Objective To investigate methods of weaning acute brain stem hemorrage patients with respiratory failure from mechanical ventilation.Methods This was a retrospective analysis of 45 acute brain stem hemorrage patients with respiratory failure requiring mechanical ventilaiton.Results 15(33.3%)patients were successfully weaned from mechanical ventilation for the first time;the other 30(66.7%)patients failed in the first place,then succeeded after 3~7 days of and occasional disconnection from ventilation.The time of mechanical ventilation varied from 6 to 35 days.Conclusion It is difficult to wean acute brain stem hemorrage patients with respiratory failure from mechanical ventilation.Occasional disconnction from ventilaiton,antiinfection and nutritional supplementation might contribute to successful weanning.

Objective To study the effects of naloxone on ?-endorphin (?-EP) in plasma and on myocardial ultrastructure during myocardial ischemia-reperfusion (I/R) injury in rabbits.Methods The myocardial ischemia models and myocardial ischemia -reperfusion injury models in rabbits,by ligating the left anterior descending branch of coronary artery,were used to investigate the changes of ?-EP and ET-1 in plasma during I/R injury, and after treatment with naloxone, an antagonist of opiate receptor. 20 New Zealand rabbits were randomly assigned to 2 groups (each 10 rabbits in naloxone treatment and ischemia-reperfusion group). The bloods were taken at different times in each group. The concentrations of ?-EP and ET-1 were detected with radioimmunology method.The changes of myocardial ultrastructure in samples of myocardial ischemia,were observed through electron microscope.Rseults The levels of ?-EP were significantly improved after I/R injury compared with those before ischemia (P0.05). For ischemia-reperfusion group, most of cardiac muscles were in the contracting state, the myofibril dissolved and broke locally. The edema was found on the circumference of nucleus. For naloxone treatment group, the structure of myofibril was clear and its arrangement was in good order, and no obvious breakage was found. The contracting of myofibril, the edema of mitochondria and kytoplasm were moderating. Conclusion Naloxone may effectively control the levels of ?-EP and the synthesis and secreting of ET-1 after myocardial ischemia and during I/R injury;and reduce the injury to the myocardial ultrastructure and decrease the injury to blood vessel and myocardium.

Objective Discussing the clinical features, early diagnosis and therapeutic methods of aortic dissection (AD). Methods We analyzed and concluded the clinical datum of 33 AD patients in our hospital. Results The rate of male to female was 5.6 to 1 among all patients, average age 60, hypertension accounted for 81.8 percent. There were 26 patients (78.8 percent) suffered an acute pain, of who 22 patients got a pain in anterior chest.There were 22 of 26 patients diagnosed AD through echocardiography, 20 and 11 patients confirmed AD by MRI or CT respectively among all 33 patients. 13 patients had abnormal ECG, 10 ST-T segment changed, 12 left ventricular hypertrophy or hyper-voltage. Hypertension patients were treated through a infusion of nitroglycerin or nitroprusside by intervenous drop or by vein pump firstly to decend systolic blood pressure to the level of 100~120 mmHg and heart rate to 60~70 bpm,combining with the use of beta blocker, calcium antagonist and rennin- angiotensin inhibitor. 27 patients’ pain alleviated gradually even disappeared after controling their blood pressure, whose state of illness became to stable. 2 persons did the operation of aortic replacement in emergency. 6 persons died for aortic dissection broken in one week or one month. Conclusions The clinical manifestations of AD are complex, and the rate of false or leak diagnosis is high. Radiology studies including echocardiography, MRI or CT may be very important to enhance the ability of diagnosing AD early and to guide the treatment. Taking medical treatment is primary in emergency. Operating the replacement of aorta is an effective measure to treat AD.

Objective To evaluate plasma BNP level change in acute pulmonary embolism and its clinical value.Methods 33 cases were diagnosed by CT pulmonary angiography or DSA.they were divided into two groups:the group with right ventricular(RV)dysfunction group and the group without right ventricular(RV)dysfunction.Plasma BNP was detected by Triage BNP test.otherwise,we observed severe clinical presentation、 death rate and mechanical ventilation in two groups.Results Plasma BNP level is higher in the group with RV dysfunction(288?102pg/ml)than that in the group without RV dysfunction(61?32pg/ml)(P

Objective To investigate the change and significance of electrocardiogram and myocardial damage index in patients with acute organophosphorus pesticide (AOPP).Methods 71 hospitalized patients in EICU with AOPP from January 2000 to June 2006 were recorded.The patients were divided into 3 groups: mild poisoning group (n=18),moderate poisoning group(n=22) and severe poisoning group (n=31).Electrocardiogram(ECG), serum creatine kinase(CK), serum creatine kinase isoenzyrne MB(CK-MB),lactate dehydrogenase(LDH) and TnI were detected,the relation between the above-mentioned indexes and the toxical degree were analyzed.Results Abnormal ECG had a rasied tendency along with increase of the poisoning degree.The incidence of Ⅱ~Ⅲ atrioventricular block, atrial premature beats, ventricular premature contraction, ventricular tachycardia and ventricular fibrillation in severe poisoning group significantly increased compared with that in mild poisoning group and moderate poisoning group(P

Objective To explore effects of hcmoperfusion on toxic ingredients in plasma of rabbiis with a-cute intoxication of Radix Aconiti Kusmezoffii Monkshood.Method Sixteen male Japanese Giant Ear Rabbits were randomly divided into acute poisoning(AP)group and acute poisoning + hemoperfusion(AH)group(8 an-hnals in each group).Acute poisoning models were established in rabbits of both groups with intragastric adminis-tration of Radix Aconiti Kusmezoffii Monkshood liquid in dose of 1 mL/kg in order to produce arrhythm which oc-curred within ode hour after intragastric administration was regarded as the criteria of successful animal model.and then hemoperfusion with active carbon was performed for 2 hours in AH group.The pathological chanses of brain,myocardium and hepatic tissues were observed.The plasma concentrations of toxicants including mesaconitine,a-conitine and hypaconitine were measured by using HPLC-MS at 1 h,2 h,3 h,and 6 h after poisoning.Student's T test was used to identify the significance.Results The brain.myocardium and hepatic tissues of the rabbits in AP group showed hyperemia and edema which were attenuated after hemoperfusion.The plasma concentrations of mesaconitine,aconitine and hypaconitine revealed no significant differences between AP group and AH group with-in one hour after poisoning(P＞0.05),while at 2 h and 3 h after poisoning,the plasma concentrations of mesaconitine were(2.11±1.08)ng/mL,(2.02±1.46)ng/mL,respectively,aconitine(39.70±9.31)ng/mL,(19.71±16.06)ng/mL,respectively,and hypaconitine(1.70±0.71)ng/mL,(2.12±1.33)ng/mL,respec-fively in AH group,and they were significantly lower than those in AP group(P＜0.05).Conclusions The the plasma concentrations of mesaconitine,aconitine and hypaconitine were lower and the histopathological changes were attenuated after hemoperfusion.Hemoperfusion is a good intervention for acute intoxication of Radix Aconiti Kusmezoffii Monkshood.

Objective To observe the release of glutamate (Glu)and γ-amino butyric acid (GABA) from PC 12 cells induced by aconitine,and to study the intervention of Shuanghuanglian on the injury of these cells. Methods The cell proliferation test agent in cell counting kit(CCK-8)was applied to assay the aconitine toxicity to PC12 cells and to establish the PC12 cell injury model induced by aconitine. The PC12 cells during logarithmic growing phase were randomly divided into the following groups:blank control group(complete medium containing 0.1% dimethyl sulfoxide was added), Shuanghuanglian control group (complete medium containing 50 μg/mL Shuanghuanglian),baicalin control group(complete medium containing 20 μmol/L baicalin),aconitine toxic group(complete medium containing 100 μmol/L aconitine),Shuanghuanglian intervention group(complete medium containing 100μmol/L aconitine and 50μg/mL Shuanghuanglian)and baicalin intervention group(complete medium containing 100 μmol/L aconitine and 20 μmol/L baicalin). The cells in all groups were incubated for 24 hours respectively. The changes of PC12 cell absorbance(A)values were detected by CCK-8 assay before and after intervention by Shuanghuanglian and baicalin. The PC12 cell apoptosis was determined by flow cytometry. Glu and GABA contents in cell culture medium were determined by chromatometry and enzyme-linked immunosorbent assay (ELISA). Results Compared with blank control group,after the PC12 cells treated with 100 μmol/L aconitine for 24 hours,their cytoactivity was decreased markedly(A value:1.003±0.042 vs. 1.685±0.030,P<0.05),then afterwards in the experiment,the incubation of 100 μmol/L aconitine with PC12 cells for 24 hours was considered as the intervention concentration. In blank control group,the normal PC12 cells accounted for 95.89%,while in the aconitine toxic group,the rate of injured PC12 cells reached 64.27% and early apoptosis rate reached 45.46%, and in Shuanghuanglian intervention group and baicalin intervention group,the early apoptosis rate was decreased to 33.24% and 28.22% respectively. Compared with blank control group,there were no significant differences in cytoactivities and the contents of Glu and GABA released by PC12 cells in Shuanghuanglian control group and baicalin control group(all P<0.05),while in the aconitine toxic group,the cytoactivity was significantly decreased(A value:1.056±0.039 vs. 1.722±0.083),and the contents of Glu and GABA were significantly increased〔Glu(μmol/L):5.295±0.137 vs. 3.433±0.138;GABA(μmol/L):0.769±0.020 vs. 0.528±0.012,both P<0.05〕. Compared with aconitine toxic group,the cytoactivities of PC12 were significantly elevated(1.202±0.059 and 1.180±0.032),the levels of Glu were significantly reduced(4.055±0.086 and 3.984±0.057),and the contents of GABA were obviously increased(0.809±0.016 and 0.930±0.021)in the cell culture medium of the Shuanghuanglian intervention group and baicalin intervention group(all P<0.05). The increase of cytoactivity in Shuanghuanglian intervention group was more marked than that of baicalin intervention group(P<0.05). There were no statistical significant differences in contents of Glu and GABA between Shuanghuanglian intervention group and baicalin intervention group(both P>0.05). Conclusions The changes of Glu and GABA may be one of the mechanisms of neural toxic effect of aconitine. Shuanghuanglian possibly can decrease Glu level and increase GABA content by way of its main component baicalin to antagonize the aconitine neurotoxicity.

Objective To investigate clinical features,treatments and prognostic factors of the patients with necrotizing fasciitis caused by vibrio infections and thus provide reference for the early treatment and prognostic assessment.Methods A retrospective analysis was conducted on clinical data of 56 patients with vibrio necrotizing fasciitis admitted to the emergency center of our hospital from May 1995 to June 2011.The clinical characteristics and treatments of the patients were summarized,and differences of clinical factors between the survival group and death group were compared.The possible influencing factors for prognosis were also analyzed.Results The main clinical manifestations included fever (61％),shock (84％) and organ dysfunction,of which renal insufficiency (88％) was the most common,with case fatality of 43％.Early pathological changes of limbs were only local swelling and pain,while skin ecchymosis,tension blood blisters,necrosis and subcutaneous crepitation were the signs of advanced stage.Comprehensive treatment regime including early administration of sensitive antibiotics plus surgical incision and drainage and medicine support was given.A series of factors were significantly different between the survival and death groups including the duration from the presentation of symptoms to hospital admission (P ＜ 0.05 ),limb lesions involving the trunk (P ＜ 0.01 ),creatine kinase level (P ＜ 0.05 ),and emergency incision and drainage ( P ＜ 0.01 ).Conclusions The most prominent clinical manifestations of vibrio necrotizing fasciitis are rapidly progressive local symptoms and signs,and sharp deterioration of systemic conditions.Delayed visiting,severe local lesions,and failure to emergency surgery may be the factors for poor prognosis.

Objective To investigate the interference effect of baicalin on acute brain injury induced by aconitine in rats and its mechanism. Methods A total of 200 Sprague-Dawley(SD)rats were randomly divided into five groups:normal control,baicalin control,aconitine poisoning,baicalin 15 mg/kg intervention and baicalin 30 mg/kg intervention groups(each,n=40). Aconitine(20μg/kg)was given via tail vein in aconitine poisoning group. The rats in the normal control group and baicalin control group were respectively injected with saline 2 mL/kg and baicalin 30 mg/kg via tail vein. The aconitine poisoning rats were given with baicalin at the dose of 15 mg/kg and 30 mg/kg respectively in the low and high dose baicalin intervention groups within 2-3 minutes after injection of aconitine. Rats in all groups in the study were anesthetized and sacrificed at 1,6,12,24 hours after various agents were respectively given in the groups,the rat cerebral cortex samples were collected,the histological changes in normal and baicalin control groups and pathological changes of the aconitine poisoning rats were observed,the levels of glutamate(Glu),aspartate(Asp),γ-aminobutyric acid(GABA),glycine(Gly)were detected and the apoptotic cells were determined at the above time points. Results Compared with the normal control group,the aconitine poisoning group had significantly higher levels of excitatory amino acids Glu and Asp and the number of apoptotic neurons. After exposure to aconitine for 1 hour, the levels of inhibitory amino acids of GABA and Gly were markedly decreased in the rat cortex in the poisoning group compared to the normal control group(both P<0.05),at 6 hours and 12 hours they were significantly increased and after 24 h,they began to decline,but still maintained at relatively high levels. Compared with the aconitine poisoning group, after baicalin intervention for 1 hour,in the 15 mg/kg and 30 mg/kg baicalin intervention groups,the levels of Glu and Asp were markedly decreased〔Glu(μmol/L):309.39±14.59,307.22±23.69 vs. 370.46±40.31,Asp(μmol/L):143.43±8.36,129.12±4.86 vs. 222.97±6.26〕,while the levels of GABA and Gly were increased〔GABA(μmol/L):55.91±4.76,59.61±13.11 vs. 32.05±2.20,Gly(μmol/L):32.33±1.85,33.90±0.66 vs. 21.96±4.75〕,and the number of neuronal apoptosis was obviously decreased(cell/mm2:18.65±4.10,14.80±1.89 vs. 58.15±3.68,both P<0.05). Under microscope and electron microscope,the pathological and ultrastructural changes indicated that the aconitine poisoning group had the most marked cerebral cortex damage at 12 hours after poisoning,while the two baicalin intervention groups showed milder damage than that in aconitine poisoning group. Conclusions The neural toxic effect of aconitine in rats may be related to the imbalance between the neurotransmitter contents of excitatory Glu. Asp and inhibitory GABA,Gly in the cerebral cortex. Baicalin can decrease the contents of excitatory amino acid and elevate the inhibitory amino acid,therefore it may ameliorate the cerebral injury of acute aconitine intoxication in rats.

Objective To investigate the effects of transient receptor potential vanilloid 1 activation by capsaicin on the oxidative stress in lipopolysaccharide-induced lung injury in mice in order to elucidate the potential mechanisms.Methods A total of 108 specific pathogen free (SPF) ICR male mice were randomly divided into six groups:normal control group (n =18),capsaicin control group (CAP control group,n =18),capsazepine control group (CAPZ control group,n =18),acute lung injury group (n =18),capsaicin treatment group (CAP treatment group,n =18) and capsazepine treatment group (CAPZ treatment group,n =18).After modeling,superoxide dismutase (SOD),catalase (CAT) and malondiachehyche (MDA) levels in lung were measured with the method of chromatometry,and the expression of heme oxygenase 1 (HO-1) in lung tissue was assessed with enzyme linked immunosorbent assay (ELISA),while the level of NF-E2-related factor-2 (Nrf2) was determined by western blotting and the expression of Nrf2 mRNA was measured by RTPCR.Pathological changes of lung tissue were observed under light microscope.Results The activities of SOD and CAT in lung tissue at 3,8,16 h were dramatically lower in acute lung injury group than those in normal control group (P ＜ 0.05),while the level of MDA was higher.Compared with acute lung injury group,the lung levels of SOD and CAT at 8 h and 16 h were higher in CAP treatment group (P ＜0.05),while the lung level of MDA was lower (P ＜ 0.05).The levels of SOD and CAT in CAPZ treatment group were decreased at 8 h and 16 h,while the levels of MDA in this group were increased at 3,8,16 h (P ＜0.05).The pulmonary levels of HO-1,Nrf2 and expression of Nrf2 mRNA were significantly higher in acute lung injury group than those in normal control group (P ＜ 0.05).Compared with acute lung injury group,the levels of HO-1,NRF2 and expression of NRF2 mRNA were increased markedly in CAP treatment group (P ＜ 0.05)and were obviously decreased in CAPZ treatment group (P ＜0.05).At 8 h,16 h after modeling,the degree of lung damage was ameliorated in CAP treatment group compared with acute lung injury group under light microscope,while the lung damage was aggravated in CAPZ treatment group.Conclusions The activation of TRPV1 could apparently up-regulate the levels of CAT,SOD,Nrf2,HO-1,and reduce the MDA level in lung tissue of mice with acute lung injury,ultimately protecting the endotoxemia mice from oxidative stress.