| The research reason purpose Pulmonary thromboembolism is a serious cardiovascular disease,which damages human health, the patients of millions with pulmonary embolism around the world are diagnosed each year. the number of pulmonary embolism has rised gradually year by yearin our country, if not treatment, mortality rates will attrive leveal as high as 30%, especially, the patients of pulmonary thromboembolism with right ventricular failure is highly death rate. Clinical found that pulmonary thromboembolism is the cause of death in patients with pulmonary hypertension and right ventricular dysfunction and failure, is also the cause of pulmonary hypertension and right ventricular dysfunction and myocardial damage. Therefore,It is key factor to reduce pulmonary artery pressure and myocardial damage for patient’s treatment. Myocardial troponin as a key indicator of early myocardial damage that is confirmed by many foreign research, and its plasma concentration was significantly negative correlation with the degree of the myocardial damage and prognosis of patients with pulmonary thromboembolism. Nitric oxide is a potent vasodilator, foreign studies have confirmed that inhalation nitric oxide in chronic patients who suffered heart disease from lung disorders can reduce pulmonary vascular resistance andright ventricular afterload, improve the cardiac function of cor pulmonale. In order to verify the foreign researchers’ conclusion,that inhaled nitric oxide can improve myocardial damage in patients with acute pulmonary thromboembolism, that myocardial troponin is a main indicator of myocardial damage, Tht investigation of inhalation nitric oxide to reduce pulmonary artery pressure and to prevent myocardial damaged is designed; If this assumption is successful, what is the mechanism which inhaled nitric oxide can protect heart muscle?Our studies have found that Ctn I, v WF, GP b/ a, GMP Ⅱ Ⅲ- 140, ET- 1 plays an important role about the occurrence and development of blood clots in thrombotic disease, so, whether plays an important role t about these factors in the process of myocardial damage in patients with pulmonary thromboembolism,and whether inhaled nitric oxide through influencinge these factors will protect myocardial or no? The problemes will be thounk.The subject is designed baseding on the idea. Objective: to want to pass the subject investigation, more theoretical basis are provide about the clinical diagnosis and treatment of patients with acute pulmonary thromboembolism. Research significance: by the research, to clarify further the cause of myocardial damage in patients with acute pulmonary thromboembolism. content 1.to established a rabbit model of acute massive pulmonary thromboembolism: 2. c Tn I and pulmonary artery mean pressure changes were investigated before and after inhaled nitric oxide in rabbit with acute massive pulmonary thromboembolism. 3. relationship of plasma v WF, GP b/ Ⅱ Ⅲwith c Tn I and after inhaled nitric oxide in acute massive pulmonary thromboembolism rabbit. 4. the change of plasma ET 1 and GMP- 140 and c Tn I in acute massive pulmonary thromboembolism rabbit and after nitric oxide inhaled. 5. the change of plasma TXA2 and PGI2 and c Tn I were investigated in acute massive pulmonary thromboembolism rabbit before and after nitric oxide inhaled. methods The first part: establish a rabbit model of acute massive pulmonary thromboembolism: The homemade pulmonary artery catheter and micro artery catheter are inserted respectively through to the left jugular vein and right carotid artery, the preparation of good thromboembolus into 5 ml syringe is injected repeatedly via right jugular vein of the pulmonary artery catheter, each injecting embolus 0.5 ml, with 2 ml saline injection,is repeated every 3 minutes, embolus is injected continuously until the rabbit average pulmonary blood pressure reach to 45 mm Hg, rabbit mean arterial blood pressure drop to the base value of measurement of 20-40%, the state of low blood pressure of rabbit maintained about 55 to 60 mm Hg, this status last about 40 minutes, rabbit pulmonary thromboembolism reachs the level of massive pulmonary embolism, stop injecting embolus at this time. in the process of Model preparation, if rabbit appeared obvious difficulty breathing, breathing machine would be applicated brief, the pressure is controlled in 20 cm water column pressure, 28 times/min breathing rate. The second part: after the success of the model preparation, inhaled nitric oxide therapy, blood more time, myocardial troponin is measured by chemical method(c Tn I) concentrations, and multi-channel physiological parameter analysis data recorder, synchronous detection average average artery pressure and pulmonary artery pressure. The third part: the application of chemical testing method before and after the detection of acute massive pulmonary thromboembolism with rats inhaled nitric oxide plasma v WF, GP Ⅱ/ a and b c TnⅢI levels change, discusses their relationship. The fourth part: the application of chemical testing methods of acute massive pulmonary thromboembolism rabbit plasma before and after inhaled nitric oxide TE-1 and GMP- 140 and c Tn I levels change, discusses their relationship. The fifth part: the application of chemical testing method before and after the detection of acute massive pulmonary thromboembolism rats inhaled nitric oxide, the concentration of plasma TXA2 and PGI2 and c Tn I changes, discusses their relationship. Results The first part: The serum cardiac troponin have become positive at the 4 hours after beginning of the embolism, myocardial troponin peak plasma concentration time 16.6±3.5 h, plasma cardiac troponin positive duration 38±7.2 h, myocardial troponin peak plasma concentration is 0.42±0.1 mu g/l The second part: 1.4 h after massive pulmonary embolism on rabbit, The myocardial troponin(CTn I) all is positive, the peak concentration in the required time is 16.6±3.5 h, myocardial troponin positive duration 38.6±5.2 h, the myocardial troponin peak value is 0.42±0.12 mu g/l, rabbit myocardial troponin concentration had no correlation with average artery pressure and average pulmonary artery pressure, myocardial troponin peak concentration is obviously correlation with pulmonary artery mean pressure range of the time point(r, 0.98, P < 0.05). 2. Its peak myocardial troponin concentrations in positive duration is significantly shortened than that control group patients(P =0.048; P =0.036), also is significantly reduced in the treatment group than the control group(P=0.047; P=0.03), myocardial troponin peak concentrations were decreased obviously in control group than experimental group(P=0.039), is significantly decreased in treatment group than the control group(P=0.014). 3. In control group, first a rising average pulmonary artery pressure change curve after thrombolysis has happened, peak after,gradually reduce, the treatment group average pulmonary artery pressure curve has a lower first, then rise, gradually decrease after the peak, when random several time point were selected on the curve of average pulmonary artery pressure,the average pulmonary artery pressure have obvious difference in control group and treatment group. The third part 1. The rabbit myocardial damage animal model of massive pulmonary thromboembolism is provided successfully fter 16 hours, the myocardial troponin concentrations significantly higher than the control group(0.41±0.07, 0.08±0.009, P < 0.05), was lower after inhaled nitric oxide 16 hours in treatment group than that in the experimental group(0.31±0.07, 0.41±0.07, P < 0.05). 2. The plasma v WF level obviously is higher in embolization rabbit with acute massive pulmonary thromboembolism after 2 hours and 16 hours than the control group(153.8±26.2, 212.7±28.4, P < 0.05; 111.2±24.6, 111.2±25.1, P < 0.05), its levels significantly decreased comparing with the experimental group after nitric oxide inhaled for 16 hours(131.8±25.4, 212.7±28.4, P < 0.05). the plasma level of GP b/ a significantly higher Ⅱ Ⅲ in rabbit with acute massive pulmonary thromboembolism after 2 hours and 16 hours than that the control group(14.04±6.01, 23.03±6.70, P < 0.05; 2.14±0.82, 2.14±0.79, P < 0.05), inhaled nitric oxide for 24 hours after its levels significantly decreased compared with the experimental group(10.4±7.1, 23.03±6.70, P < 0.05). 4. The serum cardiac troponin and plasma,v WF, GP b/ was significantly Ⅱ Ⅲpositive correlation after 16 hours of experimental model(r, 0.99, P < 0.01; r, 0.99, P < 0.01); the plasma cardiac troponin and plasma v WF, GP b/ was significantly Ⅱ Ⅲpositive correlation after inhaled nitric oxide for 16 hours(r, 0.98, P < 0.01; r, 0.98, P < 0.01).The fourth part 1. The myocardial troponin concentrations is significantly higher in rabbit with massive pulmonary thromboembolism after 16 hours of the model successful preparation than that the control group(0.41±0.07, 0.08±0.009, P < 0.05), 16 hours after treatment in group inhaled nitric oxide, it was lower than that in the experimental group(0.31±0.07, 0.41±0.07, P < 0.05). 2. the plasma levels of endothelin- 1 is significantly higher in rabbit with acute massive pulmonary thromboembolism after 2 hours and 16 hours of model successful embolization than that control group(62.20±5.98, 46.58±5.25,P < 0.05; 68.09±5.04, 68.09±5.30, P < 0.05), 16 hours after treatment in group inhaled nitric oxide, it was lower than that in the experimental group(47.78±5.33, 68.09±5.04, P < 0.05). the plasma protein alpha particles concentration level is significantly higher in rabbit with massive pulmonary thromboembolism after 16 hours of the model successful preparation than that the control group(31.04±4.86, 16.80±5.16, P < 0.05; 36.09±4.56, 36.09±5.04, P < 0.05), 16 hours after treatment in inhaled nitric oxide group, it was lower than that in the experimental group(18.96±3.59, 36.09±4.56, P < 0.05). 4. The experimental model successful preparation after 16 hours,the of plasma cardiac troponin and plasma endothelin- 1 alpha particles plasma protein was significantly positive correlation(r, 0.96, P < 0.05; r, 0.93, P < 0.05); Inhaled nitric oxide after 16 hours,the plasma cardiac troponin and plasma endothelin- 1 alpha particles was significantly positive correlation(r, 0.95, P < 0.05; r, 0.96, P < 0.05). The fifth part 1. In animal model of acute massive pulmonary thromboembolism, myocardial troponin concentrations in plasma increased significantly after 4 hours, 16 h(0.46±0.10) reached its peak, compared with that the control group,compared with inhaled nitric oxide group, 4, 12 reached its peak concentrations, were statistically significant,; plasma TXB2 peaked at 12 h in rabbit with acute massive pulmonary thromboembolism,it have statistical significance comparing with the control group.At inhaled nitric oxide group,highest concentrations is 12, which were significantly lower than that rabbit with acute massive pulmonary thromboembolism 2. PGI2 has a peak at 16 h in rabbit with acute massive pulmonary thromboembolism after,which were statistically significant comparing with the control group At inhaled nitric oxide group, highest concentrations were significantly lower, a than that rabbit with acute massive pulmonary thromboembolism 3. correlation analysis at plasma peak about cardiac troponin, 6- K- PGF plasma TXB2 : plasma cardiac troponin were significantly positive correlation with plasma TXB2(r, 0.99, P < 0.05), plasma cardiac troponin and PGI2 were significantly positive correlation(r, 0.99, P < 0.05). conclusion 1. pulmonary thromboembolism in large area of can cause myocardial damage,cause myocardial troponin release, pulmonary embolism and myocardial infarction, its mechanism of myocardial troponin released into the bloodstream is different. 2. inhalation nitric oxide can obviously reduce the average pulmonary artery pressure and cardiac troponin concentration in rabbit with large area of pulmonary thromboembolism inhalation nitric oxide has obvious protection to myocardial damage. 3. plasma v WF and GP b/Ⅱ Ⅲin rabbit with large area of pulmonary thromboembolism are increased, which is the main factors of myocardial damage, inhalation nitric oxide can reduce its concentration,which is the main mechanism of protecting myocardial damage. 4. endothelin- 1 concentration in plasma is increased in rabbit with large area of pulmonary thromboembolism,which is a main cause of myocardial damage, inhalalation nitric oxide can reduce its concentration,which is the main mechanism of protecting myocardial damage. 5. TXA2 concentrations in plasma is increased in rabbit with large area of pulmonary thromboembolism,which is a main cause of myocardial damage, inhalalation nitric oxide can reduce its concentration,which is the main mechanism of protecting myocardial damage. |
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