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外力打擊兔頸動(dòng)脈竇壓力感受器引起動(dòng)物死亡心肌組織ANP及血漿兒茶酚胺含量變化規(guī)律的研究

發(fā)布時(shí)間:2019-07-08 20:00
【摘要】: 研究目的:觀察外力打擊兔頸動(dòng)脈竇壓力感受器后引起動(dòng)物死亡,觀察組組織形態(tài)學(xué)變化和分析測(cè)定心肌組織ANP及血漿兒茶酚胺含量的差異,探討引起死亡的機(jī)制。 方法:機(jī)械性外力打擊兔頸動(dòng)脈竇壓力感受器后造成動(dòng)物神經(jīng)源性休克死亡模型,觀察組織形態(tài)學(xué)的變化,運(yùn)用Western blot檢測(cè)心肌組織ANP水平,高效液相-電化學(xué)法(HPLC-ECD)檢測(cè)兒茶酚胺含量,并與對(duì)照組比較。 結(jié)果:1、形態(tài)學(xué)研究:實(shí)驗(yàn)組死亡動(dòng)物經(jīng)過(guò)檢驗(yàn)未發(fā)現(xiàn)器質(zhì)性病變,其死亡均由頸動(dòng)脈竇壓力感受器被打擊后所致。形態(tài)學(xué)觀察發(fā)現(xiàn)頸動(dòng)脈竇外膜損傷表現(xiàn)為灶性片狀出血、神經(jīng)纖維斷裂、神經(jīng)纖維軸漿溶解;心肌組織表現(xiàn)為急性缺血性損傷改變;無(wú)明顯肺水腫表現(xiàn)。而存活組亦有部分頸動(dòng)脈外膜灶性出血、輕度急性心肌缺血性損傷改變。 2、與對(duì)照組與存活組比較,死亡組右心耳ANP含量較低。 3、死亡組血漿兒茶酚胺較對(duì)照組含量明顯增高(3-10倍)。 結(jié)論:頸動(dòng)脈竇壓力感受器受外界壓力刺激引起死亡的改變有:頸動(dòng)脈竇外膜損傷表現(xiàn)為灶性片狀出血、神經(jīng)纖維斷裂、神經(jīng)纖維軸漿溶解,急性心肌缺血性損傷改變;心肌組織ANP含量減少;血漿兒茶酚胺含量明顯升高。
文內(nèi)圖片:兔頸內(nèi)動(dòng)脈打擊部位外膜出血HE×20Fig-1haemorrhageofrabbit’sinternalcarotidarteryadventitiabyhit(HE10×20)
圖片說(shuō)明:兔頸內(nèi)動(dòng)脈打擊部位外膜出血HE×20Fig-1haemorrhageofrabbit’sinternalcarotidarteryadventitiabyhit(HE10×20)
[Abstract]:Objective: to observe the animal death caused by external force striking carotid sinus baroreceptor in rabbits, to observe the morphological changes of myocardial tissue and the difference of plasma catecholamine content in myocardial tissue, and to explore the mechanism of death. Methods: the animal model of neurogenic shock was established after mechanical external force hit the carotid sinus baroreceptor in rabbits. The histomorphological changes were observed. The level of ANP in myocardial tissue was measured by Western blot, and the content of catecholamine was detected by high performance liquid phase electrochemical method (HPLC-ECD) and compared with the control group. Results: 1. Morphological study: no organic lesions were found in the dead animals in the experimental group, and the deaths were caused by the attack of carotid sinus baroreceptor. Morphological observation showed that the injury of carotid sinus adventitia showed focal flake hemorrhage, broken nerve fibers and axonal plasma dissolution of nerve fibers, acute ischemic injury in myocardial tissue and no obvious pulmonary edema. In the survival group, some focal hemorrhage of carotid artery and mild acute myocardial ischemic injury were also found. 2. Compared with the control group and survival group, the ANP content of right atrial appendage in the death group was lower than that in the control group and survival group. 3. The content of plasma catecholamine in the dead group was significantly higher than that in the control group (3 鈮,

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