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Objective To investigate the effect of desflurane post-processing on the expression of glucose transporter 4 (GIUT4)in myocardial ischemia-reperfusion injury.Methods Twenty-four male New Zealand white rabbits were randomly divided into 4 groups (n =6 each):normal control group (group NC),ischemic-reperfusion group (group IR),ischemic-reperfusion postconditioning group (group IRP),desflurane aftertreatment group (group Des).Myocardial ischemia-reperfusion model was established by ligating the left coronary artery.Plasma glucose,Insulin and myocardial glucose uptake rate were measured at the time point before ischemia (T0),30 min after ischemia (T1),30 min (T2),60 min (T3) and 120 min (T4) after reperfusion,for dynamic comparison;the expression of GLUT4 mRNA in myocardium was detected by quantitative RT-PCR,and GLUT4 protein was detected by Western blot.Results Compared with group NC,the levels of blood glucose at T2-T4 increased in group IR (P＜0.05),but blood glucose in group Des was significantly lower than that in groups IR and IRP at T2-T4 (P＜0.05).Compared with group NC,serum insulin levels in groups IR,IRP and Des were significantly higher at T1-T3 (P＜0.05).The level of serum insulin in groups IRP and Des at T1 and T2 was significantly higher than that in group IR (P＜0.05),while that in group Des was higher than that in group IRP (P＜0.05).Blood glucose uptake rate in group IR at T2-T4 was significantly lower than that in groups NC,IRP and Des (P＜0.05),while the blood glucose uptake rate was higher in group Des than that in group IRP (P＜0.05).compared with group NC,the expression of GLUT4 mRNA and protein in groups IR,IRP and Des decreased (P＜0.05),but compared with groups IR and IRP,GLUT4 mRNA and protein expression increased in group Des (P＜0.05).Conclusion Postconditioning of desflurane can improve myocardial ischemia-reperfusion insulin resistance and increase myocardial glucose uptake,which may be related to the increase of myocardial GLUT4 expression.
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Objective To compare the anesthetic effects of interscalene brachial plexus combined with ulnar nerve and axillary brachial plexus block guided by nerve stimulator. Methods Eighty patients belonging to ASA ⅠorⅡ and undergoing replantation of severed palm or wrist were divided randomly into 2 groups, Each group had 40 patients. Nerve stimulator guided nerve block. Patients in groupⅠreceived interscalene brachial plexus combined with ulnar nerve block, and those in groupⅡreceived axillary brachial plexus block. The onset time, hold time, tourniquet tolerance of radial nerve, median nerve and ulnar nerve of two groups was recorded. The phrenic nerve block, Horner′s syndrome and recurrent laryngeal nerve block was compared between two groups. Results The onset time of radial nerve, median nerve and ulnar nerve in group Ⅰwas (5.13 ± 0.76), (7.13 ± 1.04), (3.23 ± 0.62) min , in group Ⅱ was (9.23 ± 1.61), (12.35 ± 1.76), (8.83 ± 1.13) min, and there were significant differences (P<0.05). The excellent rates of sensory block of radial nerve, median nerve and ulnar nerve in group Ⅰ were 90.0%(36/40), 85.0%(34/40), 97.5%(39/40), in group Ⅱ were 72.5%(29/40), 65.0%(26/40), 70.0%(28/40), and there were significant differences (P<0.05). The full rates of motor block of radial nerve, median nerve and ulnar nerve in groupⅠwere 75.0%(30/40), 37.5%(27/40), 80.0%(32/40), in groupⅡ were 47.5%(19/40), 40.0%(16/40), 45.0%(18/40), and there were significant differences (P < 0.05). The tourniquet tolerance rate in group Ⅰwas significantly higher than that in groupⅡ:90.0%(36/40) vs. 62.5%(25/40) , P<0.05. In groupⅠ, phrenic nerve block occurred in 2 patients, and Horner syndrome occurred in 1 patient. None had laryngeal recurrent nerve block in both group. Conclusions The interscalene brachial plexus combined with ulnar nerve block guided by nerve stimulator is more suitable for a long time microsurgery of the palm or wrist, because it takes action faster, has better sensory and motor block effects, improves the rate of tourniquet tolerance without increasing untoward reaction.
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The treatment of vascular malformations has been a difficult clinical subject. At present, the main therapeutic methods include embolization/sclerotherapy, surgical excision, laser treatment, etc. However, it is often difficult to obtain a satisfactory clinical effect. As it can induce the vascular endothelial denudation resulting in protein degeneration, ethanol embolization can obtain the effect of complete obliteration of the diseased vascular lumen. Although ethanol embolization of vascular malformations has already achieved satisfactory clinical effect, the fear of cardiac and pulmonary accidents has limited the application of this technique in clinical practice. This paper aims to make a comprehensive review concerning the effect of ethanol embolization for vascular malformations on the cardiopulmonary functions.
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Objective To evaluate the role of cyclic adenosine monophosphate-protein kinase A (cAMP-PKA) signal transduction pathway in lidocaine-induced up-regulation of the expression of surfactant protein-A (SP-A) in rat alveolar epithelial type Ⅱ cells (AEC Ⅱ).Methods Healthy male Sprague-Dawley rats were sacrificed and AEC Ⅱ were isolated,purified and incubated in 24-well culture plates (100μd/hole) with density of 1 × 106/ml.After being incubated for 2 h,the culture medium was replaced with serum-free medium DMEM.The cells were randomly divided into 4 groups (n =48 each):control group (group C),forskolin (adenylate cyclase agonist) group (group F),lidocaine 200 μg/ml group (group L),and PKA inhibitor H89 + L group (group P+ L).Forskolin 10 μmol/ml was added to DMEM in group F.Lidocaine 200 μg/ml was added to DMEM in group L.H89 10μnol/ ml was added to DMEM and AEC Ⅱ were incubated for 10 min,and then lidocaine 200 μg/ml was added in group P + L.At 6,12 and 24 h of incubation (T1-3),cAMP content and PKA activity (using ELISA),and expression of SP-A mRNA (by real-time fluorescent quantitative PCR) and SP-A (by Western blot) were measured.Results Compared with group C,the expression of SP-A mRNA and SP-A was significantly upregulated,and cAMP level and PKA activity were increased at T1-3 in group F and at T2,3 in group L.Compared with group L,the expression of SP-A and SP-A mRNA was down-regulated,PKA activity was decreased,and no significant change was found in cAMP level at T1-3 in group P + L.Conclusion Lidocaine can up-regulate the expression of SP-A in AEC Ⅱ of rats through activating cAMP-PKA signal transduction pathway.
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Objective To evaluate the clinic effects of perioperative psychological intervention combined appropriate sedation by target-controlled infusion of midazolam during operation via symptom check List 90 (SCL-90) and observers assessment of alertness/sedation scale (OAA/S) in patients undergoing thumb or finger reconstruction.Methods Eighty patients undergoing thumb or finger reconstruction were randomly divided into group A,B,C,and D (n =20 cases per group).All patients were received brachial plexus block and spinal-epidural combined anesthesia.Patients in group A were given perioperative psychological intervention combined appropriate sedation by target-controlled infusion of midazolam during operation; patients in group B were received routine treatment; patients in group C were given perioperative psychological intervention; and patients in group D were sedated with midazolam during operation.The vital signs and the scores of OAA/S were observed during operation.The scores of visual analogue scale (VAS) and SCL-90 were recorded after operation.Results The OAA/S grade in groups A and D were stability than that in groups B and C (P ＜ 0.05) ; the scores of VAS and the results of psychological status assessment by SCL-90 in group A were superior to groups B,C,and D (P ＜ 0.05).Conclusions Perioperative psychological intervention combined appropriate sedation in operation on thumb or finger reconstruction is a excellence anaesthesia processing method.It might have beneficial effects on postoperative recovery profile,and strengthen the tolerance to pain and improve the patient's psychological status during operative period.
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Objective To investigate the effect of high concentration carbon dioxide preconditioning on lipid peroxidation during myocardial ischemia-reperfusion (I/R) in rabbits. Methods Twenty-four New Zealand white rabbits weighing 2.0-3.9 kg were randomly divided into 3 groups ( n = 8 each): sham operation group (group S) , I/R group, high concentration carbon dioxide preconditioning group (group H) . The amimals were tracheal intubated and mechanically ventilated. In groups S and I/R, fresh gas flow was set at 0.3 L/min (100% O2 ), respiratory rate 30-40 bpm and tidal volume IS ml/kg, and PETCO2 was maintained at 40-50 mm Hg for 30 min. In group H, fresh gas flow was set at 0.3 L/min (100% O2), respiratory rate 20-30 bpm and tidal volume 10 ml/kg, PETO2 was maintained at 75-85 mm Hg for 5 min, and then all the ventilatory parameters were adjusted to the same as those in groups S and I/R. Myocardial I/R was produced by occlusion of left anterior descending branch of coronary artery for 30 min followed by 3 h reperfusion after preconditioning in groups I/R and H. The animals were sacrificed at the end of reperfusion and myocardial tissues obtained for determination of the superoxide dismutase (SOD) activity and malondialdehyde (MDA) content and examination of the ultrastnicture of myocardium with the transmission electron microscope. Results The SOD activity was significantly lower, while MDA content higher in group I/R than in group S ( P ＜ 0.01) . The SOD activity was significantly higher, while MDA content lower in group H than in group I/R ( P ＜ 0.01) . The myocardial injury was attenuated in group H compared with group I/R. ConclusionHigh concentration carbon dioxide preconditioning can reduce myocardial I/R injury in rabbits through inhibiting lipid peroxidation.
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Objective: To investigate the function of the ATP-sensitive K+(KATP) channel activation on the protective effect of hypercarbonic acidosis preconditioning on rabbit myocardial cells. Methods: Thirty-two rabbits were randomly divided into 4 groups (n = 8 for each group): pseudo-operation group (group P), ischemia and reperfusion group(group IR), hypercarbonic acidosis group(group H) and hypercarbonic acidosis+ glybenzcyclamide group (group H+G). Animals were ventilated normally in group IR and group P, tidal volume 15 mL/kg, breathing rate 35 bpm .The PETCO_2 was maintained at the level of 40-50 mm Hg for 30 minutes. Animals received low-frequency, low volume ventilation in group H group H+G, tidal volume 10 ml/kg, breathing rate 25 bpm to achieve hypercarbonic acidosis. The target value of PETCO_2 was 75-85 mm Hg. This value was maintained for 5 minutes. The animals then were ventilated normally to make the PETCO_2 return to 40-50 mm Hg. Animals were injected with 0.3 mg/kg glybenzcyclamide 10min before achieving hypercarbonic acidosis with hypoventilation in group H+G. Animals received ligation of left anterior branch artery for 30 minutes and reperfusion for 180 minutes in each group except P group. The myocardial ischemia area, the myocardial infarction area and their ratios were calculated by the ismaeil methods. Results: The ratio of the myocardial infarction area to the myocardial ischemia was significantly less in group H than those of group IR and group H+G (P 0.05). Conclusion: Hypercarbonic acidosis preconditioning can protect the cardiomyocytes by activating the KATP channel.
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This study observed the protective effect of hypercapnic acidosis preconditioning on rabbit heart suffered from ischemia-reperfusion injury. Hypercapnic acidosis was established in animals with mechanical hypoventilation before ischemia-reperfusion. Thirty-two rabbits were randomly divided into 4 groups, with each having 8 animals in term of the degree of acidification: hypercapnic acidosis group A (group A), hypercapnic acidosis group B (group B), hypercapnic acidosis group C (group C), ischemia and reperfusion group (group IR). Animals in group IR were ventilated normally (tidal volume: 15 mL/kg, breathing rate 35 bpm). The PETCO(2) was maintained at the level of 40-50 mmHg for 30 min. Animals in groups A, B, C received low-frequency, low-volume ventilation to achieve hypercarbonic acidosis and the target levels of PETCO(2) were 75-85,65-75, 55-65 mmHg, respectively, with levels being maintained for 5 min. The animals then were ventilated normally to lower PETCO(2) to 40-50 mmHg. The left anterior branch artery of all the animals was ligated for 30 min and reperfused for 180 min. Then the infarct size was calculated. The cardiomyocytes were morphologically observed and ECG and hemodynamics were monitored on continuous basis. Acid-base balance was measured during procedure. Our results showed that the infarct size was (48.5+/-11.5)% of the risk area in the control group and (42.4+/-7.9)% in group C (P>0.05). Mean infarct size was significantly smaller in group B (34.5%+/-9.4%) (P<0.05 vs control group) and group A (31.0%+/-9.1%) (P<0.01 vs control group). It is concluded that HA-preconditioning can effectively protect the myocardium.
Subject(s)
Acidosis, Respiratory/physiopathology , Hypercapnia/physiopathology , Ischemic Preconditioning, Myocardial/methods , Myocardial Reperfusion Injury/prevention & control , Random AllocationABSTRACT
BACKGROUND: Recent studies have indicated that cellular apoptosis might be related with the pathological process of diabetic penis erection function disorder. OBJECTIVE: To observe the expression of apoptosis inhibiting gene Bcl 2 and apoptosis inducing gene Bax in the penis cavernosal tissue of diabet ic rats based on the diabetic rat model. DESIGN: A randomized controlled experimental study. SETTING: The Central Laboratory of Jiamusi University. MATERIALS: Fifty male adult Wistar rats were selected. The rats wererandomly divided into normal control group (n=10) and the model group(n=40). The rats in the model group were divided into subgroups according to whether they had diabetes mellitus, namely alloxan medicine control group (n=9) and diabetes mellitus group (n=12). METHODS: The experiment was conducted at the Central Laboratory of Jiamusi University. 20 g/L Alloxan was injected intravenously into the tails of the rats in the model group at a dose of 50 mg/kg. Urine and blood sugar were examined 48 hours after the injection. Diagnosis of diabetes was established when urine sugar was (+++)～ (++++) and blood sugar was above 16.67 mmol/L. The rats in the alloxan group (n=9) were not found to have diabetes mellitus. The rats in the diabetic group were found to have diabetes mellitus, and dead rats were excluded. The blood sugar and urine sugar were measured before experiment and 48 hours, 2, 4, 6and 8 weeks after the experiment. After 8 weeks, the penises were harvested and fixed in 10% neutral formaldehydum polymerisatum. The remaining structures were thoroughly embedded in paraffin, and sections were obtained. Then, apoptosis and the protein of Bcl-2 and Bax were detected in the erectile tissues. 0.5 cm of the middle-section of bulbocavernosus body was collected, and it was then fixed in 10 g/L neutral formaldehydum polymerisatum at 4 ℃ for 24 hours. Then, 5-7 μ m paraffin sections were obtained. The cellular apoptosis was detected with in situ end labeling method. Bcl-2 and Bax gene expressions were detected with histochemical staining. MAIN OUTCOME MEASURES: Cellular apoptosis in the erectile tissues of the rats and genes Bcl-2 and Bax expressions. RESULTS: Nineteen rats died after model establishment and 31 rats entered the stage of the result analysis. ①Cellular apoptosis of the erectile tissues of the rats: The apoptosis rate in the diabetic group was significantly higher than that in the normal control group and alloxan group (16.26±6.63)%,(0.38±0.02)%, (0.40±0.03)%,(q=4.45, P ＜ 0.01). ② Expression of Bcl-2gene of the erectile tissues of the rats: Bcl-2 gene expression of the diabetic group was significantly lower than that in the normal control group and alloxan group [(12.04±2.30)%,(20.88±3.02)%,(21.23±2.58)%,q=4.45,P＜0.01].③Expression of Bax gene in the erectile tissues of the rats: Bax gene expression of the diabetic group was significantly higher than that in the normal control group and alloxan group [(18.35±2.00)%, (9.33±0.56)%,(10.32±0.63)%, (q=4.45, P ＜ 0.01)]. ④ The ratio of Bcl-2 to Bax: The ratio of Bcl-2 to Bax of the diabetic group was significantly lower than that in the normal control group and alloxan group. CONCLUSION: That the cellular apoptosis of the erectile tissues in rats with diabetes mellitus increased suggests that cellular apoptosis is related with diabetic erectile dysfunction. Also, Bcl-2/Bax was down-regulated,and this indicates that Bcl-2 and Bax cooperates in the cellular apoptosis in the diabetic erectile tissues.
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<p><b>OBJECTIVE</b>To investigate the relationship between apoptosis and the expression of Bcl-2 and Bax in the penis cavernosal tissues of diabetic rats.</p><p><b>METHODS</b>Fifty male adult Wistar rats were divided into two groups: 10 as normal control and 40 used to induce diabetes by intravenous injection of alloxan (AXN) (50 mg/kg). After 8 weeks, their penises were harvested. Apoptosis was evaluated by means of terminal deoxynucleotidyl transferase mediated d-UTP nick end labeling (TUNEL). Immunohistochemistry was employed to detect the protein of Bcl-2 and Bax.</p><p><b>RESULTS</b>Compared with those in the control group, apoptotic cells were more in number (P<0.01) and the expression of Bcl-2 was absent in the penis cavernosal tissues of the diabetic rats. However, there was upregulation of Bax and decrease in Bcl-2/Bax ratio in the diabetic group.</p><p><b>CONCLUSION</b>The high rate of apoptosis in diabetic rats may play a role in the pathophysiology of erectile dysfunction. The change in Bcl-2 and Bax activities may be responsible for apoptosis in diabetic penis erectile tissues.</p>
Subject(s)
Animals , Male , Rats , Apoptosis , DNA, Neoplasm , Genetics , Diabetes Mellitus, Experimental , Metabolism , Pathology , Disease Models, Animal , Gene Expression , Penis , Metabolism , Pathology , Proto-Oncogene Proteins c-bcl-2 , Genetics , Rats, Wistar , bcl-2-Associated X Protein , GeneticsABSTRACT
Purpose: To study the clinical efficacy, toxicity of preoperative chemotherapy and survival time with Gemicitabine-Cisplatin combination in the treatment of stage Ma( N2) NSCLC. Methods: Thirty patients with stage IIIa( N2) NSCLC were included. Gemicitabine was administered on dl, 8 and 15 at a dose of 1000 mg/m" and Cisplatin at a dose of 100 mg/m on d2. The chemotherapy was repeated every 28days. Results: Thirty patients were evaluable for response. The overall response rate was 70%. Surgical'excision rate after preoperative chemotherapy was 93%. Total surgical excision rate was 70%. Median survival time was 15 months, one year survival rate was 67%. The main toxicity was hematological, thrombocytopenia of grade III-IV appeared in 46% course of treatment, but it did not lead to hemorrhage. Conclusions: Preoperative chemotherapy with Gemicitabine-Cisplatin combination is effective and well-tolerated in the treatment of stage IIIIa( N2) NSCLC. So it is worthy to be further studied and popularized.
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Objective To comparatively analyze the DNA extracted from sweat latent fingerprints on the adhesive side of tapes by three kinds of methods. Methods DNA was extracted from sweat latent fingerprint on the adhesive side of tapes using silicon bead test,QIA micro Kit and combined silicon bead-QIA micro Kit. STR loci were detected by multiplex PCR procedures. The PCR product was electrophoresed on an ABI 3100 Genetic Analyzer. Results 36%of the sweat latent fingerprints on the adhesive side of tapes was successfully genotyped using combined silicon bead-QIA micro Kit, and 21% using QIA micro Kit. Conclusion DNA genotyping of the sweat latent fingerprints on the adhesive side of tapes reveals higher possibility using combined silicon bead-QIA micro Kit than using QIA micro Kit and is less time-consuming.