3K inhibitor group (Spc+W group), and PI3K inhibitor group (W group). Myocardial I/R model was established by ligation of the anterior descending branch of the left coronary artery for 30 min followed by reperfusion for 120 min. Sufentanil was administered in 3 doses via the femoral vein before the occlusion, each at 1 µg/kg infused within 5 min at a 5-min interval. In Spc+W and W groups, PI3K inhibitor wortmannin (15 µg/kg) was given intravenously 5 min before sufentanil preconditioning and 35 min before ischemia, respectively. Heart rate and mean arterial pressure (MAP) were continuously monitored during I/R. At the end of reperfusion, blood samples were obtained to determine plasma activation of CK-MB and LDH. Acute infarct size was measured by triphenyltetrazolium chloride staining, and the myocardial tissues were obtained to detect the expression of phosphorylated Akt using Western blotting. RESULTS: Phosphorylated Akt expression was significantly up-regulated in I/R and Spc groups as compared with the sham group, and was significantly higher in Spc group than in I/R group. After reperfusion, sufentanil preconditioning significantly decreased myocardial infarct size (P<0.01) and lowered the levels of CK-MB (P<0.01) and LDH (P<0.01) compared with those in the I/R group. The I/R , Spc+W and W groups showed no significant differences in myocardial infarct size or the levels of CK-MB and LDH. CONCLUSION: The protective effect of sufentanil preconditioning against myocardium against I/R injury in rats may involve PI3K/Akt signaling pathway activation.

Asunto(s)

Precondicionamiento Isquémico Miocárdico/métodos , Daño por Reperfusión Miocárdica/prevención & control , Proteínas Proto-Oncogénicas c-akt/metabolismo , Sufentanilo/farmacología , Animales , Masculino , Daño por Reperfusión Miocárdica/metabolismo , Ratas , Transducción de Señal

RESUMEN

BACKGROUND: To evaluate the potential efficacy of preventive effect of ulinastatin in esophagectomy patients. METHODS: Eighty patients with esophageal cancer were preoperatively allocated at random into two equal groups. Ulinastatin was administered to the treatment group (U) whereas the control group (C) received a placebo. The arterial oxygen tension and carbon dioxide tension were measured and the respiratory index (RI) was calculated. Plasma levels of circulating T lymphocyte subsets and interleukin 6 (IL-6) were measured and clinical courses of patients in the two groups were compared. RESULTS: RI in the U group was significantly lower than that in the C group. The rate of postoperative complications and the duration of ICU stay were significantly lower in the U group. Ulinastatin significantly increased the rate of CD3+ and CD4+ cells, and ratio of CD4+/CD8+, but decreased the rate of CD8+ cells and release of IL-6 compared to the C group on postoperative days 1 and 3. Patients within the C group showed worse recurrence free survival. Multivariate analysis revealed that ulinastatin administration significantly decreased the incidence of recurrence. CONCLUSIONS: Ulinastatin had a preventive effect on postoperative complications and immunosuppression in esophagectomy patients, thereby prolongingrecurrence free survival.

Asunto(s)

Neoplasias Esofágicas/tratamiento farmacológico , Esofagectomía/efectos adversos , Glicoproteínas/uso terapéutico , Recurrencia Local de Neoplasia/tratamiento farmacológico , Complicaciones Posoperatorias/prevención & control , Subgrupos de Linfocitos T/efectos de los fármacos , Adenocarcinoma/tratamiento farmacológico , Adenocarcinoma/mortalidad , Adenocarcinoma/cirugía , Adulto , Anciano , Dióxido de Carbono/metabolismo , Estudios de Casos y Controles , Neoplasias Esofágicas/mortalidad , Neoplasias Esofágicas/cirugía , Esofagectomía/mortalidad , Femenino , Estudios de Seguimiento , Humanos , Tolerancia Inmunológica/efectos de los fármacos , Terapia de Inmunosupresión , Interleucina-6/metabolismo , Masculino , Persona de Mediana Edad , Recurrencia Local de Neoplasia/mortalidad , Recurrencia Local de Neoplasia/cirugía , Estadificación de Neoplasias , Oxígeno/metabolismo , Pronóstico , Mecánica Respiratoria , Tasa de Supervivencia , Inhibidores de Tripsina/uso terapéutico , Adulto Joven

RESUMEN

BACKGROUND: Propofol is one of the most commonly used intravenous anaesthetic agents during cancer resection surgery, but the effect of propofol on gallbladder cancer is not clear. NF-E2-related factor 2 (Nrf2) is abundantly expressed in cancer cells and relates to proliferation, invasion, and chemoresistance. The aims of the current study were to evaluate effects of propofol on the behavior of human GC cells and role of Nrf2 in these effects. METHOD: The effects of propofol on cell proliferation, apoptosis, and invasion were detected by MTT assays, flow cytometry, and transwell assay. Also, activation of Nrf2 was determined by western blot, RT-PCR, and immunofluorescence assays. Nrf2 was knocked-down in GBC-SD cells by shRNA before evaluating the role of Nrf2 in the influence of propofol on biological behaviors. RESULTS: Propofol promoted the proliferation of GBC-SD cells in a dose- and time- dependent manner. After exposure to propofol for 48 h, GBC-SD cells showed decreased apoptosis and increased invasion. Also, propofol over-expressed Nrf2 at both the protein and mRNA levels and induced translocation of Nrf2 into the nucleus. Finally, loss of Nrf2 by shRNA reversed the effect of propofol on cell proliferation, apoptosis, and invasion. CONCLUSION: Propofol induces proliferation and promotes invasion of GC cells through activation of Nrf2.

Asunto(s)

Neoplasias de la Vesícula Biliar , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Factor 2 Relacionado con NF-E2 , Propofol/administración & dosificación , Animales , Apoptosis/efectos de los fármacos , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Neoplasias de la Vesícula Biliar/genética , Neoplasias de la Vesícula Biliar/metabolismo , Técnicas de Silenciamiento del Gen , Humanos , Ratones , Factor 2 Relacionado con NF-E2/genética , Factor 2 Relacionado con NF-E2/metabolismo , Invasividad Neoplásica/prevención & control

RESUMEN

OBJECTIVE: To observe the effect of ischemic postconditioning on phosphatidylinositol-3-OH kinase (PI3K) and extracellular signal-regulated protein kinase 1/2(ERK1/2) in rats after hepatic ischemia reperfusion in rats and investigate the mechanism of ischemic postcoditioning of the liver. METHODS: Three cycles of 1 min-off-1 min-on ischemic postconditioning regime were used in a rat model of 70% hepatic ischemia-reperfusion injury. The changes in the liver function, hepatocyte apoptosis, phosphorylation of Akt and ERK1/2 were assessed in rats treated with sham operation, LY294002+sham operation (LY+S), PD98059+sham operation (PD+S), ischemia reperfusion (IR), ischemic postconditioning (IPO), LY294002+ ischemic postconditioning (LY+IPO), or PD98059+ischemic postconditioning (PD+IPO). RESULTS: Ischemic postconditioning significantly alleviated hepatic ischemia-reperfusion-induced liver function injury and hepatocyte apoptosis and increased phosphorylation of Akt and ERK1/2. LY294002 and PD98059 antagonized the effects of ischemic postconditioning in the liver. CONCLUSION: Activation of PI3K and ERK1/2 may mediate the protective effect of ischemic postconditioning against hepatic ischemia- reperfusion injury in rats.

Asunto(s)

Quinasas MAP Reguladas por Señal Extracelular/metabolismo , Poscondicionamiento Isquémico , Fosfatidilinositol 3-Quinasas/metabolismo , Daño por Reperfusión/metabolismo , Animales , Cromonas/farmacología , Flavonoides/farmacología , Hígado/irrigación sanguínea , Masculino , Morfolinas/farmacología , Inhibidores de las Quinasa Fosfoinosítidos-3 , Ratas , Ratas Sprague-Dawley

RESUMEN

OBJECTIVE: [corrected] To assess the effects of metallothionein on myocyte apoptosis and energy supply of isolated rabbit heart muscle during perfusion with ropivacaine.. METHODS: Sixty New Zealand white male rabbits were randomized into 3 equal groups. In group I, the rabbits received a intreaperitioneal injection of distilled water 24 h before isolation of the heart with perfusion by Langendoff model; in group II, distilled water was injected intreaperitioneally, and 24 h later the heart was isolated and perfused with Langendoff model and ropivacaine; in group III, 3.6% ZnSO(4) was injected intreaperitioneally and the isolated heart was perfused with Langendoff model and ropivacaine. The myocardial metallothionein content, myocyte apoptosis, and myocardial ATP, ADP and AMP content were detected. RESULTS: The myocardial metallothionein content was significantly higher in group III than in the other two groups; the percent of myocyte apoptosis was the highest in group II, and was significantly higher in group III than in group I. The myocardial content of ATP was the highest in group I, and was significantly higher in group III than in group II. CONCLUSION: Metallothionein can significantly inhibit myocyte apoptosis and alleviate energy supply disorder induced by ropivacaine.

Asunto(s)

Amidas/farmacología , Apoptosis/efectos de los fármacos , Metabolismo Energético/efectos de los fármacos , Metalotioneína/farmacología , Miocitos Cardíacos/citología , Animales , Técnicas In Vitro , Masculino , Miocardio/citología , Miocardio/metabolismo , Miocitos Cardíacos/metabolismo , Perfusión , Conejos , Ropivacaína

RESUMEN

The current study was designed to investigate the mechanisms by which ropivacaine may act within the central nervous system (CNS) to produce cardiotoxicity. Eighty New Zealand rabbits were divided into four groups randomly. In Group 1, 20 rabbits received intracerebroventricular (icv) saline, and then received icv ropivacaine 30 min later. In Group 2, 20 rabbits received icv ropivacaine. Whenever dysrhythmias continued for more than 5 min, 0.1 ml saline was administered into the left cerebral ventricle. Ten minutes later, 0.1 ml midazolam was given into the left lateral ventricle. In Group 3, 20 rabbits received icv ropivacaine, and once the dysrhythmias developed, the inspired isoflurane concentration was increased from 0.75% to 1.50%. In Group 4, 20 animals received an intravenous (iv) phenylephrine infusion until dysrhythmias occurred. In Group 1, the rabbits did not develop dysrhythmias in response to icv saline, whereas dysrhythmias did develop in these animals after icv ropivacaine. In Group 2, icv saline had no effect on the dysrhythmias; however, icv midazolam terminated cardiac dysrhythmias. In Group 3, an increase in the concentration of the inspired isoflurane had no effect on dysrhythmias. In Group 4, icv midazolam had no effect on dysrhythmias in response to iv phenylephrine. Ropivacaine administered directly into the CNS is capable of producing cardiac dysrhythmias; midazolam terminated dysrhythmias presumably by potentiation of γ-aminobutyric acid (GABA) receptor activity. Our results suggest that ropivacaine produces some of its cardiotoxicity not only by the direct cardiotoxicity of the drug, but also by the CNS effects of ropivacaine.

Asunto(s)

Amidas/efectos adversos , Arritmias Cardíacas/tratamiento farmacológico , Moduladores del GABA/farmacología , Midazolam/farmacología , Anestésicos Locales/efectos adversos , Animales , Arritmias Cardíacas/inducido químicamente , Arritmias Cardíacas/metabolismo , Presión Sanguínea , Sistema Nervioso Central/efectos de los fármacos , Infusiones Intraventriculares , Masculino , Conejos , Ropivacaína , Factores de Tiempo

RESUMEN

AIM: To detect the effect of low dose propofol on the proliferation, apoptosis, migration, and invasion of esophageal squamous cell carcinoma cell line Eca109. METHODS: The proliferation, apoptosis, migration, and invasion of esophageal squamous cell carcinoma cell line Eca109 were detected by MTT assay, flow cytometry, transwell assay respectively. The effect of low dose propofol on expression of heme oxygenase-1 (HO-1) was confirmed by Real-time quantitative PCR. RESULTS: Low dose propofol could inhibit the proliferation, migration, invasion and promate the apoptosis of esophageal squamous cell carcinoma cell line Eca109. And low dose propofol increased the expression of HO-1 mRNA in a dose-dependment manner. CONCLUSION: Low dose propofol affects the biological behavior of esophageal squamous cell carcinoma cell line Eca109, which has a relationship with increasing the expression of HO-1.

Asunto(s)

Neoplasias Esofágicas/patología , Propofol/farmacología , Apoptosis/efectos de los fármacos , Carcinoma de Células Escamosas , Línea Celular Tumoral , Movimiento Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Hemo-Oxigenasa 1/genética , Humanos , Invasividad Neoplásica

RESUMEN

Postoperative pain is the most common complaint after laparoscopic cholecystectomy. This study was carried out to evaluate whether preoperative administration of intramuscular dezocine can provide postoperative analgesia and reduce postoperative opioid consumption in patients undergoing laparoscopic cholecystectomy. Patients (ASA I or II) scheduled for laparoscopic cholecystectomy were randomly assigned into intramuscular dezocine group (group 1) or intramuscular normal saline group (group 2). Dezocine and equal volume normal saline were administered intramuscularly 10 min before the induction of anesthesia. After operation, the severity of postoperative pain, postoperative fentanyl requirement, incidence and severity of side-effects were assessed. Postoperative pain and postoperative patient-controlled fentanyl consumption were reduced significantly in group 1 compared with group 2. The incidence and severity of side effects were similar between the two groups. Preoperative single-dose administration of intramuscular dezocine 0.1 mg/kg was effective in reducing postoperative pain and postoperative patient-controlled fentanyl requirement in patients undergoing laparoscopic cholecystectomy.

RESUMEN

In order to detect and measure the brain activity variation under different depth of anesthesia (DOA), the Spectral Entropy (SE) of electroencephalogram (EEG) of the SD rat was studied in this paper. The SE of EEG was measured under different DOA and the relationship between SE and the DOA was analyzed. The SE of EEG will decrease quickly while the DOA is from light to deep and vice versa, so it can be used to distinguish light and deep anesthesia, but it can not distinguish awake and light anesthesia accurately. Compared with power spectrum, we can see the change of SE is opposite to that of power spectrum. Besides EEG SE analysis, the SE variations of four rhythms of EEG (delta, theta, alpha and beta) also are analyzed. The study shows SE of delta rhythm dynamic change leads to the change of EEG and the delta rhythm is the dominant rhythm of rat during anesthesia.