| Background: Carbon monoxide is a colorless and odorless gas,it is the most common gas that can induce asphyxia. The population of carbon monoxide poisoning and the dead after carbon monoxide poisoning lists the first place among all poisoning in our country. Especially delayed encephalopathy after carbon monoxide poisoning (DEACMP) will happen to some people after carbon monoxide poisoning. Because the clear pathogenesis of the disease has not been discovered until now, there are many kinds of hypotheses. There is no effecive way inclinical treatment. Among the many hypotheses, hypoxic-ischemic mechanism play an important role in exploring the mechanism of brain injury of carbon monoxide poisoning. In recent years, many studies showed the existence of brain injury of the neorascularization phenomenon in the surrounding region of ischemia. It is important for the survival of the hypoxic-ischemic neurons after carbon monoxide poisoning.CD34 antigen is a hallmark of detecting the angiogensis, it can selectively express in human and mouse hematopoietic stem cells/progenitor cells but also in vascular endothelial cells and other tissues.It can adhess and accelerate the accumulation of vascular endothelial precursor cells for the formation of blood vessel, and control the proliferation and differentiation of hematopoietic cells It can be used to measure the density and size of the microvascucar in tumor and ischemia tissue, it can detect the formation of new microvascular. CD133 is a new hematopoietic cells It can be used to measure the density and siza of the microvascucar in tumor and ischemia tissue, it can detect the formation of new microvascular.CD133 is a new hematopoietic stem progenitor cell glycoprotein antigen, it selectively express in the bone marrow and peripheral blood stem cell and endothelial precursor cells, but it doesn't express in mature endothelial cells. Thus CD133 can be used as the surface markers of vascular endothelial precursor cells. EPC is a kind of stem sell, they can update by themselves and proliferate into endothelial cells. It is a very important role of promoting the formation of new blood vessels and making injured blood vessels to reendothelialization. EPC can home to ischemic and involve in angiogenesis site, increase blood flow to protect endorgan. There were no literatures about CD133 and CD34 expressing in mice brain tissues after carbon monoxide poisoning. We observe the expression of CD34 antigen and CD133 antigen in the mice brain tissue after carbon monoxide poisoning ,study the effect of carbon monoxide poisoning to endothelial precursor cells, speculate the role of the formation of the new blood vessels in DEACMP.Objective: In this experiment, we observe the effect of carbon monoxide poisoning to the brain vascular endothelial systems in the level of animal, provide new ideas for prevention and treatment to clinical acute carbon monoxide poisoning and DEACMP.Methods: 108 healthy Kunming male mouse, were divided into Air control group, Carbon monoxide poisoning group,54mouse in every group. Each group is divided into nine sub group, as follows:6h,1d,2d,3d, 4d,7d,14d,21d,28d groups, 6 mouses in every group. Carbon monoxide poisoning model of mouse was established with intraperitoneal injection. We check the brain tissue of mouse in each group according to every time point. Observing the ultrastructure of capillary endothelial cells by electron microscopy. Observing neovascularization of mouse tissue by HE, count the formation of vascular cavities and no significant muscular vessel wall of the microvessel count. All datas were expressed by mean±sd, statistical analysis software of SPSS13.0 t-test was employed. P<0.01 is statistical different.Result:1.In air control group, no positive expression of CD34.In carbon monoxide poisoning group,CD34 positive microvessels can be seen in hippocampus of mice brain vascular endothelial cells. In 28 days,CD34 showed changes in two stages in carbon monoxide poisoning group: apearing a peak in 1d-2d once, a peak in 4d-7d twice. The level of CD34 down in the stage of 14d-28d.Each time point with the control group had significant difference.2.In air control group, no positive expression of CD133.In carbon monoxide poisoning group. Expression of 6h group is more active,1d-3d group down,4d-7d group increase to a peak.14d-28d group down. Each time point with the control group had significant difference.3.By light microscope, we can see brain edema ,increased perivascular space, nerve cells around the gap widened, focal ischemic softening, blood cell overflow, neuronal apoptosis, inflammatory cell infiltration. Neurons structure is normal in the control group.4.By light microscope, we can see their are more microvessel in carbon monoxide poisoning group than control group.7d-14d increase obviously, reach to a peak,14d slowly decline. The general trend is that microvessel counts increase within 28 days.6h,1d,2d,3d groups are no significant different with the control group. The rest of the time points are different statistically with the control group.Conclusion:1.We observe in hippocampus of mice brain vascular endothelial cells in the cytoplasm positive for CD34 antigen expression, suggesting new angiogenesis in the brain after carbon monoxide poisoning.2.We observe in hippocampus of mice brain vascular endothelial cells in the cytoplasm positive for CD133 antigen expression, suggesting the mice's own EPC participate in the composition of local vascular endothelial and vascular construct after carbon monoxide poisoning.3.HE staining for microvessel count, it shows that their are more microvessel in carbon monoxide poisoning group than control group. |
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