心肌肌钙蛋白I诊断轻中度急性一氧化碳中毒患儿心肌损伤的临床研究

急性一氧化碳中毒(ACOP)是临床常见的急症之一,心脏是除了脑以外常见的受累器官,可引起急性心肌缺血,导致心律失常、心肌损伤、心功能不全甚至心肌梗死等;心肌肌钙蛋白(cTnI)是近年来应用于临床的检测心肌损伤的标记物,可以检测出心肌微小病变[1].本研究对30例轻、中度ACOP患儿的血清cTnI水平进行检测,并与常见的心肌酶学及心电图检查进行对比,探讨cTnI在ACOP心肌损伤诊断中的意义.

细胞移植治疗慢性心功能不全的研究进展

近几十年来,对于许多心肌病变终末期所致的顽固性心力衰竭(简称心衰)临床上好的解决方法是心脏移植.这种方法在一定时期内可以改善患者心功能不全的症状,但即使在使用免疫抑制剂(如环孢菌素)以及供体心脏与受体之间严格进行免疫配型的情况下,二者之间仍不可避免地发生不同程度的免疫排斥反应,造成移植心脏的免疫损伤;移植心脏的供血障碍和术后感染等因素也常常导致心脏移植的失败[1].此外,供体心脏的获之不易也制约着心脏移植在临床上的广泛应用.

AIM: To study the protecitve mechanism of Ligustrazine (LT), Shenmai Parenteral Injection (SPI), combination of Ligustrazine and Shenmai Parenteral Injection (LSP) to myocardial injury after brain ischemia-reperfusion in aged rats from the change in ATPase and free radical in order to provide theoretical basic for prevention and cure of cerebral infarction. METHODS: Aged rats (more than 20 months) were divided into model group, control group, Nimotop group, LT group, SPI group and LSP group. We measured the following items in aged rats with 60 min of reperfusion after 30 min of brain ischemia: the content of MDA, the activities of superoxide dismutase (SOD), lactic dehydrrogenase (LDH), creatine phosphokinase (CPK), ATPase. RESUTLS: The CPK and LDH activities in the model rats increased obviously. The serum CPK activity in the LSP group, the LT group, nimotop group was lower than those in the model group obviously. The serum LDH activities in LT group and SPI group were obviously lower compared with those in the model group. The activity of Na＋-K＋-ATPase and Ca2＋-ATPase in model group was decreased. Contrast to the model group, the activity of Na＋-K＋-ATPase in LSP group, Nimotop group, LT group and the activities of Ca2＋-ATPase in the LSP group were higher. The serum MDA/SOD ratio was larger than that in the control group. The decrease in myocardial SOD activity and the increase in the MDA level, MDA/SOD ratio in the model group showed significant difference compared with that in the control. The MDA level in the LSP group was lower than that in the model group. The increase in myocardial SOD activity and decrease in MDA, MDA/SOD ratio were obvious in the LSP group compared with the model group. CONCLUSION: The myocardial injury after brain ischemia-reperfusion in aged rats was related to the decrease in the activity of Na＋-K+-ATPase and injury of free radical. LT, SPI, LSP and Nimotop could prevent this inury. Nimotop and LT could enhanced the activity of Na+-K+-ATPase obviously. SPI could enhance the activity of Ca2＋-ATPase and restrain the injury of free redical and lipid peroxidation. This may be the mechanism of restraining myocardial injury after brain ischemia-reperfusion.

AIM: To study the mechanism of myocardial injury after brain ischemia-reperfusion in aged rats from the changes in Dopamine (DA), Noradrenalin (NE), Epinephrine(E) and Neuropeptide Y(NPY).METHODS: Young (5 months) and aged (20 months or more) rats were divided into model groups and normal control groups, respectively. We observed the following items in rats with 60 minute reperfusion after 30 minute brain ischemia: the pathological changed of myocardium, the activities of lactic dehydrrogenase(LDH), creatine phosphokinase(CPK), the contents of NE, DA, E, NPY. RESULTS:The CPK and LDH activities in the young model rats were higher than those in the young control rats was higher than that in the young control rats (P＜0.05). The serum CPK activity in the aged control rats was higher than that in the young control rats (P＜0.05). The myocardial CPK activity was higher in the aged model rats compared with the young molel rats (P＜0.05) and was higher in aged control rats compared with the young control rats (P＜0.01). The myocardial LDH activity was lower in the aged control rats than that in the young control rats (P＜0.05) and aged model rats (P＜0.01). The serum NE level, the level of NE and DA in the hypothalamus were higher obviously than those in the young control rats. The serum NE contents in the two model groups (young and aged) were higher respectively than the two control rats (young and aged). The following items’ contents were higher in the aged model rats than in the young model rats: serum NE, serum E, hypothalamus NE. The hypothalamus NE and E content was lower in the aged model rats than in te aged control rats. NPY level in the brain tissue was lower in the aged control rats than that in the young control rats and aged model rats (P＜0.05).CONCLUSION: The myocardial injury after brain ischemia-reperfusion was concerned with the enhanced excitability of sympathetic-adrenal system, espectially in the aged rats. However, the change in myocardial enzyme was not serious in the aged rats compared with young rats.

心肌肌钙蛋白Ⅰ检测缺血性心肌损害的诊断价值

在缺血性心脏病的诊断中,除了病历、身体检查和心电图以外,生化标记物的测量一直是一个重要的评估指标,大量的临床实践发现,约有25%的急性心肌梗死(AMI)病人发病早期没有典型的临床症状,约50%左右的AMI病人缺乏心电图(ECG)的特异改变,在这种情况下,心肌损伤生化指标物的检测在诊断AMI时尤为重要.

严重烧伤后早期心肌损害的细胞分子机制与防治策略研究进展

缺血缺氧性损害一直是妨碍严重烧伤治愈率进一步提高的关键问题,尽管伤后及时给予复苏,但缺血缺氧性损害仍难以避免.究其原因,一是烧伤后血液灌流不足,除了毛细血管通透性增加使有效血容量减少外,是否还有别的启动因素参与尚不清楚;二是细胞病理性缺氧的机制未明了,因而临床上缺乏有针对性的措施.近年来,在观察并证实严重烧伤后早期存在心肌损害的基础上,人们针对其细胞分子机制与防治策略进行了深入的研究.

烧伤后早期心肌损害的分子机制及防治研究进展

研究显示,烧伤后5 min患者心输出量即下降,10 min即可降至正常值的50%,60 min降至正常值的1/3, 而此时血容量仅降至正常值的69%,表明烧伤早期心功能损害的程度明显重于血容量下降的程度.心肌受损将导致有效血容量进一步降低,加重全身组织器官的缺血缺氧损害,因此,烧伤后早期心肌损害是严重烧伤缺血缺氧的启动因素之一,并提出了休克心(cardiac shock)的概念[1,2].近年来,国内外从细胞和分子水平对烧伤心肌损害的机制进行了深入广泛的研究,取得了一些重要进展,本文就此作一回顾与展望.

Objective:To detect serum chemokine RANTES content in patients with acute coronary syndrome and analyze its relationship with degree of inflammation and myocardial injury. Methods:116 cases of acute coronary syndrome (ACS) patients treated in our hospital from July 2012 to July 2014 were chosen as study group and divided into low-risk group (48 cases), moderate-risk group (33 cases) and high-risk group (35 cases) according to risk stratification; 109 cases of healthy people receiving physical examination during the same period were enrolled in healthy control group. Serum RANTES contents as well as levels of inflammatory cytokines and myocardial injury indicators in all groups were compared and the correlation was further analyzed.Results:Serum RANTES contents as well as levels of inflammatory factors and myocardial injury markers in ACS patients were all significantly higher than those in control group (P<0.05), and with the increase of coronary risk stratification, serum RANTES contents as well as levels of inflammatory factors and myocardial injury markers further rose (P<0.05); serum RANTES contents in ACS patients were positively correlated with levels of inflammatory cytokines and myocardial injury indicators.Conclusion: Increased levels of serum RANTES is one of the important factors contributing to the occurrence of ACS; it is positively correlated with levels of inflammatory cytokines and severity of myocardial injury in patients, and can guide clinical treatment and judge prognosis.