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1.
Chinese Journal of Surgery ; (12): 291-296, 2023.
Article in Chinese | WPRIM | ID: wpr-970206

ABSTRACT

Biliary tract cancer is a group of malignancies which originate from biliary epithelium, and adenocarcinoma is the main pathological type. Although surgical resection is the only radical treatment strategy, most biliary tract cancer patients are diagnosed at locally advanced stage or with distant metastasis. Biliary tract cancer is highly resistant to the conventional chemoradiotherapy and the emerging immunotherapy including immune checkpoint inhibitors, owing to the suppressive immune microenvironment. In a whole view, this paper discussed the anti-tumor and tumor-promoting immune responses of the various immune cells and stromal cells in the immune microenvironment of biliary tract cancer, as well as their correlation with prognosis. The understanding of the whole view of immune microenvironment in biliary tract cancer patients could further inform the design of clinical trials of immunotherapy or combination therapy.

2.
China Journal of Chinese Materia Medica ; (24): 2343-2351, 2023.
Article in Chinese | WPRIM | ID: wpr-981310

ABSTRACT

This study explored the molecular mechanism of acteoside against hepatoma 22(H22) tumor in mice through c-Jun N-terminal kinase(JNK) signaling pathway. H22 cells were subcutaneously inoculated in 50 male BALB/c mice, and then the model mice were classified into model group, low-dose, medium-dose, and high-dose acteoside groups, and cisplatin group. The administration lasted 2 weeks for each group(5 consecutive days/week). The general conditions of mice in each group, such as mental status, diet intake, water intake, activity, and fur were observed. The body weight, tumor volume, tumor weight, and tumor-inhibiting rate were compared before and after administration. Morphological changes of liver cancer tissues were observed based on hematoxylin and eosin(HE) staining, and the expression of phosphorylated(p)-JNK, JNK, B-cell lymphoma-2(Bcl-2), Beclin-1, and light chain 3(LC3) in each tissue was detected by immunohistochemistry and Western blot. qRT-PCR was performed to detect the mRNA expression of JNK, Bcl-2, Beclin-1, and LC3. The general conditions of mice in model and low-dose acteoside groups were poor, while the general conditions of mice in the remaining three groups were improved. The body weight of mice in medium-dose acteoside group, high-dose acteoside group, and cisplatin group was smaller than that in model group(P<0.01). The tumor volume in model group was insignificantly different from that in low-dose acteoside group, and the volume in cisplatin group showed no significant difference from that in high-dose acteoside group. Tumor volume and weight in medium-dose and high-dose acteoside groups and cisplatin group were lower than those in the model group(P<0.001). The tumor-inhibiting rates were 10.72%, 40.32%, 53.79%, and 56.44% in the low-dose, medium-dose, and high-dose acteoside groups and cisplatin group, respectively. HE staining showed gradual decrease in the count of hepatoma cells and increasing sign of cell necrosis in the acteoside and cisplatin groups, and the necrosis was particularly obvious in the high-dose acteoside group and cisplatin group. Immunohistochemical results suggested that the expression of Beclin-1, LC3, p-JNK, and JNK was up-regulated in acteoside and cisplatin groups(P<0.05). The results of immunohistochemistry, Western blot, and qRT-PCR indicated that the expression of Bcl-2 was down-regulated in the medium-dose and high-dose acteoside groups and cisplatin group(P<0.01). Western blot showed that the expression of Beclin-1, LC3, and p-JNK was up-regulated in acteoside and cisplatin groups(P<0.01), and there was no difference in the expression of JNK among groups. qRT-PCR results showed that the levels of Beclin-1 and LC3 mRNA were up-regulated in the acteoside and cisplatin groups(P<0.05), and the level of JNK mRNA was up-regulated in medium-dose and high-dose acteoside groups and cisplatin group(P<0.001). Acteoside promotes apoptosis and autophagy of H22 cells in mice hepatoma cells by up-regulating the JNK signaling pathway, thus inhibiting tumor growth.


Subject(s)
Male , Animals , Mice , Cisplatin/pharmacology , Carcinoma, Hepatocellular/genetics , MAP Kinase Signaling System , Beclin-1 , Apoptosis , Liver Neoplasms/genetics , Necrosis , Proto-Oncogene Proteins c-bcl-2/metabolism , Cell Line, Tumor , RNA, Messenger/metabolism , Autophagy
3.
Journal of Southern Medical University ; (12): 1150-1153, 2011.
Article in Chinese | WPRIM | ID: wpr-235175

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effects of simvastatin on the expression of nuclear factor-κB (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) in the lung tissue of rats with lung injury induced by ischemia-reperfusion (IR) of the hind limbs.</p><p><b>METHODS</b>Forty-eight male adult SD rats were randomized into 6 equal groups, including a sham-operated group, an IR group, 3 IR+simvastatin groups with intragastric administration of 1, 5, or 10 mg·kg(-1)·d(-1) for 3 days, and a simvastatin control group treated with 10 mg·kg(-1)·d(-1) simvastatin. IR of the hind limbs was induced in the 4 IR groups by occlusion of bilateral femoral arteries for 2 h followed by a 3-h reperfusion. The rats were sacrificed at the end of reperfusion and the arterial blood was taken for blood gas analysis. The lungs were immediately removed for pathological examination and determination of the lung Wet/dry weight ratio (W/D), myeloperoxidase (MPO) activity and polymorphonuclear neutrophil (PMN) counting. The expression of NF-κB p65 mRNA and ICAM-1 protein in the lungs was detected using RT-PCR and Western blotting.</p><p><b>RESULTS</b>Alveolar edema, localized pulmonary atelectasis and large amount of PMN infiltration were found in IR group, and these changes were ameliorated in the 3 simvastatin groups (S(1), S(5), S(10)). Lung W/D, MPO activity and PMN counting were significantly increased in IR group as compared with the sham-operated group (P<0.01). Lung W/D, MPO activity and PMN counting were significantly lowered in the 3 simvastatin groups as compared with IR group (P<0.01). IR-induced decrease in PaO(2) was significantly increased in the 3 simvastatin groups (P<0.01), which also showed significantly lowered expressions of NF-κB p65mRNA and ICAM-1 protein in a dose-dependent manner (P<0.01).</p><p><b>CONCLUSION</b>Simvastatin attenuates lung injury induced by IR of the hind limbs in rats by suppressing the activation of NF-κB and subsequent accumulation of neutrophils mediated by ICAM-1.</p>


Subject(s)
Animals , Male , Rats , Hindlimb , Intercellular Adhesion Molecule-1 , Genetics , Metabolism , Ischemia , Lung , Metabolism , Lung Injury , Metabolism , NF-kappa B , Genetics , Metabolism , RNA, Messenger , Genetics , Metabolism , Rats, Sprague-Dawley , Reperfusion Injury , Simvastatin , Pharmacology , Transcription Factor RelA , Genetics , Metabolism
4.
Chinese Journal of Applied Physiology ; (6): 166-169, 2008.
Article in Chinese | WPRIM | ID: wpr-310775

ABSTRACT

<p><b>AIM</b>To investigate a possible role for the transcription factor nuclear factor kappa-B (NF-kappaB) in preconditioning of the heart to ischemia by remote, early protection.</p><p><b>METHODS</b>48 Wistar rats were randomly divided into three experimental groups. In group I/R, the rats underwent 30 min occlusion of the left anterior descending coronary artery, and 120 min reperfusion. In group PL, the rats underwent four cycles of 5 min occlusion and reperfusion of both hind limbs using a tourniquet before the experiment was continued as in Group I/R. In Group P(L-D), we administered NF-kappaB specific inhibitor, ProDTC 125 mg/kg peritoneally, 15 min before IPG. Infarct size as a percentage of the area at risk was determined by triphenyltetrazolium chloride staining. And another 8 rats in each group were killed and myocardium were stored in liquid nitrogen for the measurement of NF-kappaB mRNA.</p><p><b>RESULTS</b>The myocardial infarct size (IS) was decreased significantly in Group PL compared with group I/R, and the IS/AAR was 34.5% +/- 7.6% and 58.5% +/- 8.5%, respectively ( P < 0.05). The IS/AAR was 54.4% +/- 8.9% in group P(L-D), and there was no significant difference compared with group I/R (P > 0.05). The NF-kappaBmRNA was weaker in P(L) group than that in I/R Group,but is stronger than that in P(L-D) group (P < 0.05). There was almost no expression of NF-kappaB mRNA in P(L-D) group.</p><p><b>CONCLUSION</b>Noninvasive limb IPC is effective in protecting the myocardium from ischemia reperfusion injury. NF-kappaB plays an important role in the mechanism of this acute remote preconditioning.</p>


Subject(s)
Animals , Male , Rats , Extremities , Ischemic Preconditioning, Myocardial , Methods , Myocardial Infarction , Pathology , Myocardium , Metabolism , NF-kappa B , Metabolism , Rats, Wistar
5.
Chinese Journal of Epidemiology ; (12): 188-190, 2008.
Article in Chinese | WPRIM | ID: wpr-287842

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the risk factors in postoperative cognitive dysfunction (POCD) induced by patient self-controlled intravenous analgesia (PCIA).</p><p><b>METHODS</b>A case-control study included 103 patients with POCD(P group), assessed by Mini-Mental-State test and 103 cognitive normal controls (NP group). The cases and controls were matched for age, gender,history of operation and PCIA volume dose. The relationship between POCD and various factors was analyzed by univariate and multivariate analysis. Spss 11.5 of statistical software was used for data analysis.</p><p><b>RESULTS</b>Data from univariate analysis showed that the history of cerebral trauma, education level and VAS score had significant differences between P group and NP group. Multivariate analysis conformed that the history of cerebral trauma, VAS score and education level were significantly related to POCD induced by PCIA and their ORs (95% CI) were 4.261 (1.344-13.508), 2.364 (1.209-4.624), 0.312 (0.170-0.573) respectively.</p><p><b>CONCLUSION</b>Patient's history of cerebral trauma and low VAS score were independent risk factors of POCD induced by PCIA and high education level seemed to be a protective factor.</p>


Subject(s)
Aged , Female , Humans , Male , Middle Aged , Analgesia, Patient-Controlled , Case-Control Studies , Cognition Disorders , Postoperative Complications , Risk Factors
6.
Acta Physiologica Sinica ; (6): 13-18, 2007.
Article in Chinese | WPRIM | ID: wpr-258694

ABSTRACT

Opening of mitochondrial permeability transition (MPT) pores leads to mitochondrial injury during oxidative stress. The peripheral benzodiazepine receptor (PBR) located at mitochondrial outer-membrane has been shown to be involved in several mitochondrial functions. In the present study, we used Ro5-4864, a PBR agonist, to test if activation of PBR could prevent MPT pore opening during Ca(2+) overloading. Cardiac mitochondria isolated from Sprague-Dawley rats were treated by 150 mmol/L Ca(2+) to induce MPT. Ro5-4864 (50, 100 and 200 micromol/L) was added into incubation buffer before adding 150 micromol/L Ca(2+). In additional group, atractyloside (ATR, 20 micromol/L), an opener of MPT pores was added 5 min before the addition of 100 micromol/L Ro5-4864. The change of absorbance at 520 nm was monitored with a spectrophotometer at 30 degrees C for 10 min. Western blot was used to detect cytochrome C loss. The mitochondrial membrane potential was monitored with the fluorescence dye JC-1. Ro5-4864 inhibited the decrease of absorbance at 520 nm compared to that in the untreated Ca(2+) group (P<0.01, P<0.05). In the presence of ATR, Ro5-4864 was not able to prevent MPT anymore. Opening of MPT pores by Ca(2+) decreased the content of cytochrome C in mitochondria, but increased cytochrome C content in cytosol. Ro5-4864 preserved cytochrome C content in mitochondria and led to less cytochrome C release to cytosol. ATR treatment reversed the protective effect of Ro5-4864 on cytochrome C content. Opening of MPT pores led to mitochondrial depolarization, whereas Ro5-4864 treatment maintained mitochondrial membrane potential. Thus, prevention of MPT by activation of PBR during calcium overloading maintains mitochondrial cytochrome C content and membrane potential. Activation of PBR during cardiac ischemia and reperfusion may be an alternative way for cardioprotection.


Subject(s)
Animals , Female , Male , Rats , Atractyloside , Pharmacology , Benzodiazepinones , Pharmacology , Carrier Proteins , Metabolism , Physiology , Membrane Potential, Mitochondrial , Physiology , Radiation Effects , Mitochondria, Heart , Physiology , Mitochondrial Membrane Transport Proteins , Physiology , Rats, Sprague-Dawley , Receptors, GABA-A , Metabolism , Physiology
7.
Chinese Journal of Applied Physiology ; (6): 46-50, 2007.
Article in Chinese | WPRIM | ID: wpr-253090

ABSTRACT

<p><b>AIM</b>To explore the effects of intrathecal injection of selective cyclooxygenase-1 (COX-1) inhibitor, SC-560, on mechanical allo dynia and spinal ERK protein expression in rats with postoperative pain.</p><p><b>METHODS</b>Rats were divided into 4 groups: control group, postoperative pain group, SC-560 group and DMSO group. Mechanical withdrawal threshold (MWT), immunohistochemical and Western blotting technique were used to evaluate mechanical hypersensitivity and the expression of phospho-ERK in the spinal cord, respectively.</p><p><b>RESULTS</b>(1) Behavior test rats developed allodynia 1 h after operation and SC-560 100 microg administrated intrathecally demonstrated a significant reduction in postoperative hypersensitivity. (2) Immunohistochemical staining Phospho-ERK positive neurons in the rat superficial spinal dorsal horn increased significantly 1 h after incision compared with that of non-incision group. Intrathecal administration of SC-560 preoperatively could significantly reduce the number of phospho-ERK positive neurons. (3) Western blot expression of phospho-ERK1/2 protein in the lumbar spinal cord increased significantly 1 h after incision and decreased by intrathecal injection of SC-560.</p><p><b>CONCLUSION</b>SC-560 administrated intrathecally can inhibit mechanical hypersensitivity induced by postoperative pain in rats and this anti-allodynic process may mediated by spinal ERK.</p>


Subject(s)
Animals , Male , Rats , Cyclooxygenase Inhibitors , Pharmacology , Extracellular Signal-Regulated MAP Kinases , Metabolism , Pain Measurement , Pain, Postoperative , Metabolism , Pyrazoles , Pharmacology , Rats, Wistar , Spinal Cord , Metabolism
8.
Acta Physiologica Sinica ; (6): 161-168, 2005.
Article in Chinese | WPRIM | ID: wpr-334191

ABSTRACT

Our previous studies showed that spinal neurons sensitization was involved in morphine withdrawal response. This study was to investigate the roles of spinal protein kinase C (PKC) alpha, gamma in morphine dependence and naloxone-precipitated withdrawal response. To set up morphine dependence model, rats were subcutaneously injected with morphine (twice a day, for 5 d). The dose of morphine was 10 mg/kg in the first day and was increased by 10 mg/kg each day. On day 6, 4 h after the injection of morphine (50 mg/kg), morphine withdrawal syndrome was precipitated by an injection of naloxone (4 mg/kg, i.p.). Chelerythrine chloride (CHE), a PKC inhibitor, was intrathecally injected 30 min before the administration of naloxone. The scores of morphine withdrawal symptom and morphine withdrawal-induced allodynia were observed. One hour after naloxone-precipitated withdrawal, Fos protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of cytosol and membrane fraction of PKC alpha and gamma in the rat spinal cord. The results showed that intrathecal administration of CHE decreased the scores of morphine withdrawal, attenuated morphine withdrawal-induced allodynia and also inhibited the increase of Fos protein expression in the spinal cord of morphine withdrawal rats. The expression of cytosol and membrane fraction of PKC alpha was significantly increased in the spinal cord of rats with morphine dependence. Naloxone-precipitated withdrawal induced PKC alpha translocation from cytosol to membrane fraction, which was prevented by intrathecal administration of CHE. During morphine dependence, but not naloxone-precipitated withdrawal, PKC gamma in the spinal cord translocated from cytosol to membrane fraction, and intrathecal administration of CHE did not change the expression of PKC gamma in the spinal cord of naloxone-precipitated withdrawal rats. It is suggested that up-regulation and translocation of PKC in the spinal cord contribute to morphine dependence and naloxone-precipitated withdrawal in rats and that PKC alpha and gamma play different roles in the above-mentioned effect.


Subject(s)
Animals , Male , Rats , Morphine Dependence , Naloxone , Pharmacology , Protein Kinase C , Metabolism , Physiology , Protein Kinase C-alpha , Metabolism , Physiology , Random Allocation , Rats, Sprague-Dawley , Spinal Cord , Metabolism , Substance Withdrawal Syndrome
9.
Acta Physiologica Sinica ; (6): 233-239, 2005.
Article in English | WPRIM | ID: wpr-334181

ABSTRACT

The present study was undertaken to explore the role of gamma-aminobutyric acid transporters in the neuropathic pain. On the chronic constriction injury (CCI) rats 4 doses (5, 10, 20, 40 microg in group N5, N10, N20, N40, respectively) of specific gamma-aminobutyric acid transporter-1 inhibitor NO-711 or normal saline (in group NS) were intrathecally administered before sciatic nerve ligation (pre-treatment) or at the third day after ligation (post-treatment). The paw withdrawl latency (PWL) from a noxious thermal stimulus and paw withdrawl mechanical threshold (PWMT) of von Frey filament was used as measure of thermal hyperalgesia and tactile allodynia respectively. The results demonstrated that post-treatment of NO-711 significantly suppressed thermal hyperalgesia and allodynia in CCI rats (P<0.05, P<0.01), the inhibitory effect lasted for 2 h (N40 group) and 4 h (N20 group) respectively. NO-711 inhibited thermal hyperalgesia induced by CCI in a dose-dependent manner. Intrathecal pretreatment with different doses of NO-711 delayed the occurrence of thermal hyperalgesia, but could not delay the emergence of allodynia induced by CCI. This study indicates that gamma-aminobutyric acid transporter inhibitor has anti-thermal hyperalgesia and anti-tactile allodynia effects in neuropathic rats.


Subject(s)
Animals , Male , Rats , GABA Antagonists , Pharmacology , Hyperalgesia , Drug Therapy , Injections, Spinal , Neurotransmitter Uptake Inhibitors , Pharmacokinetics , Nipecotic Acids , Pharmacology , Oximes , Pharmacology , Pain , Rats, Sprague-Dawley , Sciatic Neuropathy , Drug Therapy
10.
Chinese Journal of Surgery ; (12): 998-1001, 2005.
Article in Chinese | WPRIM | ID: wpr-306149

ABSTRACT

<p><b>OBJECTIVE</b>To explore the feasibility of transferring fusion gene of dihydrofolate reductase (DHFR) gene and cytidine deaminase (CD) gene into mouse bone marrow cells in order to observe the drug resistance of high dose methotrexate (MTX) and cytosine arabinoside (Ara-C) in the bone marrow cells and to improve the tolerance of myelosuppression following combination chemotherapy.</p><p><b>METHODS</b>Human double-mutant dihydrofolate reductase-cytidine deaminase fusion gene was transferred into two mice bone marrow cells by retroviral vector. Resistant colony-forming unit granulocyte-macrophage (CFU-GM) assays were performed in mouse bone marrow cells by retroviral infection and after treatment by drugs (Ara-C, MTX, and Ara-C + MTX). DNA was extracted from mouse bone marrow cells. The expression of drug resistant genes in mouse bone marrow cells after transferring by retroviral vector was checked by polymerase chain reaction (PCR).</p><p><b>RESULTS</b>Bone marrow cells after coculture with the retroviral producer cells transduced with the genes (SFG-F/S-CD) showed the drug resistance colonies yield (Colony formation after exposure to Ara-C, MTX and Ara-C + MTX were 56%, 22% and 14%, respectively) and the increase in drug resistant to both MTX and Ara-C (P < 0.005). Expression of DHFR and CD gene in extracted DNA of transfected mice were demonstrated by PCR.</p><p><b>CONCLUSIONS</b>Double drug resistant gene can not only integrate and co-express in mice bone marrow cells but also increase the drug resistance to MTX and Ara-C.</p>


Subject(s)
Animals , Humans , Male , Mice , Antimetabolites, Antineoplastic , Pharmacology , Artificial Gene Fusion , Bone Marrow Cells , Cell Biology , Cells, Cultured , Cytarabine , Pharmacology , Cytidine Deaminase , Genetics , Drug Resistance, Multiple , Genetics , Drug Resistance, Neoplasm , Genetics , Genetic Vectors , Methotrexate , Pharmacology , Mice, Inbred BALB C , Tetrahydrofolate Dehydrogenase , Genetics , Transfection
11.
Chinese Medical Journal ; (24): 1723-1727, 2005.
Article in English | WPRIM | ID: wpr-320706

ABSTRACT

<p><b>BACKGROUND</b>This study aimed at assessing the effect of noninvasive limb preconditioning on myocardial infarct size, and determining whether nitric oxide and neurogenic pathway play an important role in the mechanism of acute remote ischemic preconditioning (IPC).</p><p><b>METHODS</b>Forty Wistar rats were randomly divided into four experimental groups. In Group I, the rats underwent 30-minute occlusion of the left anterior descending coronary artery, and 120-minute reperfusion. In Group PL, the rats underwent four cycles of 5-minute occlusion and reperfusion of both hind limbs using a tourniquet before the experiment was continued as in Group I. In Group PL-N and Group PL-H, we administered L-nitro-arginine methyl ester (L-NAME) 10 mg/kg or hexamethonium chloride 20 mg/kg intravenously, 10 minutes before IPC. Infarct size as a percentage of the area at risk was determined by triphenyltetrazolium chloride staining.</p><p><b>RESULTS</b>There were no statistically significant differences in mean arterial pressure and heart rate among these groups at any time point during the experiment (P>0.05). The myocardial infarct size (IS) was decreased significantly in Group PL and Group PL-H compared with Group I, and the IS/AAR was 34.5%+/-7.6%, 35.9%+/-8.6% and 58.5%+/-8.5%, respectively (P< 0.05). The IS/AAR was 49.1%+/- 6.5% in Group PL-N, and there was no significant difference compared with Group I (P>0.05).</p><p><b>CONCLUSIONS</b>Noninvasive limb IPC is effective in protecting the myocardium from ischemia reperfusion injury. Nitric oxide plays an important role in the mechanism of acute remote IPC, in which the neurogenic pathway is not involved.</p>


Subject(s)
Animals , Rats , Blood Pressure , Extremities , Heart Rate , Ischemic Preconditioning, Myocardial , Myocardial Infarction , Myocardial Reperfusion Injury , Rats, Wistar
12.
Chinese Journal of Surgery ; (12): 1014-1017, 2004.
Article in Chinese | WPRIM | ID: wpr-360965

ABSTRACT

<p><b>OBJECTIVE</b>To observe the effect of sevoflurane on membrane permeability of alveolar capillaries in rats with acute lung injury and the ratio of inflammatory cells in bronchoalveolar lavage fluid in rats with acute endotoxin lung injury.</p><p><b>METHODS</b>48 Wistar rats were selected and divided into group C, L, S1L and S2L after injection evans blue 50 mg/kg in random with 12 rats in each group. Group C was taken as control group, 1.2 ml normal saline was injected into the rats via femoral vein and then the rats were mechanically ventilated for 4 hours; The rats in group L were also mechanically ventilated for 4 hours after injection of endotoxin 5 mg/kg via the same vein. For the rats in group S1L and S2L, 1.0 or 1.5 minimal alveolar concentration (MAC) sevoflurane was inhaled with mechanical ventilation after injection of endotoxin 5 mg/kg. Evans blue was not injected into 6 rats of each group in order that the 6 rats could be used for pathological examination and alveoli lavage, lung pathomorphological score of the lung, lung wet/dry weight ratio, the content of lung water, lung permeability index, content of evans blue, total amount and ratio of inflammatory cells in bronchoalveolar lavage fluid (BALF) were all determined.</p><p><b>RESULTS</b>Sevoflurane of 1.0 MAC and 1.5 MAC made lung wet/dry weight ratio and content of lung water change insignificantly; lung permeability index, content of evans blue and pathomorphological score in group S1L decreased from 4.86 +/- 0.82, 112.21 +/- 11.44 ng/mg, 9.17 +/- 0.90 to 3.98 +/- 0.50, 92.85 +/- 11.80 ng/mg, 7.50 +/- 0.96; group S2L decreased to 3.91 +/- 0.34, 96.33 +/- 8.79 ng/mg, 7.67 +/- 0.75. Sevoflurane of 1.0 MAC and 1.5 MAC did not have a significantly effect on total amount and ratio of inflammatory cells in BALF.</p><p><b>CONCLUSION</b>Membrane permeability of alveolar capillaries after acute endotoxin lung injury decreased by inhalation of sevoflurane of 1.0 MAC and 1.5 MAC and pathological injury of lung tissue relieved.</p>


Subject(s)
Animals , Female , Male , Rats , Blood-Air Barrier , Physiology , Bronchoalveolar Lavage Fluid , Cell Biology , Capillary Permeability , Physiology , Endotoxins , Toxicity , Methyl Ethers , Pharmacology , Rats, Wistar , Respiratory Distress Syndrome , Pathology
13.
Chinese Journal of Surgery ; (12): 856-860, 2003.
Article in Chinese | WPRIM | ID: wpr-311190

ABSTRACT

<p><b>OBJECTIVE</b>To observe the effects and mechanisms of endotoxin pretreatment on the rat lung in endotoxemia.</p><p><b>METHODS</b>Eighty-four male Wistar rats were divided into seven groups (each group containing 12 rats): saline control and lipopolysaccharide (LPS)-treated 2 h, 4 h, 6 h groups and LPS-pretreated 2 h, 4 h, 6 h groups. LPS-pretreated rats were administrated with intraperitoneal injection of 0.25 mg/kg LPS. After 24 hours, they were injected with 0.5 mg/kg of LPS. Saline control and LPS-treated rats received an equivalent amount of saline. After 72 hours, LPS-treated and LPS-pretreated rats were intravenously injected with 10 mg/kg of LPS. An equivalent amount of saline was injected in the control rats. Blood was drawn from the carotid artery in LPS-treated and LPS-pretreated rats and sacrificed after intravenous injection of LPS 2, 4, 6 hours. Following saline injection of control rats, blood was drawn from the carotid artery after 6 hours. Arterial blood was drawn for blood gas analysis. The lungs were removed for detecting the mRNA levels of intercellular adhesion molecule-1 (ICAM-1) by reverse transcription polymerase chain reaction and the protein levels of inhibitor kappa B-alpha (I kappa B-alpha) by immunohistochemical staining. Bronchoalveolar lavage was performed in the right lung. Cell counts were evaluated with a light microscopy. The supernatant of bronchoalveolar lavage fluid (BALF) was assayed for the level of protein. The whole lung was weighed and the value was used to determine the lung-body index. The tissue was homogenized and centrifuged for the determination of myeloperoxidase enzyme (MPO) activity.</p><p><b>RESULTS</b>The rats exposed to LPS alone demonstrated an increase in lung-body index, protein in BALF, and MPO activity in the lung tissue. In contrast, the rats exposed to LPS pretreatment exhibited a significant decrease in lung-body index, protein in BALF, and MPO activity. There was a significant decrease in the level of arterial bicarbonate in the LPS-treated rats in comparison with saline-treated and LPS-pretreated animals at 2 hours to 6 hours after LPS administration. The decrease of arterial bicarbonate was compensated by alveolar hyperventilation in LPS-treated animals, with a significant decrease in partial pressure of carbon dioxide. At the same time, partial pressure of oxygen decreased significantly compared with saline control animals and LPS-pretreated animals. LPS-treated rats showed a significant gradually increase in ICAM-1mRNA in the lung in comparison with the saline group. In contrast, ICAM-1mRNA levels in rats pretreated with LPS was lower than that in LPS-treated rats. In LPS-treated animals, LPS caused a decrease of I kappa B-alpha protein expression at 2 hours, returned to control level at 4 hours, and remained at 6 hours. There was no decrease of I kappa B-alpha protein expression in LPS-pretreated animals.</p><p><b>CONCLUSION</b>The results in this study showed that administration of a small dose of LPS 72 hours before endotoxemia caused a attenuation effect on lung injury, which may be correlated to I kappa B-alpha expression induced by LPS pretreatment.</p>


Subject(s)
Animals , Male , Rats , Carbon Dioxide , Blood , Endotoxemia , Metabolism , I-kappa B Proteins , Metabolism , Immunohistochemistry , Intercellular Adhesion Molecule-1 , Genetics , Lipopolysaccharides , Pharmacology , Lung , Metabolism , Pathology , NF-KappaB Inhibitor alpha , Oxygen , Blood , Peroxidase , Metabolism , RNA, Messenger , Rats, Wistar
14.
Acta Physiologica Sinica ; (6): 38-42, 2002.
Article in English | WPRIM | ID: wpr-272987

ABSTRACT

The present study investigates the vasodilative action of carbon monoxide on rat pulmonary artery in vitro. After isolation of the pulmonary artery rings (PAR) from Wistar rats, an ACh concentration-response curve was generated; the PARs were incubated with the NOS inhibitor L-NAME (30 micromol/L, n=10) or the heme oxygenase inhibitor ZnPPIX (10 micromol/L)+L-NAME (30 micromol/L, n=10) for 30 min. After that, a second ACh concentration-response curve was elicited. Other isolated PARs were randomly divided into two groups: endothelium-intact group (n=8) and endothelium-denuded group (n=8). The effect of exogenous carbon monoxide (CO) on pulmonary arterial vessel tone was observed. The results showed that ACh induced a concentration-dependent pulmonary vasorelaxation. This relaxation disappeared after endothelium was denuded. The ACh induced relaxation was attenuated after pretreatment with 30 micromol/L L-NAME, and attenuated further after pretreatment with 10 micromol/L ZnPPIX+30 micromol/L L-NAME. Exogenous carbon monoxide relaxed pulmonary artery in both the endothelium-intact group and the endothelium-denuded group. These data suggest that ZnPPIX inhibits ACh induced endothelium-dependent pulmonary artery relaxation and that CO is an endothelium-derived relaxation factor, and exogenous CO can relax pulmonary artery.


Subject(s)
Animals , Rats , Acetylcholine , Pharmacology , Carbon Monoxide , Pharmacology , Dose-Response Relationship, Drug , Endothelium, Vascular , Heme Oxygenase (Decyclizing) , In Vitro Techniques , NG-Nitroarginine Methyl Ester , Pharmacology , Nitric Oxide Synthase , Protoporphyrins , Pharmacology , Pulmonary Artery , Rats, Wistar , Vasodilation
15.
Chinese Journal of Anesthesiology ; (12)1997.
Article in Chinese | WPRIM | ID: wpr-673780

ABSTRACT

Objective Hypoxic-ischemic brain damage (HIBD) is a life-threatening neonatal disease during perinatal stage. Since excitatory amino acids (EAAs) and their receptors are involved in the pathogenesis. Sodium hydroxybutyrate ( r-OH ), an intermediate metabolite of GABA, may have beneficial effects on HIBD. Methods One-hundred seven-day (7d) SD rat pups were randomly assigned to one of three groups:(Ⅰ) control group (n= 20);(Ⅱ) sham operation group (n=20)and (Ⅲ) r-OH group which was further divided into 3 subgroups according to the dose of r-OH 50 mg?kg-1 (r-OH1) (n=20),100 mg?kg-1 (r-OH2) (n=20),200mg?kg-1 (r-OH3) ( n=20).Animals in control group and r-OH group were subjected to left carotid artery ligation followed by 2 h of hypoxia (O2 :N2=8%:92%).Normal saline ( NS) was administered ip immediately after sham operation or hypoxia,then 3 times a day for 7 days in group Ⅰ and Ⅱ.In r-OH group r-OH was administered ip instead of NS. Brain damage was evaluated by survival rate, pathology, the ratio of weight of left to right hemisphere on the 28 th day after ischemia-hypoxia and the capacity of learning and memory using Y-Maze test. Results (1) The survival rate on the 28 th day after hypoxia or sham operation was significant lower in control group (60%) than that in the other groups (85%-95% ) (P

16.
Chinese Journal of Anesthesiology ; (12)1994.
Article in Chinese | WPRIM | ID: wpr-674214

ABSTRACT

Objective To investigate the development of absorption atelectasis in healthy adult volunteers breathing 100% oxygen.Methods Six healthy volunteers aged 31-36 yrs weighing 60-80 kg were recruited into this study.Chest computed tomograph(CT)of the layer of interventricular septum was performed at the end of normal expiration(FRC)at 6 time points:(1)the baseline(T_1);(2)after 5 min maximal expiration(close to residual volume)(T_2);(3)immediately after 10 maximal inspiration and expiration(T_3);(4)after breathing 100% O_2 through face mask at tidal volume for 30 min(T_4);(5)after breathing 100% O_2 at maximal expiration for 5 min(T_5)and(6)breathing room air deeply 10 times(T_6).The area of atelectasis and poorly ventilated lung were expressed as percentage of the total lungs.Results There was no atelectasis or poorly ventilated lung at T_1. At T_2 the poorly ventilated lung accounted for 22.9%?5.0%,but there was no atelectasis.There was no atelectasis and poorly ventilated lung at T_3 and T_4.At T_5 atelectasis accounted for 4.5%?1.1% which was reduced to 0.9%?0.4% at T_6.Conclusion Breathing 100% oxygen at reduced lung volume can result in atelectasis.

17.
Chinese Journal of Anesthesiology ; (12)1994.
Article in Chinese | WPRIM | ID: wpr-674144

ABSTRACT

Objective To investigate the effect of intrathecal(IT)mibefradil on the mechanical and thermal hyperalgesia following chronic compression of dorsal mot ganglion(CCD)in rats,trying to elucidate the role of T-type calcium channels in the nociceptive signal transmission at spinal level.Methods Forty-eight male SD rats weighing 230-250 g were randomly divided into 6 groups(n=8 each):group Ⅰ sham operation;group Ⅱ CCD;group Ⅲ CCD+normal saline(N.S.)and group Ⅳ,Ⅴ,Ⅵ CCD+mibefradil 50 ?g(Ⅳ),100 ?g (Ⅴ),200 ?g(Ⅵ).The animals were anesthetized with intraperitoneal(IP)1% pentobarbital 40 mg?kg~(-1). Intrathecal catheter was placed according to the technique described by Yaksh et al.Five days after IT catheter placement L_4 and I_5 dorsal root ganglion(DRG)compression(CCD)was performed in group Ⅱ-Ⅵ.In sham operation group(Ⅰ)only L_(4-5) transverse processes and intervertebral foramina were exposed but DRGs were not compressed.In group Ⅳ,Ⅴ,and Ⅵ 5 days after CCD model was established a bolus of mibefradil 50,100 and 200 ?g in 10 ?l NS was given IT.In group Ⅲ NS 10 ?l was given IT instead of mibefradil.Mechanical withdrawal threshold(MWT)using Von Frey filament and thermal withdrawal latency(TWL)using radiant heat applied to the plantar surface were measured before CCD(baseline)and 1,3,5,7,14 and 21 days after CCD in group Ⅰ and Ⅱ and before and 30,60,120,240 and 480 min after IT mibefradil in group Ⅲ-Ⅵ.Results The animals in group Ⅱ(CCD group)developed mechanical and thermal hyperalgesia from the 1st day after operation to the end of the experiment.IT mibefradil 50,100 and 200 ?g can all attenuate both mechanical and thermal hyperalgesia induced by CCD.Conclusion Spinal T-type calcium channel may play an important role in the pathogenesis of neuropathic pain.

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