ABSTRACT
Objective To explore the effects of hyperbaric oxygen preconditioning on ischemia-reperfusion inflammatory reaction of rats after skin flap transplantation.Methods Fifty-six Sprague-Dawley rats were randomly divided into 3 groups:a sham ischemia-reperfusion (SH) group,an ischemia-reperfusion (IR) group and a hyperbaric oxygen reconditioning (HBO) group.Both IR group and HBO group were further divided into 3 subgroups,respectively,according to the time points of serum sampling for test post establishment of the IR model of the abdominal pedicle skin flap transplantation.The IR model of the abdominal pedicle skin flap transplantation was established in all the animals except those in the SH group,with those in the HBO group were preconditioned with HBO twice daily for 3 days before the operation.The blood was sampled at 1,3 and 5 day post-operation to test the level of IL-23 using enzyme-linked immunosorbeut assay (ELISA).The survival skin flaps were sampled from all the animals at 3 and 5 days after the operation for histological observation and evaluation.Results The average IL-23 level of HBO 3 d subgroup (17.80 ± 14.78) was significantly lower than that of the IR 3 d subgroup (38.91 ± 12.26).The average histological scores of the IR 3 d and 5 d subgroups,as well as HBO 3 d and 5 d subgroups were (2.66 ±0.44)and (3.2 ±0.53),(1.85 ±0.31) and (2.29 ±0.32),significantly higher than SH group (0.38 ±0.10).Moreover,the average histological score of the HBO 3 d and 5 d subgroups was significantly lower than IR 3 d and 5 d subgroups respectively.Conclusion Hyperbaric oxygen preconditioning can relieve the ischemia-reperfusion inflammatory reaction through reducing the serum level of IL-23 in rats after skin flap transplantation.
ABSTRACT
Objective To observe the effects of hyperbaric oxygen (HBO) exposure on the expression of aquaporin-1 (AQP1) and aquaporin-5 (AQP5) in rats with simulated high-altitude pulmonary edema (HAPE).Methods Fifty-six rats were randomly divided into five groups:control (normal),HAPE (high altitude pulmonary edema model),1 HBOT (HAPE model and HBO therapy for 1 time),2 HBOT (HAPE model and HBO therapy twice) and NOT (normal pressure oxygen therapy) groups,and was intervened accordingly.Western blotting and real-time PCR techniques were used to analyze the expression of AQP1 and AQP5 in their lungs.The wet-todry (W/D) weight ratio and morphology of the lungs was also examined.Results The protein and gene expression of AQP1 and AQP5 in the HAPE group decreased significantly compared with the control group.There were obvious differences in the protein and mRNA expression of AQP1 and AQP5 between the 2 HBOT group and the HAPE group and between the 2 HBOT group and the 1 HBOT group.Compared with the control group and the 1 HBOT group,marked lung injury could be seen in the HAPE group.Compared with the NOT group and the 1 HBOT group,lung injury in the 2 HBOT group was relieved significantly.Conclusions HAPE in rats is associated with down-regulation of the expression of AQP1 and AQP5 in the lungs.This down-regulation can be attenuated and lung injury can be alleviated by HBOT.Two sessions of HBOT could be more helpful than one for promoting this improvement.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate cardiac function and myocardial perfusion during 48 h after cardiopulmonary resuscitation (CPR), further to test myocardial stunning and seek indicators for long-term survival after CPR.</p><p><b>METHODS</b>After 4 min of untreated ventricular fibrillation, fifteen anesthetized pigs were studied at baseline and 2 h, 4 h, 24 h, and 48 h after restoration of spontaneous circulation (ROSC). Hemodynamic data, echocardiography and gated-single photon emission computed tomography myocardial perfusion images were carried out.</p><p><b>RESULTS</b>Mean arterial pressure (MAP), coronary perfusion pressure (CPP) and cardiac troponin I (CTNI) showed significant differences between eventual survival animals and non-survival animals at 4 h after ROSC (109.2 ± 10.7 mmHg vs. 94.8 ± 12.3 mmHg, P=0.048; 100.8 ± 6.9 mmHg vs. 84.4±12.6 mmHg, P=0.011; 1.60 ± 0.13 ug/L vs. 1.75 ± 0.10 ug/L, P=0.046). Mitral valve early-to-late diastolic peak velocity ratio, mitral valve deceleration time recovered 24 h; ejection faction and the summed rest score recovered 48 h after ROSC.</p><p><b>CONCLUSION</b>Cardiac systolic and early active relaxation dysfunctions were reversible within survival animals; cardiac stunning might be potentially adaptive and protective after CPR. The recovery of MAP, CPP, and CTNI could be the indicators for long-term survival after CPR.</p>
Subject(s)
Animals , Male , Blood Pressure , Cardiopulmonary Resuscitation , Coronary Circulation , Heart Arrest , Hemodynamics , Myocardial Contraction , Physiology , Myocardial Stunning , Swine , Time Factors , Ventricular FibrillationABSTRACT
Objective To study the effect of preconditioning hyperbaric oxygenation on skin flap is-ehaemia tolerance. Methods 18 male SD rats were divided into the control and HBO preconditioning groups. In control group, an extended epigastrie adipocutaneous flap was raised, based on the right su-perficial epigastric artery and vein. 3-hours flap ischemia was induced by clamping the pedicle vessels with microvascular clamp. At the end of ischemia induction, the clamp was removed and the flap was sutured back. Rats in HBO preconditioning group were treated with HBO two days before operation. Flap surger-y began 1 hour after the last HBO treatment. The operation was the same as the control group. On the fifth postoperative day, the condition of the flap was recorded with transparent paper. Mean flap necrosis area was calculated with Acrobat software. Data were analyzed with SPSS software. Results The aver-age designed flap area was (51.59±6.62)cm2 and (52.71±2.05)cm2 in the control group and the HBO preconditioning group. The average flap survival area was (7.38±2.49)cm2 and (15.82±5.95)cm2. The difference was significant between the control and HBO preconditioning groups (t= 4. 14, P<0.01) in average flap survival area. Conclusion HBO preconditioning can rise flap ischaemia tolerance and enhance flap survival.
ABSTRACT
BACKGROUND: Gene chip of expression spectrum is used to make contrastive analysis of the changes of gene expression of histocytes derived from different individuals, tissues, cell cycles, developmental stages, differentiating stages, physiological and pathological status, and stimulating conditions.OBJECTIVE: To investigate gene expression changes of cerebral tissues of mice at different phases after ischemia/reperfusion injury, and screen out and understand genes related to cerebral ischemic/reperfusion injury.DESIGN: A randomized and controlled animal study.SETTING: Laboratory of the Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital affiliated to Capital University of Medical Sciences;Laboratory of Shanghai Biostar Gene Chip Co., Ltd.MATERIALS: The experiment was performed in the Laboratory of Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital affiliated to Capital University Medical Sciences, and the Laboratory of Shanghai Biostar Gene Chip Co., Ltd. from September 2002 to October 2003. Totally 20 male mice of C57BL/6 species were selected and randomized into 4 groups with 5 in each group: 48-hour and 10-day sham-operation groups and 48-hour and 10-day cerebral ischemia-reperfusion groups.METHODS: The bilateral common carotid arteries of mice in cerebral ischemia/reperfusion group were blocked with clamp for 20 minutes to establish models of cerebral ischemia/perfusion injury. The bilateral common carotid arteries of mice in sham-operation group were separated without clamp. We killed the mice by breaking off their necks at the 48th hour and 10th day after operation. Expression changes of cerebral tissues of mice were detected with BiostarM-20 s gene chip of expression spectrum.MAIN OUTCOME MEASURES: Changes of gene expression of cerebral tissues of mice in each group.RESULTS: A total of 20 mice were involved in the result analysis. ①Differential expression gene in 48-hour sham-operation group and 48-hour cerebral ischemia/reperfusion group showed that the number of up-regulated expression genes was 30. Among them the most obvious up-regulated gene was related to DNA synthesis, repair and transcription. The number of down-regulated expression genes was 119. Among them the most obvious down-regulated gene was protein phosphatase 1 (PP1) gene related to cellular signal and transferrin protein. ② Differential expression gene between 10-day sham-operation group and 10-day cerebral ischemia/reperfusion group showed no up-regulated gene, but 7 down-regulated genes, and the most obvious down-regulated gene was the one that related to cell apoptosis.CONCLUSION: At the 48th hour after cerebral ischemia/reperfusion, upregulated gene is the one that related to DNA synthesis, repair and transcription, which is helpful for cerebral tissue repair after cerebral ischemia/reperfusion. Genes related to cell signal and transferrin are down-regulated, and can level off barrier of endothelial cells and relieve cerebral ischemia/reperfusion injury. At the 10th day after cerebral ischemia/reperfusion, cell apoptosis-related gene is down-regulated, and can accelerate apoptosis and aggravate injury of cerebral cells, which may be related to delayed neuronal necrosis.
ABSTRACT
Objective To observe the effects of rapid decompression on serum level of IL-1?,IL- 6 and IL-10 in mice and investigate the role of cytokines in the pathogenesis of decompression sickness. Methods Twenty-one mice were randomly divided into rapid decompression group (14 mice) and normal control group (7 mice). Mice in the rapid decompression group were exposed to 600kPa compressed air for 60 minute,which was then rapidly decompressed to normal pressure in one minute. The serum level of IL-1?,IL- 6 and IL-10 was measured by enzyme-linked immuno-sorbent assay in mice in rapid decompression group after decompression and in normal control group. Results There were no significant changes in the serum level of IL-1?,IL- 6 at the 1st hour after decompression in the rapid decompression group when compared to that of and the normal control group. The serum level of IL-1?,IL- 6 in rapid decompression group at the 3rd hour after decompression was significantly higher than that of the normal control group(P