Objective To discuss the clinical effect of using autologous quadriceps tendon fixed by a patellar block as the graft to reconstruct posterior cruciate ligament (PCL ) under arthroscopy on a single-bundle way .Methods We treated 21 patients with damaged PCL using autologous quadriceps tendon fixed by a patellar block as the graft and absorbable interference screw fixation to reconstruct PCL under arthroscopy on a single-bundle way .Their functional recovery was evaluated by Lysholm scoring ,Tegner scoring and International Knee Documentation Committee (IKDC) criteria .Results All 21 patients got successful surgery on PCL reconstruction and multiple trauma ,no patients lost to follow-up .The subjective symptoms were improved after operation ,the post-operative Lysholm score and Tegner score were both significantly enhanced and showed statistical significance compared with the preoperative scores(P<0 .01) .Conclusion Using autologous quadriceps tendon fixed by a patellar block as the graft to reconstruct PCL on a single-bundle way leads to satisfactory short term clinical effects ,however ,the long term clinical effects remain to be eval-uated .

Objective To explore the effect of positive end expiratory pressure (PEEP) on arterial oxygenation and intrapulmonary shunt during one-lung ventilation (OLV) and pulmonary function during perioperation. Methods Forty patients with normal pulmonary function,ASA I - II :scheduled for pulmonary lobectomy, were divided into control group and PEEP group by random digits table with 20 cases each. Patients were induced by double-lumen tubes under intravenous anesthesia and were received 10 ml/kg tidal volume, 12 frequents/min breathing rate during the two-lung ventilation (TLV), secondary reduced to 6 ml/kg tidal volume, 16-18 frequents/min breathing rate without PEEP (control group) or with 5 cm H2O cm H2O =0.098 kPa) PEEP (PEEP group) during OLV.Hemodynamics and respiratory mechanical parameters were continuously monitored, lung function before operation and at 72 h after operation was detected. Results Compared to before OLV,arterial oxygen tension (PaO2), arterial oxygen saturation (SpO2), oxygenation index (OI) were decreased and intrapulmonary shunt ratio (Qs/Qt) was increased in control group and PEEP group at 30 min after OLV (P < 0.01 or < 0.05). However,PaO2 and SpO2 and OI were higher and Qs/Qt was lower in PEEP group than that in control group at the same time point (P<0.05). In addition, FEV1%, FVC% and FEV1/FVC were (121.8 ± 25.0% ,(117.2 ± 24.3)% , (87.6 ± 15.7)%before operation and (84.9 ± 21.6)%, (77.2 ± 18.3)% , (70.5 ± 12.5)% at 72 h after operation respectively in control group, (116.9 ±24.5)% , (112.1 ±23.6)% , (85.3 ± 13.8)% before operation and (96.3 ± 20.4)%, (88.1 ± 19.8)% , (78.4 ± 10.2)% at 72 h after operation respectively in PEEP group. Although decreased in control group and PEEP group at 72 h after operation comparing with preoperation (P< 0.01 or < 0.05 ), FEV1%, FVC% and FEV1/FVC were higher in PEEP group than those in control group at 72 h after operation (P<0.05). Conclusion Appropriate PEEP increases arterial oxygenation,reduces Qs/Qt and improves pulmonary function during OLV,reduces the risk of hypoxernia and lung injury induced by OLV during perioperation.

Objective:To assess the severity of hypoxic-ischemic brain damage (HIBD) in neonatal rats and predict the occurrence of subsequent neurobehavioral abnormalities after brain injury by scoring and magnetic resonance imaging (MRI).Methods:7-day-old of 60 Sprague-Dawley (SD) rats were randomly divided into control group (14 rats), sham operation group (14 rats) and HIBD model group (32 rats). HIBD model was established by right common carotid artery dissection with Rice-Vannucci method and hypoxia. Within 24 h after modeling, the rats in the model group were evaluated by general condition score and Longa score, and the surviving rats with moderate and severe HIBD were selected for the experiment. 24 h after modeling, 5 rats of the model group were randomly selected for 2,3,5-triphenyltetrazole chloride staining to verify cerebral infarction. 1 week after modeling, 6 rats from each group were randomly selected for hematoxylin-eosin staining to observe HIBD brain injury. 4 weeks after modeling, 4 rats were randomly selected from the control group and the sham operation group, and 8 rats from the remaining model group were used to evaluate the volume of brain damage by MRI. 5-6 weeks after modeling, the remaining 8 rats from each group were subjected to the Cylinder test, and at 13 weeks, they underwent the Morris water maze test to evaluate their neurobehavior.Results:In HIBD model group, 19 rats with moderate to severe HIBD were selected from 32 rats. 24 h after modeling, cerebral infarction was verified in all rats, indicating moderate to severe HIBD. Brain tissue pathology observed 1 week after modeling revealed predominantly gray matter brain damage. MRI showed that 7 out of 8 rats had moderate to severe HIBD. Compared to the control and sham operation groups, the model group exhibited a significant decrease in the usage rate of the left forelimb in the Cylinder test at 5-6 weeks after modeling ( P<0.05), and the latency period in Morris water maze test was significantly prolonged at 13 weeks after modeling ( P<0.05), and the times of crossing platform quadrant were significantly reduced ( P<0.05). There was no significant difference in the right brain injury volume between 24 h and 4 weeks model group ( P>0.05). The brain injury volume in model group was negatively correlated with the usage rate of left forelimb in cylinder test at 5-6 weeks and the times of crossing platform quadrant in Morris water maze test at 13 weeks ( P<0.05), and positively correlated with latency period in Morris water maze test at 13 weeks ( P<0.05). Conclusions:Within 24 h of HIBD modeling, the severity of brain injury can be preliminarily predicted by general condition score and Longa score. 4 weeks after modeling, in the chronic phase of brain injury, MRI was proved to be an excellent predictor for mid-term and long-term neurobehavioral abnormalities in HIBD rats.

Objective    To investigate the effect of simvastatin and mechanical pretreatment on intimal hyperplasia of venous graft and its mechanism. Methods    Twelve New Zealand rabbits were selected and randomly divided into 4 groups: a blank control group, a simvastatin topical treatment group, a mechanical precondition group and a combined group (n=3 in each group). Ultrasound was used to evaluate the changes of graft wall and blood flow velocity in the graft, and pathological section was used to evaluate the intimal hyperplasia. Human umbilical cord endodermal cells were cultured in vitro. A simvastatin group and a solvent control group were set to detect YAP phosphorylation, downstream target gene expression and cell proliferation. Results    Vascular ultrasound showed that except the simvastatin topical treatment group, the flow velocity in vein grafts in the other three groups significantly increased 21 days after surgery compared with 7 days after surgery (P<0.01). Pathological sections showed that the thickness of new intima in the simvastatin topical treatment group, mechanical precondition group, combined group and blank control group were 45.56±4.11 μm, 201.28±16.71 μm, 143.57±7.82 μm, 249.45±13.33 μm, respectively, and there were statistical differences compared with the blank control group (P<0.05). In vitro results showed that compared with the solvent control group, cell death was observed in high concentration simvastatin (5 mmol/L) group, cell proliferation was inhibited in low concentration simvastatin (2.5 mmol/L) group (P<0.05), the expression of YAP protein in the simvastatin group was unchanged, but the expression of phosphorylated YAP protein significantly increased (P<0.05), and the expression of downstream target gene ccn1 was down-regulated (P<0.001). Conclusion    Intravascular local application of simvastatin and mechanical preconditioning alone or in combination can inhibit intimal hyperplasia of venous graft. High concentration of simvastatin has cytotoxicity, while low concentration of simvastatin has inhibitory effect on cell proliferation. Simvastatin can inhibit the formation of new intima by inhibiting the entry of YAP into the nucleus and reducing the transcription of cell proliferation-related target gene ccn1.