共查询到20条相似文献,搜索用时 265 毫秒
1.
<正> 由于克山病主要病变在心肌,所以用造成心肌缺氧缺血的条件来进行实验性心肌坏死的研究,近年来在克山病病因研究方面已进行了大量工作。自从北京军区卫生部报告克山病病区水中亚硝酸盐含量较高以来,曾有不少单位进行了用亚硝酸盐灌胃与病区粮两种复合因素以引起大白鼠心肌坏死的观察。1978年我们对四川省西昌地区18例死亡病人心肌进行几种酶组化观察,发现其中11例亚急型克山病人心肌坏死区周围组织细胞中有酸性磷酸酶活性升高的现象。Duve报导缺血性心肌溶酶体改变对心肌坏死起着重要作用。Ferrans曾根导用异丙基肾上腺素注射大鼠引起心肌细胞中溶酶体数目增加。我们采用亚硝酸钠灌胃,引起大鼠缺氧以观察心肌中两种酶的组织化学改 相似文献
2.
3.
急性心肌梗死的临床护理 总被引:1,自引:0,他引:1
急性心肌梗死是指因冠状动脉供血急剧减少或中断,使相应的心肌严重而持久地缺血导致心肌坏死。笔者结合多年的临床经验,将有关的体会总结如下。1 疼痛的护理1.1 卧床休息 机体活动可使心肌的耗氧量增加,而心肌的血氧供应主要来自冠状动脉,由于心肌梗死病人冠状动脉急剧闭塞,若增加机体活动量,可使心肌进一步缺血缺氧,增加梗死面 相似文献
4.
5.
<正>一般情况下,急性心肌梗死的诱因大多数由心肌坏死引起的,导致心肌坏死的原因是冠状动脉持续性或者急性缺氧造成的。冠状动脉供血变少或者中断,造成心肌长时间的缺血低氧,在临床上主要表现的症状多为有持久和强烈的胸骨后疼痛,休息以及用药物不能全部缓解,同时伴随着血清心肌酶的活性增高以及进行性心电图的变化,心律失常、心力衰竭以及休克 相似文献
6.
钡对免疫器官的毒性作用 总被引:1,自引:0,他引:1
钡广泛存在于自然界,随着工业发展,其被应用于很多领域。有研究表明,可溶性钡盐对机体有较强毒性,不溶性钡盐在胃内受胃酸作用可变成可溶性氯化钡而具有毒性。钡离子可作用于全身肌肉,引起肌肉的兴奋而后麻痹;可使机体多种酶发生改变;且有性腺毒和致畸等作用.本实验对经氯化钡染毒小鼠的免疫器官进行了病理组织学检查,旨在探讨氯化钡是否对免疫系统具有毒性作用。 相似文献
7.
姚志麒 《国外医学:卫生学分册》1980,(6)
据1974年报告,美国伊利诺易斯州有16个城市和2个分区,其饮水中钡浓度超过暂定标准1 mg/l,影响人口15万以上。这些给水均取自深层岩井或钻井的地下水,受天然地球化学污染物的影响。动物和人接触钡引起的最典型急性作用,表现为对平滑肌、横纹肌和心肌的强烈刺激。 相似文献
8.
1、参芪扶正注射液对心肌缺血、心肌梗死及相关冠脉血流量、心肌耗氧量和血液生化有明显改善作用由不同病因造成局部冠状动脉狭窄或冠状动脉闭死形成心肌缺血或心肌梗死时,其它冠状动脉分支代偿性扩张和开放,可使心肌缺血或心肌梗死得到缓解。当心肌发生大面积缺血和广泛性梗死,这种代偿能力“得不偿失”时,则造成心肌坏死和不可逆损伤,发生生命危险。实验观 相似文献
9.
长期的血压升高常会累及心脏,使心脏的结构和功能发生改变。早期时。可使心室舒张功能减退.继而使心肌所需血供增加,从而引起心肌相对缺血。后期时则可使心脏收缩功能减退、心脏扩大,发展为心力衰竭。 相似文献
10.
11.
Appendicitis associated with recent barium study. 总被引:1,自引:0,他引:1
There have been several reports of "barium-induced" appendicitis in the literature. When confronted with a possible case of this phenomenon, a review of the literature on the subject was carried out. The suggestion is made that there is no evidence to support a cause-effect relationship between barium retained in the appendix and appendicitis. Diseased appendices can be marked by retained barium and a higher likelihood may then exist for the subsequent development of appendicitis. Following the finding of prolonged retention of barium after contrast study, it is recommended that the patient be instructed as to the possibility of developing symptoms of acute appendicitis. Patients who present with symptoms of appendicitis should be questioned as to history of recent barium study, and x-rays should be reviewed with the possibility of finding appendoliths. 相似文献
12.
Epidemiological studies indicate a strong relationship between dietary Mg intake and the incidence of sudden cardiac death. The mechanism by which dietary Mg leads to an increased incidence of cardiovascular disease is unknown but may involve alteration of electrolyte balance. In the present study, tissue electrolyte levels and myocardial pathology were investigated in adult hamsters fed a diet containing no added Mg. Control animals were fed the same diet supplemented with Mg or standard laboratory chow. Hamsters were killed after 4, 8, 12, or 18 days on the test diet, and levels of Na, K, Ca, and Mg were measured in the serum, myocardium, bone, and kidney. The earliest change induced by the test diet was a decrease of the serum Mg and an increase in the Na concentration of the myocardium and other tissues. Following the rise in myocardial Na, the myocardial Ca rose, attaining a fourfold increase by 18 days. K fell in heart and kidney, but not significantly. Although there was no significant change in myocardial Mg, foci of myocardial necrosis, considered to be typical of acute severe Mg deficiency, were found. Myocardial necrosis and the increase in myocardial Ca occurred in parallel. Because of the pattern of observed changes in electrolyte levels, and the potential role of Ca in myocardial injury, the occurrence of myocardial necrosis in these Mg-deficient hamsters is attributable to the increased level of myocardial Ca, rather than to any change in intracellular Mg levels. It is postulated that reduced extracellular Mg levels increase [Na]i through reduction of sarcolemmal (Na+ + K+)-ATPase activity. This would lead to an increase in [Ca]i through Na-Ca exchange. 相似文献
13.
14.
Epidemiological evidence suggests that magnesium deficiency may be a factor in the etiology of cardiovascular and renal disease. During moderate magnesium deficiency in rats, caused by feeding 80 mg Mg/kg, however, magnesium levels in the soft tissues were previously shown to vary little. Consequently, in the present study, rats were fed either 80 or 500 mg Mg/kg for 6 weeks, and the concentrations of sodium, potassium, calcium, phosphate and magnesium were determined in serum, heart, kidneys, urine and feces to see whether changes in the levels of these elements, caused by the magnesium deficiency, play a role in the pathogenesis of these diseases. The concentration of oxalate was also determined in the urine. In the heart, both sodium and calcium were increased, while magnesium was decreased slightly in the deficient animals. In the kidney, nephrocalcinosis occurred, along with an increase in sodium and phosphate concentration. The feces contained increased levels of sodium and potassium. The data suggest that magnesium deficiency alters sodium transport. In the case of the heart, this may alter the membrane potential and could account for the cardiac arrhythmias associated with magnesium deficiency. 相似文献
15.
16.
《Nutrition reviews》1976,34(1):25-27
Iron deficiency is often associated with thrombocytosis but if severe, it may conversely produce thrombocytopenia. Recent experimental observations suggest a mechanism for these observations. 相似文献
17.
18.
Mohsen H Faouzi A Khaldoun BH Fatma A Hanéne H Zohra D Habib G Fethi B Faouzi M Mohamed BF 《La Tunisie médicale》2005,83(11):675-680
Myocardial infarction with normal coronary artery is ussually inaugural, with electric and clinical characteristics similar to those with atheroma. The role of constitutional or acquired abnormalities of haemostasis has been more incriminated in the pathogenesis of myocardial infarction with normal coronary. The aim of our study was to research abnormalities of haemostasis in patients with myocardial infarction and angiographically absolutely normal coronary arteries. PATIENTS AND METHODS: Thirty nine patients with myocardial infarction and normal coronary arteries where included in our study. They were 33 males and 6 females aged between 22 and 75 years (44 + 13 years), in whom the deficiency in protein C and S. antithrombin, activated protein C resistance and antiphospholipid antibodies were assessed. RESULTS: Concurrent abnormalities of haemostasis were found in 10 patients: Antiphospholipid antibodies, found in 5 patients constitute the most frequent abnormality. The other abnormalities were deficiency in protein C in two cases, deficiency in protein S 2 cases, deficiency in antithrombin in 2 ceses and activated protein C resistance in 3 cases . CONCLUSION: In our study. in face of the high prevalence of these abnormalities, it seems reasonable to research them, especially in young patients with myocardial infarction with normal coronary artery. This should have an impact on the management of these patients. 相似文献
19.
The electrocardiogram was recorded and serum and bulk myocardial electrolytes were determined in male Sprague Dawley rats, subjected to dietary magnesium deficiency for various periods, to assess the time course of development and cessation of the enhanced arrhythmogenic action of isoproterenol (150 micrograms/kg, subcutaneously) and to establish possible relationships between electrolyte changes and severe ventricular dysrhythmias. Ventricular fibrillation occurred within 60 min following isoproterenol injection in 25, 25, 62.5, 50, and 62.5% of rats on magnesium deficient diet for 4, 7, 11, 15, and 19 days (N = 8), respectively, and resulted in death in most animals (83%). Reintroduction of normal chow following a 30-day period on magnesium-deficient diet normalized serum magnesium (from 1.42 +/- 0.23 to 1.90 +/- 0.08 mEq/liter, mean +/- SD) but did not significantly reduce the incidence of ventricular fibrillation. Magnesium deficiency did not produce statistically significant alterations in bulk myocardial content of sodium, potassium, magnesium, and calcium. However, sodium was elevated and potassium diminished in hearts from rats that died in ventricular fibrillation, but not in those that had recovered. Magnesium-deficient rats sacrificed 30 min after isoproterenol injection, that is before the occurrence of ventricular fibrillation, exhibited hypomagnesemia and hypokalemia as well as elevated sodium and diminished potassium and magnesium in the myocardium. In contrast, rats on Purina Chow exhibited hypermagnesemia, but also showed hypokalemia and diminished cardiac potassium. The results indicate that magnesium deficiency enhances the arrhythmogenic propensity of isoproterenol and that the development of ventricular fibrillation is preceded by serum and myocardial electrolyte alterations. 相似文献