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目的研究成年大鼠快速减压致中枢神经系统(CNS)损伤后神经组织细胞凋亡的变化及高压氧(HBO)暴露的效用。方法SD大鼠40只,按随机数字法分为10组,每组4只,即正常对照组、安全减压组、快速减压4个组(1.0 MPa暴露5.5 m in后快速(50 s)减至常压后6,24,48,72 h组)、HBO4个组(快速减压后5 h给予0.25 MPa HBO暴露60 m in)。大鼠均分别于快速减压后6,24,48和72 h同期取大脑,用原位末端TUNEL法标记凋亡细胞,光学显微镜下观察形态学改变和高倍镜计数阳性细胞计算凋亡指数。结果正常对照组和安全减压组未标记出TUNEL阳性细胞;快速减压致伤动物6 h组CNS组织内仅见少量散在阳性细胞;24 h组凋亡指数较6 h组增加(P<0.01);48和72 h组明显增加,达到高峰(P<0.01);TUNEL阳性凋亡细胞主要为神经元细胞。HBO暴露组24 h组神经元凋亡指数明显较快速减压组相同时间组降低(P<0.05),48 h和72 h组降低更加显著(P<0.01)。结论神经元凋亡是快速减压致CNS损伤中神经元丧失的重要形式之一。HBO暴露能够减少损伤后期的神经元凋亡,对保存神经元、改善预后起到重要作用。
Objective To study the changes of apoptosis of nerve tissue and the effect of hyperbaric oxygen (HBO) exposure after the central nervous system (CNS) injury caused by rapid decompression in adult rats. Methods Forty SD rats were randomly divided into 10 groups (4 rats in each group): normal control group, safe decompression group and rapid decompression group (fast (50 s) after exposure to 5.5 m in 1.0 MPa) Reduced to 6,24,48,72 h after the normal pressure group), HBO4 groups (0.25 MPa HBO exposure 60 min after the rapid decompression 5 h). The rats were sacrificed at 6, 24, 48 and 72 h after the rapid decompression, respectively. The apoptotic cells were labeled by TUNEL in situ and the morphological changes under light microscope were observed. Results TUNEL-positive cells were not labeled in the normal control group and the safety decompression group. Only a few scattered positive cells were found in the CNS tissue in the 6-h group after rapid decompression. The apoptotic index in 24 h group was higher than that in the 6-h group (P <0.01) ; 48 and 72 h group increased significantly, reaching the peak (P <0.01); TUNEL positive apoptotic cells are mainly neuronal cells. The apoptotic index of neurons in HBO exposed group was significantly lower than that in rapid decompression group (P <0.05), and decreased more significantly in 48 h and 72 h groups (P <0.01). Conclusion Neuronal apoptosis is one of the important forms of neuron loss during CNS injury induced by rapid decompression. HBO exposure can reduce neuronal apoptosis in the late stage of injury and plays an important role in neuron preservation and prognosis.