ObjectiveTo study the concepts and pathophysiology of intraabdominal hypertension (IAH) and abdominal compartment syndrome (ACS). MethodsRelevant information was gathered from previous original articals,and by checking the latest issues of appropriate journals. Meantime computerised MEDLINE search from 1998 to August 2001 was conducted using the Medical Subject Heading and textwords “abdominal”, “compartment syndromes”, “intraabdominal” and “hypertention” and “pressure”.Then the literature in the recent two years about the advances of IAH and ACS were reviewed. Especially the concepts, pathophysiology and clinical application of IAH and ACS were mainly summarized.ResultsAkin to compartment syndrome, the pathophysiological effects of increased intraabdominal pressure developed well before any clinical evidence of compartment syndrome. These changes included ①reduction of gastrointestinal blood flow，②increase of respiratory airway pressure whereas decrease of pulmonary compliance，③decline in cardiac output but rise in peripheral vascular pressure，④oliguria even anuria，⑤increase of intracranial pressure，⑥decrease of hepatic blood flow，⑦decrease of abdominal wall compliance.ACS can be defined as dysfunction of various organs caused by a progressive unphysiologic increase of the intraabdominal pressure. Clinically the syndrome is characterised by inadequate ventilation, tensely distended abdomen and oliguria or anuria.Early decompression by simple laparotomy and delayed closure is the treatment of choice. ConclusionThe concepts of IAH and ACS have been increasingly accepted. They mainly affects the respiratory,cardiovascular and renal systems; secondarily affect gastrointestinal, central nervous systems,liver and abdominal wall. The reduction of cardiac output and pulmonary compliance are probably promoting factors inducing organ dysfunction.
OBJECTIVE: To investigate the changes of regeneration and conduction function for peripheral nerve after neurolysis by nerve special staining and electrophysiology. METHODS: Sixty Sprague-Dawley male rats were randomly divided into four groups(n = 15), four methods were designed on rats models of sciatic nerve compression. There were simple decompression as group A, internal neurolysis after decompression as group B, lemithason(0.5 mg/kg) injected in the epineurium after decompression as group C, and lemithason(0.5 mg/kg) injected around the epineurium after decompression and internal neurolysis as group D. Motor nerve conduction velocity(MNCV) and motor latency (Lan) were monitored at 1,2,3,4,5 weeks after decompression, sections were regularly taken from the previously compressed area to perform morphometric analysis. RESULTS: After 2 weeks of decompression, the significant recovery were observed in both MNCV and Lan of four groups. Up to the 5th week of decompression, recovery of electrophysiology was significantly faster in group C and D than that of group A and B, particular in group C(P lt; 0.05), while group A compared with group B, there was no statistical difference in both MNCV and Lan(P gt; 0.05). Morphometric analysis showed that a lot of neural regeneration fibers were observed in group C and D after 3 weeks of decompression. CONCLUSION: Decompression can improve nerve conduction function significantly, while injection of lemithason in epineurium after decompression can promote the structure and function recovery of injured nerve.
The pathogenesis of diabetic retinopathy is complicated. The vast network of multiple factors including unifying mechanism, inflammatory reaction, neuron degeneration and metabolic memory of glucose, and the four established pathogenic molecular pathways are hotspots of mechanism research for diabetic retinopathy. Nevertheless, these researches may be only one corner of the ldquo;icebergrdquo; of DR mechanism, and we still face enormous challenges in DR mechanism research. Collaboration with multiple disciplines to study the relationship between DR and diabetes and other systemic diseases, search novel therapy targets may increase the result in an unexpected windfall for DR basic research.
Objective To observe the oxidative damage of mtDNA, apoptosis and expression of adhesion molecules in retinal capillary cells of diabetic rat with different disease courses. Methods One hundred Sprague-Dawley rats were randomly divided into the control group and the experimental group. The rats of experimental group were induced with streptozotocin (STZ) injection creating a diabetic model. Then they were divided into DR1m, DR2m DR3m group according to disease courses. The rats of control group were divided into NR1m, NR2m, NR3m group. Rat retinal capillaries were prepared, and then the contents of undamaged mtDNA were examined by Southern blot combined with Fpg. The expression of cyclooxygenase (COX)-1 encoded by mtDNA and transcription factors A (mtTFA) mRNA were detected by real-time quantitative polymerase chain reaction (RT-PCR). Apoptosis and expression of intercellular adhesion molecule-1 (ICAM-1) were detected by terminal dUT nick endlabeling (TUNEL) immuno-fluorescence and immunohistochemistry respectively. Results The contents of undamaged mtDNA in rats of DR1m, DR2m, DR3m were less than those of NR1m、NR2m、NR3m. The contents of undamaged mtDNA in diabetic rats decreased with the increase of disease courses. In addition, the mRNA levels of COX-1 and mtTFA were downregulated in diabetic rats. The positive cells of TUNEL and ICAM-1TUNEL and ICAM-1 in diabetic rats increased with the increase of disease courses. Conclusion With the increase of disease courses, mtDNA damage and apoptotic cells are increased, while the expression of mRNA encoded by mtDNA and ICAM-1 decreased in retinal capillary cells in diabetic rats.
Objective To observe the expression of cyclin dependent kinase 5 (Cdk5) and p25 in the pathogenesis of retinitis pigmentosa (RP) in Royal College of Surgeon (RCS) rats and its relationships with apoptosis. To explore the mechanism of Cdk5 and p25 induced photoreceptor apoptosis in the pathogenesis of RP. Methods Retinas of RCS and RCS-rdy+ rats were obtained at the ages of postnatal day 17, 25, 35, 60. The retinal structure and thickness of outer nuclear layer were measured by optical microscopy. The expression of Cdk5, p25, cleave-caspase 3 in the retina was evaluated by immunohistochemistry. The protein expression of cleave-caspase 3 in the retina was determined by Western blot. The apoptosis of retinal cells was examined by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL). The mean absorbance value of apoptotic cells was analyzed by SPSS 17.0 software. Results The retinal thickness of the RCS rats was significantly reduced in comparison to the RCS-rdy+ rats as the postnatal days progressed, particularly in the layer of rods and cones and the outer nuclear layer. The expression level of Cdk5, p25, cleave-caspase 3 of RCS rats increased from postnatal 17 days to postnatal 35 days, while decreased on postnatal 60 days; but there was no obvious change of above indexes in RCS-rdy+ rats. The protein expression of cleave-caspase 3 in the RCS rats was significantly increased with progression of postnatal days to postnatal 35; but there was no obvious similar change in RCS-rdy+ rats. The results of TUNEL showed that the apoptotic cells significantly increased in the outer nuclear layer of RCS rats from postnatal 17 days to postnatal 35 days, while decreased on postnatal 60 days; but there was no obvious change of above index in RCS-rdy+ rats. This study showed that there were significant correlations between the following variables: Cdk5 expression and p25 expression, Cdk5 expression and cleave-caspase 3 expression, Cdk5 expression and apoptotic cells, p25 expression and cleave-caspase 3 expression, p25 expression and apoptotic cells, cleave-caspase 3 expression and apoptotic cells. The partial correlation coefficients were 0.949, 0.808, 0.959, 0.887, 0.979, 0.852, respectively and the P value was 0.000. Conclusions The apoptotic cells significantly increases and the expression level of Cdk5, p25, cleave-caspase 3 of RCS rats increases from postnatal 17 days to postnatal 35 days. The tendency of apoptotic cells to increase is consistent with the change of Cdk5, p25, cleave-caspase 3 expression. The apoptosis of photoreceptor cells is related to increasing expression of Cdk5 and p25 in RCS rats. Cdk5 may be involved in the development of RP in RCS rats.
Objective To observe the effect of ginsenoside Rg3 on the proliferation, migration, and tube formation of human retinal capillary endothelial cell (HRCEC) cultured in normal and hypoxia condition. Methods HRCEC was cultured in normal condition and treated with 0.0 mmol/L (group A), 0.1 mmol/L (group B) and 0.5 mmol/L (group C) ginsenoside Rg3. HRCEC was also cultured in hypoxia condition and treated with 0.0 mmol/L (group D), 0.1 mmol/L (group E) and 0.5 mmol/L (group F) ginsenoside Rg3. The effects of ginsenoside Rg3 on HRCEC proliferation were measured by methylthiazoletrazolium assay in 24, 48 and 72 hours after culture. In 24 hours after culture, the effect of cell migration was evaluated by transwell chamber; the effect of tube formation was evaluated by Matrigel; the expression of vascular endothelial growth factor (VEGF) protein and mRNA were detected by Western blot and real-time quantitative reverse transcription-polymerase chain reaction. Results Ginsenoside Rg3 could inhibit proliferation of HRCEC, depending on the concentration (F=30.331 and 33.402 in normal and hypoxia condition, respectively; P＜0.05) and time (F=85.462 and 136.045 in normal and hypoxia condition, respectively; P＜0.05). The number of cell migration was 103.33plusmn;3.54, 92..25plusmn;3.68, 78.64plusmn;4.66 in group A, B and C, the difference among three groups was statistically significant (F=28.801, P＜0.05). The number of cell migration was 125.76plusmn;3.11, 90.27plusmn;3.55, 77.81plusmn;5.01 in group D, E and F, the difference among three groups was statistically significant (F=117.594, P＜0.05). The number of tube formed in Matrigel was 24.3plusmn;2.2, 15.7plusmn;1.7, 10.1plusmn;2.3 in group A, B and C, the difference among three groups was statistically significant (F=35.364, P＜0.05). The number of tube formed in Matrigel was 26.2plusmn;1.9, 15.1plusmn;2.6, 8.6plusmn;1.9 in group D, E and F, the difference among three groups was statistically significant (F=50.989, P＜0.05). The expression of VEGF mRNA was 1.00plusmn;0.06, 0.79plusmn;0.06, 0.68plusmn;0.02 in group A, B and C, the difference among three groups was statistically significant (F=31.303, P＜0.05). The expression of VEGF mRNA was 3.88plusmn;0.12, 2.83plusmn;0.09, 1.15plusmn;0.05 in group D, E and F, the difference among three groups was statistically significant (F=682.668, P＜0.05). The expression of VEGF protein was 0.62plusmn;0.03, 0.41plusmn;0.02, 0.32plusmn;0.02 in group A, B and C, the difference among three groups was statistically significant (F=125.471, P＜0.05). The expression of VEGF protein was 0.91plusmn;0.03, 0.82plusmn;0.03, 0.71plusmn;0.02 in group D, E and F, the difference among three groups was statistically significant (F=41.045, P＜0.05). Conclusion Ginsenoside Rg3 can inhibit the proliferation, migration, and tube formation of HRCEC through the inhibition of VEGF expression.
Objective To observe the retinal apoptosis of laser-induced retinal injury in mice after bone marrow mesenchymal stem cells transplantation. Methods Green fluorescent protein (GFP) labeled MSCs from C57BL/6 mice were cultured in vitro. A total of 135 C57BL/6 mice were divided into three groups including normal control group (15 mice), injured control group (60 mice) and MSCs treatment group (60 mice). Laser retinal injuries were induced by laser photocoagulation. One day after photocoagulation, 02 ml cell suspension, which contained 1times;106 GFP-MSCs, were injected into the mice in treatment group via tail vein, and the mice in injured control group were given equal volume of phosphate buffer solution. Animal were execute on three, seven, 14 and 21 days following laser damage. Hematoxylin and eosin (HE) staining was performed to assess the changes of injured retinas. The diameters of laser spots and areas with total loss of cells in outer nuclear layer (ONL) were analyzed by image processing software. The apoptosis of retinal cells was examined by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) staining. The migration of GFP-MSCs into the retina was observed by fluorescence microscope. Results HE staining showed that the retinal structures were integrated in normal control group. Retinal damages were observed both in injured control group and MSCs treatment group, but milder in the latter. Though the average diameter of area with total loss of cells in ONL of MSCs treatment group was less than the injured control group (t=5.769, P＜0.05), the diameters of laser spots show no difference (t=0.964,P＞0.05) on day three. Both the average diameter of laser spots (t=5.180, 5.417, 2.381) and area with total loss of cells in ONL (t=3.530, 3.224, 3.162) were less in the MSCs treatment group on day seven, 14 and 21 (P＜0.05). TUNEL staining shows that the apoptosis were decreased after MSCs transplantation on day three, seven, 14 and 21 (t=11.142, 7.479, 6.678, 3.953,P＜0.05). No apoptosis was observed in normal control group. Very few GFP-MSCs were observed in the retina at all time-points. They were only seen in the subretinal and choroidal neovascularization occasionally on day seven and 14. Conclusion MSCs transplantation can effectively limit the range of retinal laser damage and inhibit cell apoptosis.
Objective To observe the expression of vascular endothelial growth factor receptor-1 (VEGFR-1) and VEGFR-2 in hypoxic chorioretinal endothelial cells of monkeys (RF/6A), and to evaluate the effect of minocycline. Methods RF/6A was cultured and divided into four groups: control group, hypoxia group, hypoxia and low dose of minocycline group (0.5 mu;mol/L), hypoxia and medium dose of minocycline group (5 mu;mol/L), and hypoxia and high dose of minocycline group (50 mu;mol/L). Real-time reverse transcriptionpolymerase chain reaction (RT-PCR) and immunohistopathological staining were used to measure the mRNA and protein expression of VEGFR-1 and VEGFR-2, respectively. Results RT-PCR showed that the expression of VEGFR-1 mRNA did not vary significantly between groups (F 24 h=0.17,F 48 h=1.53,F72 h=2.04;P＞0.05). Compared with hypoxia group, the expression of VEGFR-2 mRNA in all minocycline treated groups were significantly downregulated (low minocycline, medium minocycline, high minocycline: t=4.69, 20.16, 17.12; P＜0.001). The immunohistopathological study showed the cells with positive staining of VEGFR-1 can be observed in all groups, and the staining was relatively weak and mainly located in cell membrane and cytoplasm. The optical density value analysis showed that the protein expression of VEGFR-1 did not vary significantly between groups at all time points（F 24 h=0.251,F 48 h=0.340,F72 h=0.589;P＞0.05）. The VEGFR-2 positive staining cells were also observed in all groups, and the staining was relatively high. Brown staining particles of VEGFR-2 were observed in the cell membrane with minor staining particles in cytoplasm. The staining density of VEGFR-2 was significantly higher in hypoxia group than control group. Compared with the hypoxia group, the protein expression of VEGFR-2 in minocycline treated groups was significantly lower（F 24 h=19.147,F 48 h=14.893,F72 h==11.984; P＜0.05). Conclusion The expression of VEGFR-2 is upregulated in RF/6A, and minocycline somewhat shows an inhibition effect.