| Acute extraocular muscles injury is a common disease of eyes. In injury muscles, nerves and blood vessels result in acute extraocular muscles limitation of movement. Meanwhile, diplopia and compensation head position are clinical manifestation of disease. At present, due to the anatomy and physiology features of the extraocular muscle, the reliable and stable animal model for acute extraocular muscle injury study is still underdetermined. Therefore, the fundamental and clinical research about the injury of the extraocular muscle has been limited in large extent.There are 52 years from Insulin like growth factor-1(IGF-I) that have extensive biology functions was discovered. It is a polypeptide of anabolic metabolism and promoting growth. And it can adjust and promote repair after muscle injury. Therefore,establishment of an stable and reduplicative animal model for acute extraocular muscle injury, and using the agent of promote repairing for muscles at the forepart of acute extraocular muscle injury which will become the referenced model for researching pathogenesis and medication for acute extraocular muscles injury. It is also the exploring new method for prevention and cure of acute extraocular muscles injury.Objective:To establishment of an animal model for acute extraocular muscle injury with clamping for researching of pathogenesis and treatment and to observe IGF-I promoting repair in acute extraocular muscles injury with ring clamping.Methods:1. Establishment of an animal model for acute extraocular muscle injury: 48 eyes of 24 adult male New Zealand albino rabbits were randomly divided into A, B, C groups(each of 8 rabbits). Open the conjunctiva of the left eye after the conventional disinfection to expose the superior rectus, then clamp the superior rectus by needle of 20 cm(clamping force:1200g) holder for 5min(A), 10min(B), and 20min(C), respectively. And there was no treatment in the right eye (as control group: D). All rabbits were sacrificed on the 7th day after the operation. Then the muscular strength of the superior rectus and the histopathology changes after HE dyeing were observed.2. According to results of experiment 1, and referring the grade standard of muscular movement injury, we made certain clamping time of low-grade, midrange and heavy-grade muscles injury. 36 eyes of 18 adult male New Zealand albino rabbits were used in this study and were randomly divided into E, F, G groups(each of 6 rabbits): opened the conjunctiva of the both eyes after the conventional disinfection to expose the superior rectus, then clamped holder the lateral rectus for 10min, one superior rectus muscle received a single injection of 5ug IGF-I(experimental group). The contralateral muscle received an injection of saline only (as control group). After 4d(E), 7d(F) and 14d(G), six rabbits were sacrificed. Then the muscular strength of the lateral rectus and the histopathology changes after HE dyeing were observed. In addition, proliferating cell nuclear antigen (PCNA) expressions were studied.Results:1. Histopathology observation showed that muscle fiber necrosis, fragmentation and cytoplasmic lysis have happened in the superior rectus of the experimental groups in different extent. Results(/400 light microscope field) of transaction muscle fiber counting at 40×10 light microscope showed: A:45.25±3.54,B:34.00±3.53, C:17.83±3.19,control group: 61.25±4.89. Quantity of muscle fibers counting decreased than that of the control group: 26.12%(A, P<0.05), 44.49%(B, P<0.01), 71.76%(C, P<0.01). The histopathology change after 5min, 10min, 20min clamping were accorded with muscle injuryⅡlow-grade, midrange and heavy-grade, respectively. Results(mN/cm2) of muscular strength measurements showed 40HZ: A(83.00±4.80), B(81.83±3.97), C(83.58±2.61), D(92.67±2.71); 100HZ: A(227.25±7.02), B(223.00±4.79), C(217.25±4.05), D(229.08±5.55); 200HZ: A(290.42±6.60), B(285.75±9.35), C(283.75±5.01), D(295.25±6.88). There were no statistically significant differences between the experimental groups and the control group.2. In the experiment by IGF-I treatment, results(/400 light microscope field) of transaction muscle fiber counting at 40×10 light microscope showed: experimental groups:E 39.06±3.87, F 39.72±3.75, G 39.50±2.87, control group: E 33.94±3.11, F 34.83±3.13, G 35.50±2.98. Quantity of muscle fibers counting increased than that of the control group: 15.09%(E, P>0.05), 14.04%(F, P> 0.05), 11.27%(G, P > 0.05). Results ( mN/cm2 ) of muscular strength measurements showed 40HZ: experimental groups: E ( 86.44±6.44 ), F(87.78±5.19),G(84.56±6.46), 40HZ control group: E(85.67±7.25), F(82.00±6.04), G(83.11±4.78);100HZ experimental groups:E(228.11±10.71),F(223.44±11.57),G(225.44±8.22), 100HZ control group: E(226.78±3.60), F(223.44±11.57), G(228.89±5.58) ; 200HZ experimental groups: E(300.56±14.55),F(296.89±15.10),G(277.78±17.41), 200HZ control group: E(300.11±12.72), F(286.11±12.81), G(288.11±12.39). There was no significant change in muscle force generation. Results(/400 light microscope field) of Expressing PCNA showed: experimental groups: E(106.72±9.82), F(104.39±9.85), G(71.94±8.33), control group: E(63.17±4.77), F(65.56±5.67), G(59.56±6.45). In all three of experimental groups increased than that of the control: E(P<0.01), F(P<0.01), G(P>0.05). And expressions of PCNA in the group E and group F increased than that of the group G..Conclusions:1,Clamping extraocular muscle can induce the acute injury, which can be used for the establishment of an animal model for acute extraocular muscle injury.2,IGF-I effectively promotes repairing of extraocular muscle injury by protecting muscular tissue and regulating cellular proliferation. |