| Background: Carbon monoxide is a colorless, odorless, toxic gas, which is the production environment and living environment up to see the asphyxiating gas. Acute carbon monoxide poisoning is the largest number of morbidity and mortality of acute occupational poisoning. ACOP can cause the body after multiple organ damage, of which the most severe brain involvement.Some patients a few days or weeks after the performance of normal or near normal "false Overdue", will appear again to acute dementia, a group of mainly neurological, psychiatric symptoms, known as delayed encephalopathy(delayed encephalopathy after acute carbon monoxide poisoning, DEACMP), which is the most serious type of CO poisoning, some patients left permanent neurological damage. The clinical manifestation is a series of spirit and nerve function disorder, especially acute stupid primarily energetic. Even part of the permanent neurological damage in patients with left. Because the clear pathogenesis has not been discovered, there`s no effective way in clinical treatment of DEACMP and repressor the happening trend. In recent years, caused by CO poisoning caused by vascular changes in the increasing attention of scholars.α-actin in vascular smooth muscle cell is an important functional proteins,which is specifically expressed in the VSMC.α-actin expression in VSMC for the prompt changes in the structure and function is very important, it is a sign of VSMC phenotypic. When the number ofα-actin decreased, the synthesis of the dominant type of smooth muscle cells, cell synthesis and secretion and the added value is very strong, can lead to vascular stenosis or occlusion.Ⅳcollagen and elastin in the vessel wall is an important component of the extracellular matrix.Ⅳcollagen constitutes the main component of basement membrane, Recently some scholars have smaller arteries in the glass-like outer layer of the middle and found abnormal accumulation ofⅣcollagen. Main components of elastic fiber elastin or elastic membrane, the blood vessels flexible. Many studies have found a variety of cerebral vascular diseases are associated with typeⅣcollagen and elastin changes.β-amyloid protein in normal neural cells and non-neuronal cells continuously secreted to the extracellular release into the blood and cerebrospinal fluid, in exceptional cases deposited on the wall of small blood vessels, can cause vascular amyloidosis; deposition Substance into the brain senile plaques that can lead to Alzheimer's disease. The abnormal expression of several substances not only cause the abnormal changes of the vascular wall structure, but also lead to a small artery on the nervous control and regulate biochemical reactions diminished capacity, which led to a series of vascular diseases.Objective: In this study, based on animal experiments, based on the dynamic observation of CO poisoning,α-actin,Ⅳcollagen, elastin,β-amyloid protein changes and histopathological changes in the brain. CO poisoning of the structure of brain tissue changes of the vascular wall, may elucidate the pathogenesis of DEACMP provide clues, but also for the treatment of vascular intervention DEACMP provide the experimental basis.Methods:Health Kunming male rats 108, weight 180-220g, and then randomly divided into 2 groups that a balanced air control group and the control group, all 54. Each group has 9 sub-groups (time points):6 hours (h),1 day (d),2d,3d,4d,7d,14d,21d,28d, each sub-group of 6 rats. Intraperitoneal injection with a single exposure to CO poisoning in rats was established by the control group were injected with equal amount of air. To model it after the perfusion fixed at each time point, and then to the brain tissue. Immunohistochemical detection basal gangliaα-actin,Ⅳcollagen, elastin,β-amyloid protein changes; conventional HE staining and morphological changes in brain pathology, and small vessels were counted; electron microscope vessel diameter and vessel wall observed ultrastructural changes. Data presented as mean±standard deviation, statistical analysis software used SSPS13.0 statistics, P<0.05 was statistically significant, P <0.01 are statistically significant.Result:1. By light microscope, brain edema, blood vessels around the gap increases, a red blood cell overflow. Intima of small arteries can be seen later become rough, irregular wall thickening, vessel lumen narrowed. By electron microscope, shows the late vascular smooth muscle cells increased, increasing the oval cells, the cell rough endoplasmic reticulum 2. Early poisoning group no significant changes, starting from the 14d group and the outer diameter of 30-50μm and 50-100μm small vessel's SI began to increase. compared with the control group there was statistically significant (P <0.05). The diameter> 100μm full of small vessel's SI in poisoning compared with the control group were not statistically significant. Hardening of the arteries of different diameter have significantly different index, diameter of blood vessels for the 30-50μm diameter SI higher than the other two vessels(P﹤0.05).3. Compared with the control group, early after poisoning the expression ofα-actin decreased,2d group' expression reach the minimum, 3d group expression was increased, to the 21d group reached the peak when the PU. Exposed group 2d,21d,28d of the PU with the control group was statistically significant difference (P <0.05).4. Compared with the control group, early poisoning group of collagenⅣPU values decrease, 4d the lowest, followed by the rise to the highest 28d. Exposed group 4d,21d,28d PU three time points difference with the control group was statistically significant(P <0.05).5. In poisoning group, 3d group began to appear when the brain parenchymalβ-amyloid protein expression, 7d group when the highest expression intensity, and then began to decrease expression to 28d group when disappeared. No expression in the control group. Exposed 3d,4d,7d,14d,21d group's expression difference with the control group was statistically significant(P﹤0.05).6. In poisoning group and control group were very low elasticity of protein expression. Comparison between the two was no significant difference(P﹥0.05).Conclusion:1. CO poisoning of small blood vessels in rat brainα-actin and typeⅣcollagen changes, suggesting a smooth muscle cell proliferation and typeⅣcollagen, indicating that the rat brain after CO poisoning, pathological changes in small artery hyalinosis for the class, And the smaller the diameter of small arteries, vascular wall thickening is more obvious.2. In this study, CO poisoning, first discovered in rat brainβ-amyloid protein expression, and its peak after the exposure to 14d group, speculated that CO poisoning may be delayed encephalopathy andβ-amyloid Abnormalities related to the rise. |
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