Objective Platelet aggregation, activation induced by bubbles is the main cause of decompression sick-ness.Clopidogrel(Clo) can decrease platelet aggregation through inhibiting the bind of fibrinogen and ADP .This study is designed to find if Clopidogrel can paly a protective role in decompression sickness and explore the intervention mechanism . Methods Totally 111 male SD rats divided into 3 groups:normal control group (n=20), decompression sickness(DCS) group(n=46), and DCS+Clo(Clopidogrel)treated decompression sickness (DCS+Clo)group(n=45).The rats in DCS and DCS+Clo group were placed in chamber and compressed to 1.5 MPa at speed of 2t/4 , the time of compression and res-idence was 4.5 min totally, then decompressed to surface at a speed of 3 m/s.The mortality and behavioral of rats were ob-served within 30 min post decompression .The pathology and the wet/dry ratio of lung , WBC and platelet counts in periph-eral blood, the expression of activated platelets , and immunohistochemical detection of lung tissue CD 41 expression were also been tested .Results We found Clo reduces the DCS mortality risk ( mortality rate:11/45 in DCS+Clo group vs 28/46 in DCS group, P<0.01).Clo reduced the lung injury, the wet/dry ratio of lung, the accumulation of platelet and leu-kocyte in lung , the WBC counts and activated platelets in peripheral blood .Conclusion Clo can play a protective role in decompression sickness through reducing post-decompression platelet consumption and activation , decreasing the activation of leukocytes .

Objective To study the expression levels of microRNA (miR)-16 and miR-146a in rat lungs of decompres-sion sickness (DCS) caused by fast buoyancy ascent escape or diving .Methods At 0.5 h after fast buoyancy ascent es-cape or diving, the pathological changes in rat lungs and expression levels of miR-16,and miR-146a were detected by re-verse transcription-quantitive polymerase chain reaction and compared with normal control group .Results The pathological characteristics of lungs in two DCS groups were tissue damage .At 0.5 h after DCS caused by fast buoyancy ascent escape , the lung tissue expression levels of miR-16 and miR-146a did not significantly change compared with normal control and diving DCS groups ,but the rat lung tissue expression level of miR-146 a in diving DCS group was obviously increased , com-pared with normal control group .Conclusion miR-146a may play a role in post-transcriptional regulation in the process of diving DCS .

Objective To study the pathological changes of lung tissues during fast floating escape-induced decompres-sion sickness.Methods Eighty male SD rats were randomly divided into 2 groups, 60 in fast floating escape group (escape group) , and 20 in control group .Rats in the control group were only put in a cabin under the same atmospheric pressure (ATM).Rats in escape group were pressurized to 1.5 MPa by pressure air at the 2t/7 exponential rate and stayed for 4 min till decompression.Then the rats′survival rate was observed after 0.5 h, lung tissue specimens were collected from each rat, the pathological score was taken , according to the degree of lung injury and the R language was used for statistical analysis.Results The mortality rate was 50%.Lung tissues of these rats were pathologically characterized by stromal lung thickening, edema, and hyperemia.Kruskal non-parametric test analysis found a significant difference (P=0.0016) between the two groups .Nemenyi test was used in pairwise comparison .The death and survival animals in escape group compared with the control group, the scores were significantly different (P<0.05).The scores had no significant difference between the deach and survival animal in escape group .Conclusion Decompression sickness caused by fast floating es-cape can significantly damage the blood-lung barrier to cause pulmonary edema .

Objective To study the effect of nicardipine on fast floating escape induced lung injury in animal models with decompression sickness .Methods Sixty male SD rats were randomly and evenly divided into three groups:blank control, control and nicardipine groups .The nicardipine group was given nicardipine 50 mg/kg orally 0.5 h before entrance.In the control group, rats were given an equal volume of saline 0.5 h before entrance.The blank control group only stayed in the vehicle without any pressurized procedure .The air was pressurized at the 2t/7 exponential rate to 1.5 Mpa which was maintained for 4 min, and then uniformly decompressed to atmospheric pressure .The extravehicular survival and lung pathology were observed in rats after 0.5 h, IL1-βand TNF-αexpression levels were detected by ELISA , and the Caspase 3 expression in lung tissue was detected by Western blot .Results The incidence and mortality rate were 80%and 50%respectively in control group ,and 100%and 80%in the experimental group .The surviving animals in the two groups suffered from alveolar and interstitial lung hemorrhage , with widened interstitial lung .IL1-βin the experimental group was significantly higher than in the normal control group , while TNF-αhad no significant change .After nicardipine treatment pro-caspase 3 did not change significantly , but cleaved-caspase 3 increased significantly .Conclusion Nicardipine can aggravate lung injury caused by fast floating escape-induced decompression sickness if used before decompression.

Objective To establish a closed-chest pulmonary embolism-reperfusion animal model by Swan-Ganz catheter and to explore the mechanisms of pulmonary embolism(PE)-reperfusion injury(RI). Methods Experiments were made on 14 mongrel dogs,ranging in weight from 15 to 18 kg,anesthetized with 3% pentobarbital sodium.The dogs were intubated with I.D.7 endotracheal tubes.Under sterile conditions,a 7 F Swan-Ganz catheter via the external jugular vein was positioned in the unilateral pulmonary diaphragmatic lobe(DL)artery.Occlusion/reperfusion of the DL artery was controlled with 1.2 ml diluted contrast agent filled into/drawn from the balloon.After the 24 h PE,the balloon was deflated to result in 4 h reperfusion of the DL.Measurements of blood gases and tumor necrosis factor-?(TNF-?)were made at normal condition,at 24 h PE and at 4 h reperfusion.Thin-section CT scans were performed at normal condition,24 h PE,30 min,1,2,3 and 4 h reperfusion,respectively.At the end of each experiment, tissue specimens of bilateral diaphragmatic lobes were obtained for both wet/dry(W/D)weight ratio and for pathological study.Results Reperfusion pulmonary edema(RPE)was an acute,mixed,noncardiogenic edema that was observed in all 14 dogs who had been successfully established as PE/RI animal models.RPE demonstrated heterogeneous ground-glass opacifications that predominated in the areas distal to the recanalized vessels.It manifested pathologically as an edematous lung infiltrated by inflammatory cells.The mean ofPaO_2 and TNF-? of 4 h reperfusion was(81?4)mm Hg(l mm Hg=0.133 kPa)and(16.0? 2.5)pg/ml,which were significantly different(P

OBJECTIVETo investigate the effect of different pressure oxygen pre-breathing in preventing decompression sickness of rats.

METHODSForty male SD rats were randomly divided into 4 groups: decompression sickness (DCS) group and three oxygen pre-breathing groups with 1 ATA, 2 ATA and 3 ATA pressure respectively. The rats of DCS group were placed in the hyperbaric chamber and the chamber was compressed evenly within 3 minutes to depths of 7 absolute atmosphere(ATA) and held at the designated depth for 60 min, then decompressed (3 min) at constant speed to the surface pressure. After that, the rats were taken out for further detection. While the rats of oxygen pretreatment groups pre-breathed different pressure oxygen for 20 min before entering into chamber. The mortality and behavioral of rats were observed with 30 min post decompression. The dry/wet ratio of the lung, protein levels in the bronchoalveolar lavage fluid (BALF), and the inflammatory cytokine tumor necrosis factor (TNF-alpha) expression were also tested.

RESULTSCompared with that of the DCS group, the mortality and morbidity of oxygen pre-breathe groups didn't change obviously. But the total BALF protein level and the inflammatory cytokine TNF-alpha expression of 1 ATA oxygen pre-breathe group were obviously decreased, while the dry/wet ratio of lung as obviously increased instead (P < 0.05).

CONCLUSIONAlthough preoxygenation can' t obviously change the mortality and mobidity of rats, normal pressure oxygen pre-breathing can mitigate the protein infiltration in BALF and the expression of inflammatory cytokine in lung tissue.

Animals ; Bronchoalveolar Lavage Fluid ; chemistry ; Decompression Sickness ; Diving ; Lung ; pathology ; Oxygen ; physiology ; Pressure ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; metabolism

Objective To investigate the effect of N-acetylcysteine ( NAC) on lung and heart injury of rats with a fast floating escape induced decompression sickness .Methods Eighty male Sprague-Dawley rats were randomly and evenly divided into four groups:control group and three NAC prevention groups .The NAC groups were treated with different doses of NAC(250, 500 or 1000 mg/kg)by intraperitoneal injection 1 h before entrance.In the control group, rats were given an equal volume of saline1h before entrance.The air was pressurized at the 2t/7 exponential rate to 1.5 MPa which was maintained for 4 min and then uniformly decompressed to atmospheric pressure .The extravehicular survival and pathological changes in the lung and heart tissue were detected 0.5 h after rat egress.Results The survival rate of rats treated with NAC 500 mg/kg(90%) was significantly higher than that of those treated with saline (65%)alone (P<0.05).There was large break and fusion in the structure of pulmonary alveolus of control group besides obvious erythrocyte exudation , cardiac muscle fibers edema ,and obvious denaturation and break .Conclusion NAC can play a protective role in rats with a fast floating escape induced decompression sickness by mitigating the injury to and inflammation of lung and heart tissue .

Objective To study the immune regulatory effect of natural killer cell(NKT) in the early stage of murine liver injury induced by type 5 adenovirus(Ad5). Methods Animal models were con-structed by injected C57BL/6 mice with 1.5×109-3×109 PFU Ad5 into the tail vein. Liver injury of mouse at day 0, 1, 2, 3, 4, 5 after infection was determined by HE staining and serum ALT/AST(alanine amin-otransferase/aspartate aminotransferase) level. Flow cytometry analysis was used to measure the proportion of lymphocytes, expression of Fas/FasL on the surface of NKT cells and level of IL-4, IFN-γ/in NKT cell plasma in the infected mouse liver. RT-PCR was applied to semi-quantify the chemokines and their receptors mRNA in infected mouse liver. Results NKT cells of mouse increased significantly at day 1 after infected with high titer Ads(3×109 PFU), expression of FasL on NKT cell and plasma IL-4, IFN-γ/level in NKT cells were also up-regulated, hence the obviously infiltration of lymphocytes in routine liver. Comparing with high titer Ads infection, low titer Ads infection (1.5×109 PFU) lead to little change of NKT cell proper-tion, and fewer infiltration of lymphocytes in murine liver. Hepatic chemokine RANTES, 1P-10, and MIP-1β mRNA expression in C57BL/6 was up-regulated 2 d after intravenous administration of 3×109 PFU Ad5. Corresponding chemokine receptor CCR5, CCR1, CXCR3 mRNA expression was up-regulated 3 d after in-fection. Conclusion NKT cells play an important role in lymphocytes recruitment into the liver of mouse in-fected with AdS, which may relate to up-regulatio of the plasma IL-4, IFN-γ level and expression of FasL of NKT cells, therefore facilitating the production of chemokines, e.g. IP-10 and Mig.

Objective To investigate the clinical characteristics,minimal invasive operation technique and perioperative management of lateral ventrieular tumors.Methods The clinical characteristics,image diagnosis,surgical approaches and postoperative management and surgical outcomes of 65 consecutive cases of lateral ventricular tumors were retrospectively analyzed.Results In our series,total resection was achieved in 54 cases,and subtotal resection was achieved in 11 cases.Lateral ventricular tumors were mostly found in male and in the left side.Headache caused by increased intracranial pressure was the most common clinical symptom.Ependymocytoma and astrocytic glioma are the most common pathologic diagnosis.Postoperative complications included fever (26 cases),hydrocephalus (9 cases),intraventricular hematoma (7 cases) of which 2 cases were evacuated by craniotomy,epilepsy (7 cases),wound infection (3 cases).Postoperative death was happened in 3 cases.Two of them died of respiratory failure due to postoperative epilepsy.Conclusion Early discovery of lateral ventricle tumors,meticulous operation,subtle micromanipulation and right postoperative treatment are the criticality to improve the rate of total resection of lateral ventricle tumors through microsurgical treatment and reduce postoperative complications and mortality.

The technique introduced in this paper is applied in the endocardial catheter operation, which describes the 3D heart model reconstruction before the operation for the endocardial navigation. After a series of CT images of the thorax are processed, an accurate 3D endocardial model can be reconstructed. At first, the series of 2D CT images are preprocessed for denoising and the enhancement,then they are constructed as the volume data. After the region growing segmentation in the 3D volume data according to the grey value of the voxel in the heart cavity, the heart surface rendering is got and the 3D model of endocardial cavity is reconstructed.
Cardiac Catheterization ; methods ; Imaging, Three-Dimensional ; Models, Cardiovascular ; Tomography, X-Ray Computed ; methods