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 super thin skin flaps were designed on the abdominal wall of pig.The flap were divided into6 groups. The general oppoarances,such as the color,swelling,survival of the flaps,and the bloodflow measurement of the flape were used to oherve the postoperative pathophysiology changes of theblood supply of the flaps.It、was noted that:(1)the blood flow of the flape Was increasedcompensatorily as early as 3 days after oporation and reached its highest on 5th to 7th days,thers wasgradually ...
Objective To investigate the possible effects of phosphorylated signal transduction and activator of transcription3 (STAT3) in the formation of choroidal neovascuarization (CNV) induced by photocoagulation in rats. Methods The CNV model in rats induced by photocoagulation was established, and the expression of phosphorylated STAT3 at the early stage in CNV were observed by immunofluorescence. To set up the hypoxia model, the specific inhibitor of Janus kinase 2 (JAK2), AG490 was mixed into cell culture fluid and then cultured for 0,1 hour,3,6,12,and 24 hours.Retinal pigment epithelial (RPE) cells proliferation activity were detected by flow cytometry (FCM).the expression of hypoxiainducible factor (HIF)1α and vascular endothelial grow factor (VEGF) mRNA were detected by reverse transcriptase polymerase chain reaction (RT-PCR); the expression of HIF1α protein was detected by Western blot; the content of VEGF in the supernatant of cell culture fluid was measured by enzyme linked immunosorbent assay (ELISA). Results Phosphorylated STAT3 highly expressed in CNV areas in rats 3 days after the photocoagulation. The proliferation activity of human RPE cells under hypoxia condition significantly decreased after inhibition of JAK2/STAT3 signal transduction pathway (t=1.472, 3.566,2.391,6.420; P=0.054,0.038,0.042,0.016). The expression of HIF-1α and VEGF mRNA increased gradually with increasing time of hypoxia;while the expression of HIF1α and VEGF mRNA and the activation of HIF1α protein in cultured human RPE cells with the JAK/STAT3 signal transduction pathway blocked by AG490 were suppressed obviously under hypoxia condition (t=0.07,0.02,0.01, P<0.05); the content of VEGF in RPE cells supernatant decreased significantly (t=1.330,1.106,2.828,7.742,5.610,6.894; P=0.082,0.063,0.014,0.002,0.016,0.011). Conclusion STAT3 may be involved in CNV formation, which may partly dependent on JAK2/STAT3 signal transduction pathway regulating the expression of HIF-1α and VEGF in RPE cells.
Objective To explore the feasibility of the Budd-Chiari syndrome model establishment in rat by using the inferior vena cava coarctation. Methods Fifty SD rats were randomly divided into experimental group and sham operation group， the laparotomy was performed after general anesthesia by intraperitoneal injection， and dissociated the inferior vena cava. In the experimental group， the vena cava was tightly ligated with silk thread according to partial portal vein coarctation， enclosing 23 G L-style blunt needle in the ligature to prevent complete obliteration. The diameter of the vena cava was set to about 80% of its normal size after removing the 23 G L-style blunt needle. The abdominal Doppler， liver function， blood routine examination， and liver biopsy were tested at different time （on week 1， 4， 8， and 12） after operation. Results The signs of inferior vena cava and primary hepatic venous obstruction， liver congestion and cirrhosis， ascites， hepatosplenomegaly， portal vein extension， and collateral patency occurred on week 4 in the experimental group. The levels of AST， ALT， AKP， TBIL， DBIL， and TBA in the experimental group were significantly higher than those in the sham operation group （P＜0.05）， and the WBC， PLT， RBC， HGB， and ALB in the experimental group was significantly lower than those in the sham operation group （P＜0.05）. Conclusion The inferior vena cava coarctation can be successfully used to establish a rat model of Budd-Chiari syndrome.
ObjectiveTo retrospective analysis the research progress of the acute-on-chronic liver failure (ACLF), and provide some useful advice for the early diagnosis, evaluation, and treatments of ACLF. MethodsThe literatures on ACLF which published in domestic and overseas for these years were reviewed. ResultsACLF, which is an acute deterioration of liver function results from precipitating events in patients with chronic liver disease. As an independent clinical entity and different from acute liver failure (ALF), sub-acute liver failure (SALF), and chronic liver failure (CLF). For the high short-term mortality and seldom good treatment measures, attached much people's attention. ConclusionThe research of ACLF makes great advance but still exits different in some field between the East and the West. Search dangerous etiology earlier, combine with reality and early effective treatments can develop total survival rate of ACLF.
Central serous chorioretinopathy (CSC) is one of the representative pachychoroid spectrum disease. Although fundus fluorescein angiography and indocyanine green angiography can be used as the gold standard for the diagnosis of CSC, they are invasive examinations, which may bring certain risks in clinical application and cannot help us obtain quantitative parameters. Optical coherence tomography angiography (OCTA), as a non-invasive and quantitative examination, is an important imaging tool for understanding the pathogenesis, diagnosis and treatment of CSC. With the advancement of OCTA, the swept-source OCTA has a satisfying scanning depth, a wider scanning range and a higher resolution. The development of OCTA broadens the horizons of the pathogenesis of CSC, promotes the understanding of the pathophysiology of CSC, and sheds new light for its clinical diagnosis and treatment. Based on OCTA, the choroid and retina in eyes with CSC are presented with qualitative and quantitative changes in vascular system. OCTA-guided CSC treatment and the discovery of prognostic markers based on OCTA challenge the application of traditional imaging techniques in CSC. With the continuous improvement and progress of OCTA technology, traditional angiography combined with OCTA will bring great benefits to the diagnosis and treatment of CSC. This review summarizes the quantitative application of OCTA in the pathogenesis, diagnosis and treatment of CSC.