【摘要】：目的：本實(shí)驗(yàn)通過建立大鼠側(cè)位液壓腦損傷模型，研究液壓腦損傷后損傷側(cè)和非損傷側(cè)大血管形態(tài)和生理功能改變及微血管損傷與腦水腫的關(guān)系，為顱腦創(chuàng)傷后損傷側(cè)和非損傷側(cè)腦血管改變的研究提供實(shí)驗(yàn)依據(jù)。 方法： 1、成年健康雄性SD大鼠45只，采用完全隨機(jī)法分為正常對(duì)照組、假手術(shù)組、實(shí)驗(yàn)組，實(shí)驗(yàn)組又分為液壓腦損傷后6h、24h及72h組，每組9只。利用改良的側(cè)位液壓損傷裝置建立大鼠顱腦損傷模型。應(yīng)用光鏡、透射電鏡觀察大鼠損傷側(cè)和非損傷側(cè)大腦中動(dòng)脈主干形態(tài)學(xué)改變，應(yīng)用免疫組化法檢測(cè)不同時(shí)間點(diǎn)大鼠損傷側(cè)和非損傷側(cè)大腦中動(dòng)脈縫隙連接蛋白40（connexin40, Cx40）；縫隙連接蛋白43(connexin43, Cx43)表達(dá)的改變。 2、成年健康雄性SD大鼠30只，，采用完全隨機(jī)法分為正常組、假手術(shù)組、實(shí)驗(yàn)組，其中實(shí)驗(yàn)組分為6h、24h、72h組，每組6只，利用液壓沖擊法建立大鼠顱腦損傷模型，顯微鏡觀察損傷側(cè)損傷區(qū)域和非損傷側(cè)相應(yīng)區(qū)域腦皮質(zhì)微血管改變情況，CD34標(biāo)記血管內(nèi)皮細(xì)胞(Endothelial Cell, EC)，采用微血管計(jì)數(shù)法來檢測(cè)微血管密度(Microvesseldensity, MVD)改變，干濕重法檢測(cè)腦組織含水量的變化。 結(jié)果： 1、液壓腦損傷后損傷側(cè)和非損傷側(cè)大腦中動(dòng)脈均有不同程度損傷，主要表現(xiàn)為血管管腔縮小，內(nèi)皮細(xì)胞形態(tài)結(jié)構(gòu)改變，內(nèi)彈力膜皺縮，平滑肌細(xì)胞水腫變形。損傷后72h電鏡下可見損傷側(cè)內(nèi)彈力膜斷裂，部分平滑肌細(xì)胞核固縮，異染色質(zhì)增多，非損傷側(cè)改變較輕微；與假手術(shù)組相比，實(shí)驗(yàn)組大鼠損傷側(cè)和損傷側(cè)大腦中動(dòng)脈血管壁細(xì)胞Cx40、Cx43表達(dá)增加(P0.05)，24h達(dá)蛋白表達(dá)達(dá)高峰，尤以損傷側(cè)增加明顯。 2、液壓腦損傷后大鼠兩側(cè)腦皮質(zhì)微血管均有不同程度皺縮、扭曲，血管周圍間隙增寬，損傷后24h和72h組可見微血管內(nèi)有血栓形成；與假手術(shù)組相比腦皮質(zhì)微血管計(jì)數(shù)明顯降低(P0.05)，以損傷側(cè)為重；實(shí)驗(yàn)組損傷側(cè)和非損傷側(cè)腦皮質(zhì)含水量升高，與假手術(shù)組相比差異有統(tǒng)計(jì)學(xué)意義(P0.05)；腦皮質(zhì)微血管計(jì)數(shù)與腦組織含水量呈負(fù)相關(guān)（r=㧟0.76, P0.01）。 結(jié)論： 1、液壓腦損傷后損傷側(cè)因直接受外力作用，大腦中動(dòng)脈血管結(jié)構(gòu)改變，管壁內(nèi)皮細(xì)胞出現(xiàn)凋亡表現(xiàn)，非損傷側(cè)則出現(xiàn)內(nèi)皮細(xì)胞變性脫落，平滑肌細(xì)胞水腫等改變；同時(shí)損傷側(cè)和非損傷側(cè)管壁細(xì)胞Cx40和Cx43表達(dá)均增加。提示創(chuàng)傷性腦損傷后力線作用方向和非力線作用方向均存在顱內(nèi)大血管結(jié)構(gòu)和生理功能改變。 2、液壓腦損傷后損傷側(cè)和非損傷側(cè)腦皮質(zhì)微血管扭曲變形，部分血管內(nèi)可見血栓形成，同時(shí)兩側(cè)腦組織微血管內(nèi)皮細(xì)胞密度均減低，其降低程度與腦水腫程度吻合。提示創(chuàng)傷性腦損傷后不僅外力直接作用方向微血管有損傷，遠(yuǎn)隔部位亦可見損傷性改變，腦皮質(zhì)微血管密度降低是創(chuàng)傷性腦水腫的病理基礎(chǔ)。
[Abstract]:Objective: to study the changes of the morphology and physiological function of large vessels and the relationship between microvascular injury and brain edema in the injured side and non-injured side by establishing the model of lateral fluid brain injury in rats. To provide experimental basis for the study of cerebral vascular changes in the injured and non-injured sides after craniocerebral trauma. Methods: 1. Forty-five adult healthy male SD rats were randomly divided into normal control group, sham operation group and experimental group, 9 rats in each group. The model of craniocerebral injury in rats was established by using an improved lateral hydraulic injury device. The morphological changes of the middle cerebral artery trunk in the injured and non-injured sides were observed by light microscope and transmission electron microscope. The gap junction protein 40 (connexin40, Cx40) of the middle cerebral artery at different time points was detected by immunohistochemical method. Changes of gap junction protein 43 (connexin43, Cx43) expression. 2Thirty adult healthy male SD rats were randomly divided into normal group, sham operation group and experimental group. The experimental group was divided into 6 groups with 6 rats in each group. A rat model of craniocerebral injury was established by hydraulic shock. The changes of cerebral cortical microvessels in the injured and uninjured regions were observed under microscope. CD34 labeled vascular endothelial cells (Endothelial Cell, EC),) were used to detect the changes of microvessel density (Microvesseldensity, MVD) by microvessel count. The changes of water content in brain tissue were measured by wet and dry weight method. Results: 1. The middle cerebral artery of the injured side and the non-injured side were damaged to different degrees after fluid pressure brain injury. The main manifestations were the reduction of vascular lumen, the change of endothelial cell morphology, the contraction of internal elastic membrane, and the edema and deformation of smooth muscle cells. Under electron microscope 72 hours after injury, the inner elastic membrane was broken, some smooth muscle nuclei were pyknosis, heterochromatin was increased, and the change of non-injured side was slight. In the experimental group, the expression of Cx40,Cx43 was increased in the injured side and the injured side of the middle cerebral artery (P0.05), and reached the peak at 24 hours, especially in the injured side. Compared with the sham-operated group, the cerebral cortex microvessel count was significantly decreased (P0.05), especially in the injured side. The cortical water content in the experimental group was significantly higher than that in the sham-operated group (P0.05); the cerebral cortex microvessel count was negatively correlated with the brain tissue water content (r = 0.76, P 0.01). Conclusion: 1. The injured side was directly affected by external force, the vascular structure of the middle cerebral artery changed, the endothelial cells of the wall showed apoptosis, and the non-injured side showed degeneration and shedding of endothelial cells. The expressions of Cx40 and Cx43 were increased in both injured and uninjured wall cells. It is suggested that there are changes in the structure and physiological function of intracranial macrovessels after traumatic brain injury. 2. The cerebral cortical microvessels in the injured and non-injured sides are distorted and deformed after fluid pressure brain injury. Thrombosis was seen in some of the blood vessels, and the density of microvascular endothelial cells in both brain tissues was decreased, which coincided with the degree of cerebral edema. It is suggested that not only the direct action of external force has microvascular injury after traumatic brain injury, but also the damage can be seen in the distant area. The decrease of cerebral cortex microvessel density is the pathological basis of traumatic brain edema.
【學(xué)位授予單位】：石河子大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2013
【分類號(hào)】：R651.15

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