| IntroductionThere are inflammatory reactions in the brain tissue around the hypertensive intracerebral hematoma. These reactions are related to brain cell injury, and influences the scope and degree of brain cell injury greatly. Cell adhesion molecule (CAM) is a kind of glycoprotein, located on cell membrane surface, functioning as an adhesive which regulate the combination between cells, and between cell and extracellular matrix. ICAM — 1 is the first identified ICAM. The prerequisite of inflammation of brain tissue around hematoma due to hypertensive intracerebral hemorrhage is inflammatory cells adhere to vascular endothelial cells, the process of which adhesive molecules are critical to adhesive mediation , and ICAM — 1 is pivotal. In a normal physical condition of central nervous system, ICAM -1 has low expression, but when there is a intracerebral hemorrhage , endothelial cells upgrade the expression of ICAM - 1, which is important to the leukocyte adhesion and a necessary process enhancing leukocytes' transfer through endothelium, and accelerates development and progression of brain injury. ICAM - 1 is able to adhere leukocytes to vascular endothelial cells and to develop them into an activated leukocytes, it is also able to produce large a-mount of protein hydrolases, especially those of matrix metalloproteinase, oxygen free radicals and some products of arachidonic acid, which increase permeability of blood - brain barrier resulting in vasculargenic brain edema and secondary brain injury. Using immunohistochemistry, we studied ICAM -1's expression and its significance in brain tissue around hypertensive intracerebral hematoma and in normal brain tissue.MaterialsClinical specimen included 30 patients of acute hypertensive intracerebral hemorrhage who had an open skull hematoma excision in Shenyang Brain hospital from december 2004 to may 2005, and the time from disease occurrence to specimens taken differed from 4 to 12 hours. Trail team included the brain tissues close to hematoma due to intracerebral hemorrhage and control team included relatively normal brain tissues on the surgical route.Major reagents: (1) Instantaneous immunohistochemistrical reagent box of ICAM - 1 of rabbit - anti - human monoclonal antibody. (2) SABC reagent box. ( 3 ) DAB coloration reagent box, all the above were brought from BOSTER,Wuhan company.MethodThe tissues taken in the surgeries for pathological diagnosis were fixed, buried by wax and sectioned, and were dyed by HE and immunohistochemistry, immunohistochemistrical dyeing was according to the dyeing procedure given by BOSTER,Wuhan company.Conclusion identification using immunohistochemistrcial method;positive cells were those whose cytoplasm exist specific yellow - brown granules and the number of positive cells was counted by multimedia chromatic pathologic microscopic picture analytic system MetaMorph/C5050/BX41.Statistical Management;used SPSS software for statistical management, measurement data taked the form of mean number ± standard difference (x ± s) , and compared trail team and control team with t test, P < 0. 01 had statistical significance.ResultsThis research showed that in trial team, there were ICAM -1 expression inbrain tissue around hematoma and collective expression of neuron, vascular en-dothelial cell, among these, neuron was more obvious. The expression of ICAM - 1 has a distinct up - regulation in trial team that was much higher than control team.DiscussionResearch data illustrate that there are large amount of ICAM - 1 expression in neurons around the hematoma due to hypertensive intracerebral hemorrhage. This over - expression of adhesion molecules mediate the immunologic and inflammatory reaction of hemorrhagic areas, and the inflammation participates secondary brain injury and brain edema. The positive cells accompanying the expression of ICAM — 1 in neurons appear 12 hours after disease occurrence, peak 3 days later, last for 10 days and reduce gradually. The positive cells accompanying the expression of ICAM — 1 in vascular cells appear 24 hours, peak in 7 days, last for about 14 days and reduce gradually. As it comes to the time, the expression of ICAM -1 is greatly related to the infiltration of leukocytes, that is ICAM - 1 expresses early than leukocytes infiltrate. It is the increase of ICAM -1 expression and leukocytes aggregation and infiltration guided by it that constitutes critical factors of microvascular circulation impairment of brain tissue. The marked leukocytes infiltration around hematoma is capable of obstructing micro-vassels, reducing brain perfusion, impairing blood — brain barrier and release or induce miscellaneous poisonous products, such as free radicals, cellular factors and proteinase etc, resulting in direct or indirect damage to neurons.The important mark of inflammatory reaction is leukocytes infiltration. Infil-trative neutrocytes can release multiple cellular factors, such as tumor necrosis factor - a (TNF - a) , interleukin 6 (IL - 6) , interferin7 (INF - y) , and oxygen free base etc, which aggravate brain damage, at the same time obstruct mi-crovessels and lead to local ischemia;also can release vascular active products such as thromboxanes A2 (TXA2) , hyperoxygen anion, interleukin 1 (IL - 1) , Prostaglandins, which alter the reactant activity of blood vessles and release cellular poisonous enzymes, CO and products of phospholipids cascade reactions,aggravating neuron damage;besides, elastic proteinase is released, making damage to vascular endothelial cells and basal membrane and leading to vasculo-genic brain edema.It is irreversible for the acute necrosis of neurons and axons due to intracerebral hemorrhage, however, the pathologic alternation of neurons located in areas around hematoma due to intracerebral hemorrhage /ischemic half dark strip is reversible in a certain time limitation. If some appropriate interference could be done in this time window, some injured brain tissue would regain its function.The conclusions of our research demonstrate that there is marked expression of ICAM -1 in the brain tissue around hematoma;colletive expression of neurons , vascular endothelial cells;neurons expression is extremely obvious. These suggest that in the brain tissue around hematoma due to intracerebral hemorrhage , ischemia and anoxia stimulate neurons, endothelium to express IC AM - 1 together. These expressions focus on cytoplasm and cell membrane, no nuclear expression, which is consistent with documentary reports. The positive cells which express ICAM — 1 are mostly irregular ones, ovoid ones in the second place. There exists low expression of ICAM -1 in control team, cells express it are the same ones in trial team. This research discovers that not only vascular endothelial cells and leukocytes can express ICAM — 1, but also neurons has large amounts of expression, and which may be one of the critical mechanisms of secondary brain injury due to intracerebral hemorrhage and is consistent to documentary report. This research also discovers that positive cells accompanying the expression of ICAM - 1 in neurons and vessels appear 4 hours after disease occurrence, inconsistent with the fact in animal experiments, suggesting that human expression of ICAM - 1 is much earlier. Comparing ICAM -1 expression in 4-8 hours and that of 8 - 12 hours, there is hardly a difference between the two, consistent with animal experiment, suggesting ICAM - 1 expression differs for races.Conclusions1. There exists an up - regulation of ICAM - 1 expression in brain tissue a-round hematoma due to hypertensive intracerebral hemorrhage in human.2. The up - regulation of ICAM - 1 expression may participate leukocytes infiltration of brain tissue around the hematoma, finally leding to inflammatory reaction and secondary brain injury.
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