| Objective: Cerebrovascular diseases is one of commonly and frequently encountered nervous system diseases,significantly threatens human health. It accounts for 80% of all acute cerebrovascular diseases,its mortality and disability rate are higher than other stroke diseases. Acute cerebral infarction is a very complicated pathophysiologic process, which involves local thrombogenesis,atherosclerosis, heart mural thrombus fall off, and low perfusion et al. No definitely ideal treatment is available. So, actively looking for methods reducing its morbidity and mortality is still a international academic research hot spot. Professor Atherosclerosis, as an inflammatory disease, was formulated by professor Ross in 1999, and elevating inflammatory factors expression is present in the whole pathological process of atherosclerosis and acute cerebral infarction. Studies find that there are a lot of inflammatory factors which were gathering in terribly damaged cells after acute cerebral infarction. They participate in the process of tissue damage caused by ischemic events. Result in the process of ischemia around the site of lesions developed to be an irreversibly brain-damaged. At the same time, the danger of cerebral infarction is greatly increasing. Hypertension, as a common cardiovascular diseases, consists of many complex causes, such as genetic, physiological, psychological, and endocrine factors. The morbidity and blood pressure went higher with the age increased. It is characterized by the proliferation of smooth muscle cells. At first, spasm of arterioles leads to fibrin plugs and hyaline degeneration. And then, in advanced cases, the smaller arteries have become thickened and narrowed. At last, atherosclerosis happened. Atherosclerosis is an inflammatory disease characterized by chronic inflammation in the artery wall. Hypertension is one of the main factors which promote arteriosclerosis. So it is important to probe into the changes and significance of the serum levels of TNF-αand TNF-βin patients of cerebral infarction with hypertension and in patients with cerebral infarction without hypertension. Nowadays, this research field has been emphasized on the action of TNF-αin patients of acute cerebral infarction at home and abroad. There has been a lack of conclusive evidence concerning the causal relation between TNF-βand disease of the central nervous system, especially the causal relation between TNF-βand acute cerebral infarction. Only a handful of reports have shown that TNF-βis associated with thymoma ,myasthenia gravis and post-operative complications. The study in my thesis focused on detecting and discussing the function of serum levels of TNF-αand TNF-βin patients of acute cerebral infarction with hypertension or not in the acute brain damage. It may provide a new clue for clinical diagnosis.Method: We chose 30 patients of cerebral infarction with hypertension, 30 patients with cerebral infarction without hypertension, 20 patients of hypertension without cerebral infarction and 20 normal people as subjects. Everyone must be checked at the enrolling, such as sex, age, history of hypertension, history of drug, diet, complications, smoking history and drinking history. Centrifuge the venous blood from the subject in the morning after fasting 10-12h for 10 mins at 3000r/min speed. Store the specimens in the refrigerator at -20℃. Remove hemolysis samples. Determine the content of TNF-αand TNF-βwith RIA. The kit was provided by Biotech Research Institute of Hua ying, Beijing.Results: The serum levels of TNF-αand TNF-βwere different among the four groups ( patients of cerebral infarction with hypertension, patients with cerebral infarction without hypertension, patients of hypertension without cerebral infarction and normal people) (P<0.05 ). The serum levels of TNF-αand TNF-βin patients of cerebral infarction with hypertension and in patients with cerebral infarction without hypertension respectively were significantly higher than the hypertension group and the normal group (P<0.05 ). The serum levels of TNF-αand TNF-βdid not correlate with hypertension(P>0.05). The serum levels of TNF-αand TNF-βin the severe cerebral infarction group increased significantly as compared with the moderate and mild cerebral infarction group(P<0.05 ) . The serum levels of TNF-αand TNF-βin the moderate cerebral infarction group were significantly higher than the mild cerebral infarction group (P<0.05 ). The serum levels of TNF-αand TNF-βin the large area cerebral infarction group were significantly higher than the non-massive cerebral infarction group(P<0.05 ). The serum levels of TNF-αand TNF-βhave great relation (r=0.488, P<0.05 )Conclusion:1 The serum levels of TNF-αand TNF-βin patients of cerebral infarction with hypertension and in patients with cerebral infarction without hypertension have a significantly increase . It indicated levels of TNF-αand TNF-βtake part in the pathological process of cerebral infarction.2 The different levels of TNF-αand TNF-βbetween patients of cerebral infarction with hypertension and without were not statistically significant . The result showed that hypertension was not the reason on aggravating the condition of patients with cerebral infarction.3 The serum levels of TNF-αand TNF-βin the severe cerebral infarction group increased significantly as compared with the moderate and mild cerebral infarction group. The serum levels of TNF-αand TNF-βin the moderate cerebral infarction group were significantly higher than the mild cerebral infarction group. The serum levels of TNF-αand TNF-βin the large area cerebral infarction group were significantly higher than the non-massive cerebral infarction group. Level of TNF-αand TNF-βin acute cerebral infarction patients correlated with infarct volume and nerve function. It indicated TNF-αand TNF-βmay reflect degree of cerebral infarction.4 The serum levels of TNF-αand TNF-βhave great relation. |
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