ObjectiveTo explore the feasibility of establishment of a artificial joint aseptic loosening mouse model by cobalt-chromium particles stimulation.MethodsTwenty-four 8-week-old male severe combined immunodeficient (SCID) mice were divided into experimental group (n=12) and control group (n=12). The titanium nail was inserted into the tibial medullary cavity of mouse in the two groups to simulate artificial joint prosthesis replacement. And the cobalt-chromium particles were injected into the tibial medullary cavity of mouse in experimental group. The survival of the mouse was observed after operation; the position of the titanium nail and the bone mineral density of proximal femur were observed by X-ray film, CT, and Micro-CT bone scanning; and the degree of dissolution of the bone tissue around the tibia was detected by biomechanical test and histological staining.ResultsTwo mice in experimental group died, and the rest of the mice survived until the experiment was completed. Postoperative imaging examination showed that there was no obvious displacement of titanium nails in control group, and there were new callus around the titanium nails. In experimental group, there was obvious osteolysis around the titanium nails. The bone mineral density of the proximal tibia was 91.25%±0.67%, and the maximum shear force at the tibial nail-bone interface was (5.93±0.85) N in experimental group, which were significantly lower than those in control group [102.07%±1.87% and (16.76±3.09) N] (t=5.462, P=0.041; t=3.760, P=0.046). Histological observation showed that a large number of inflammatory cells could be seen around the titanium nails in experimental group, while there was no inflammatory cells, and obvious bone tissue formation was observed in control group.ConclusionThe artificial joint aseptic loosening mouse model can be successfully established by cobalt-chromium particles stimulation.
目的 探讨川芎嗪对大鼠重症急性胰腺炎（SAP）脑损伤的保护作用。方法 将72只健康Wistar大鼠按数字表法随机均分为对照组、SAP组和川芎嗪治疗组3组。对照组仅剖腹翻动胰腺后即缝合腹壁； SAP组采用胰腺被膜下均匀注射5%牛磺胆酸钠（2ml/kg体重）制备SAP动物模型；川芎嗪治疗组在SAP建模后5min于大鼠尾静脉注射川芎嗪注射液（100mg/kg体重）。各组大鼠分别于术后第6、12及24 h观察胰腺组织及脑组织的病理改变，检测血清淀粉酶、 脑组织含水量和微血管内白细胞聚集附壁计数，以及脑组织中MDA、TNF-α和IL-1β水平。结果 对照组胰腺组织无明显改变；SAP组胰腺组织腺泡细胞坏死，结构不清，间质水肿，红细胞漏出，部分腺导管扩张，有点片状出血坏死，炎性细胞浸润；川芎嗪治疗组胰腺组织病理改变较同一时相的SAP组明显减轻。对照组脑组织无明显改变；SAP组脑组织神经元细胞水肿，微血管内白细胞聚集及附壁，脑组织内有炎性细胞增生、聚集，且随时间延长上述表现逐渐加重；川芎嗪治疗组脑组织病理改变较同一时相的SAP组明显减轻。SAP组大鼠各时相脑组织含水量和微血管内白细胞聚集附壁计数，脑组织中TNF-α、IL-1β和MDA水平，以及血淀粉酶含量均明显高于对照组（P＜0.05）；川芎嗪治疗组大鼠各时相的上述指标均明显低于SAP组（P＜0.05）。结论 大鼠脑组织中的TNF-α、IL-1β及MDA参与了SAP脑损伤的病理过程，川芎嗪对SAP大鼠脑损伤具有保护、治疗作用。
ObjectiveTo summarize the current researches and progress on experimental animal models of avascular necrosis of the femoral head. MethodsDomestic and international literature concerning experimental animal models of avascular necrosis of the femoral head was reviewed and analyzed. ResultsThe methods to prepare the experimental animal models of avascular necrosis of the femoral head can be mainly concluded as traumatic methods (including surgical, physical, and chemical insult), and non-traumatic methods (including steroid, lipopolysaccharide, steroid combined with lipopolysaccharide, steroid combined with horse serum, etc). Each method has both merits and demerits, yet no ideal methods have been developed. ConclusionThere are many methods to prepare the experimental animal models of avascular necrosis of the femoral head, but proper model should be selected based on the aim of research. The establishment of ideal experimental animal models needs further research in future.
Objective To study the effects of malondialdehyde (MDA), superoxide dismutase (SOD) and tumor necrosis factor-α (TNF-α) on brain tissue in rats with pancreatic encephalopathy (PE). Methods Thirty-six Wistar rats were randomly divided into control group (n=6) and PE model group (n=30). In control group, rats were injected with normal saline by internal carotid artery (0.1 ml/100 g) and were killed on the first day after the injection. In PE model group, rats were injected with phospholipases A2 (0.1 ml/100 g, 1 000 U/0.1 ml) by internal carotid artery, to establish animal model of PE in rat and 10 rats were killed on day 1, 3, 7 respectively after the injection. The changes of water content in the brain were measured. Leucocytes aggregation and margination in the microvessels, and the changes of cerebral cells and nerve fibers were observed. The levels of MDA, TNF-α and the activity of SOD were tested in the brain homogenate in rats. Results In PE model group, water contents of brain increased; The phenomena of leucocytes accumulation and margination, cellular edema of neurons and demyelination of nerve fibers became more obvious; The levels of MDA and TNF-α increased significantly than those in the control group, while the activity of SOD reduced (P＜0．05， P＜0.01)． Conclusion Inthe rat model of PE, MDA, SOD, and TNF-α play important roles on the occurrence and development of brain injury.
To introduce a rat model of the conversion of acute edematous pancreatitis (AEP) to necrotizing pancreatitis (ANP). One hundred and seven Sprague-Dawley rats were randomized in three experimental groups as follows: sham operation control group and AEP group and ANP group. AEP was induced by pancreatic duct ligation and exocrine stimulation, ANP was induced same as AEP，but with a large dose of dextran-110 (500mg/kg) intravenously. The serum concentration of amylase increased significantly in AEP group and ANP group. Cytosolic free Ca2+ concentration in isolated pancreatic acinar cells increased consistently after induction of ANP. Homorrhage, parenchymal necrosis and calcium deposits in acinar cells were observed in pancreas in ANP group. Ultrastructural examination showed desquamation and necrosis of the endothelium of the pancreatic capillary in ANP group. These results suggest that ischemia may induce the conversion of AEP to ANP via acinar cell Ca2+ overloading. The rat model would seem to be a suitable animal model for studying aggravating mechanism of acute pancreatitis.
In order to investigater the effect of nutritional support on nutrients metabolism after liver resection,we researched into the hepatectomy and total parenteral nutrition model in rats.The features of the model were no fasting before surgery,10% glucose subcutaneous injection prior to operation avoiding of blood loss and shortening of the surgical process.The 7-day mortality was markedly decreased.Anesthetized with phenobarbital(25mg/kg) injection in combination of ether inhalation,the rats recovered quickly from anesthesia and developed almost no infection of the respiratory tract after hepatectomy.The rats were supplied parenterally energy of 573kJ/kg and a marked improvement in survival was achieved after liver resection.By applying dual preventive rotation equipment of protective spring and IN-Stopper,nutrient solution could be safely infused.
ObjectiveTo observe the effect of using tungsten drills to prepare mouse knee osteochondral injury model by comparing with the needle modeling method, in order to provide an appropriate animal modeling method for osteochondral injury research.MethodsA total of 75 two-month-old male C57BL/6 mice were randomly divided into 3 groups (n=25). Mice in groups A and B were used to prepare the right knee osteochondral injury models by using needles and tungsten drills, respectively; group C was sham-operation group. The general condition of the mice was observed after operation. The samples were taken at 1 day and 1, 2, 4, and 8 weeks after modeling, and HE staining was performed. The depth, width, and cross-sectional area of the injury site at 1 day in groups A and B were measured, and the percentage of the injury depth to the thickness of the articular cartilage (depth/thickness) was calculated. Toluidine blue staining and immunohistochemical staining for collagen type Ⅱ were performed at 8 weeks, and the International Cartilage Research Society (ICRS) score was used to evaluate the osteochondral healing in groups A and B.ResultsAll mice survived to the completion of the experiment. HE staining showed that group C had normal cartilage morphology. At 1 day after modeling, the injury in group A only broke through the cartilage layer and reached the subchondral bone without entering the bone marrow cavity; the injury in group B reached the bone marrow cavity. The depth, width, cross-sectional area, and depth/thickness of the injury in group A were significantly lower than those in group B (P<0.05). At 1, 2, 4, and 8 weeks after modeling, there was no obvious tissue filling in the injured part of group A, and no toluidine blue staining and expression of collagen type Ⅱ were observed at 8 weeks; while the injured part of group B was gradually filled with tissue, the toluidine blue staining and the expression of collagen type Ⅱ were seen at 8 weeks. At 8 weeks, the ICRS score of group A was 8.2±1.3, which was lower than that of group B (13.6±0.9), showing significant difference (t=−7.637, P=0.000).ConclusionThe tungsten drills can break through the subchondral bone layer and enter the bone marrow cavity, and the injury can heal spontaneously. Compared with the needle modeling method, it is a better method for modeling knee osteochondral injury in mice.
Objective To establ ish the experimental animal model of perforator sural neurocutaneous flap for laying a foundation of further study on its physiology and haemodynamics. Methods Thirty-five New Zealand rabbits were divided into four groups, weighing 2.5-3.0 kg and being male or female. In group A (n=5), vivisection was performed to observe thestarting point and arrangement of sural nerve, its concomitant vessels, posterior tibial artery and perforating vessel. In groups B and C (n=5), red latex and gelatin-lead oxide were injected into the concomitant arteries of sural nerve and the posterior tibial arteries respectively to observe their arrangement, the diameter and anatomasis. In group D, forty neurocutaneous flaps based on single perforator were elevated in the twenty rabbits with a size of 7 cm × 1 cm and a pedicle of 0.5 cm. The colour and condition of flaps were observed. Results The sural nerve originated from posterior tibial nerve, passed through the lateral head of the gastrocnemius at site of the popl iteal fossa, descended obl iquely to exterior, entered in the deep fascia at about (5.42 ± 0.15) cm above lateral malleolus, and descended vertically to lateral malleolus. Its concomitant artery originated from deep femoral artery with an initial diameter of (0.73 ± 0.11) mm and extended to the lateral malleolus along the sural nerve. A perforating branch of posterior tibial artery at the position of the calcaneus originated from the midpoint of the l ine connecting between the medial malleolus and the calcaneus with an initial diameter of (0.45 ± 0.01) mm. The perforating branch traversed the calcaneus to the region of the lateral malleolus, and anastomosed to the concomitant artery of the sural nerve, forming a vascular plexus around the sural nerve. In group D, two cases were excluded due to infection. The survival rate was 78.0% ± 1.5% in other 38 flaps 10days after operation. Conclusion The perforator based sural neurocutaneous flap in rabbit is a good experimental model,which has stable anamatic features and rel iable blood distribution.