Intrauterine left chamber myocardial infarction of the heart and hydrops fetalis in the recipient fetus due to twin-to-twin transfusion syndrome

A rare complication of twin-to-twin transfusion syndrome (TTTS) is described: myocardial infarction of the recipient fetus. Myocardial infarction and hydrops are considered to be consequences of hypertension in the recipient. No other organs were affected. Pathological signs of intrauterine hypertension were estimated by the thickness of vessel walls and signs of hypertrophied myocardial cells. In the heart of the recipient fetus there was a chronic myocardial infarction near the apex cordis on the anterior wall with an aneurysm 4×5 mm in diameter. Diagnosis was based on light microscopic examination. The poor myocardial systolic function resulted in hydrops. Since the mother was administered β sympathomimetics in therapeutic doses the contribution of the drug to the myocardial infarction is uncertain, but we would like to suggest this as a possible adverse effect in TTTS. The present case is the first reported myocardial infarction in connection with the syndrome. Copyright © 2002 John Wiley & Sons, Ltd.     

Pulmonary stenosis and reactive right ventricular hypertrophy in the recipient fetus as a consequence of twin-to-twin transfusion

The present study describes an association between adverse outcome in the twin-to-twin transfusion syndrome (TTTS) and pulmonary stenosis or reactive right ventricular hypertrophy. Six discordant monozygotic twin pregnancies with TTTS are described. Ventricular hypertrophy and atrioventricular valvular regurgitation occurred in all the recipient twins with pulmonary valvular stenosis in three cases and infundibular stenosis in one case. The recipient twin in one pair and both twins in another pregnancy died as a consequence of immaturity but the remaining twins all survived. Surgical intervention was required in one baby for valvular pulmonary stenosis. Our observations suggest that elevated blood pressure in the transfusion recipient may play an important role in pathogenesis. We hypothesise that both pulmonary stenosis and right chamber hypertrophy are secondary to hemodynamic changes. Although we have found valvular pulmonary stenosis in three recipients and infundibular stenosis in only one, this (obstruction to outflow) could be due to right chamber hypertrophy. Copyright © 2001 John Wiley & Sons, Ltd.     

大气细颗粒物暴露干扰心肌细胞存活和炎性反应的主要毒性组分研究

鉴于PM_(2.5)组分呈现多样性和复杂性,其引起心力衰竭的主要毒性组分尚不清楚.由于采样地区、季节和污染源的不同,PM_(2.5)不同组分的占比也会有巨大差异,但不同浓度无法比较其不同组分间的毒性差异.因此,为了揭示大气PM_(2.5)引起心肌毒性作用的关键组分,分离复合型PM_(2.5)的3种主要组分(有机组分、金属组分和水溶性组分),综合两种浓度暴露方式,即实际占比浓度和与复合型PM_(2.5)相同的暴露浓度,染毒H9C2大鼠心肌细胞24 h和48 h,选择心肌细胞的细胞存活和炎症反应为主要评价指标,旨在揭示PM_(2.5)对心肌造成毒性损伤的关键性成分.CCK-8法检测存活结果显示,不同组分在实际环境比重下,对心肌细胞存活率没有造成显著影响.相同浓度暴露下,高剂量组分(30μg·cm~(-2))引起心肌细胞存活率显著降低,且有机组分毒性大于其他组分.根据细胞活力测定结果,选择低染毒浓度(10μg·cm~(-2))暴露细胞,采用qRT-PCR和ELISA试剂盒检测炎症因子变化.与对照组相比,金属组暴露后,炎症因子TNF-α和IL-1β显著升高,而有机组则显著升高TNF-α的含量.结果表明,造成心肌细胞存活毒性和炎症损伤的主要PM_(2.5)组分可能为有机组分和金属组分,而炎性反应对这两种组分的响应存在显著差异.     

PM2.5对小鼠和H9C2细胞心肌肥大相关因子mRNA表达的影响

用采自太原市4个不同季节的细颗粒物(PM_(2.5))对小鼠心肌细胞H9C2进行染毒后,采用荧光定量PCR技术检测心肌肥大相关因子ANP和TGF-β的mRNA水平.采用浓度分别为0、1、3、10μg·mL~(-1)的冬季PM_(2.5)处理H9C2细胞后,检测心肌肥大相关因子ANP、β-MHC、MMP2和MMP9的mRNA水平.之后分别选取4周龄、4月龄、10月龄C57BL/6雌性小鼠作为实验模型,采用咽后壁滴注的方法用3 mg·kg~(-1) PM_(2.5)暴露4周.采用苏木素-伊红染色(HE)对小鼠心脏组织病理切片进行观察,并检测ANP和β-MHC的mRNA水平.结果发现,与对照组相比,冬季PM_(2.5)诱导H9C2细胞中ANP和TGF-β的mRNA水平升高最为显著;其中,当冬季PM_(2.5)染毒浓度较高时可诱导ANP、β-MHC、MMP2和MMP9的mRNA水平均显著升高.经PM_(2.5)暴露4周后,幼年和老年小鼠心肌细胞核质比显著降低.老年小鼠心脏组织中ANP和β-MHC的mRNA表达水平显著上升.实验表明,冬季PM_(2.5)诱导心肌肥大标志物表达改变的效应要强于其他季节,且有一定的剂量效应关系,而老年小鼠对PM_(2.5)诱导的心肌肥大效应最为敏感.     

SO2污染激活AT1R改变运动大鼠心肌胶原纤维形态学并导致心功能降低

为了观察SO₂污染环境下运动对大鼠心功能的影响,从心脏局部肾素-血管紧张素系统（renin-angiotensin system,RAS）核心成员——血管紧张素Ⅱ（angiotensin Ⅱ,AngⅡ）Ⅰ型受体（AT₁R）介导的心肌胶原纤维形态结构重塑的角度出发,应用心脏插管技术观察大鼠的心脏功能;采用放射免疫技术（ELISA）、免疫组织化学和胃酶酸解法等方法对心肌局部ρ（AngⅡ）、AT₁R蛋白表达水平、w（HYP）（HYP为羟脯氨酸）及胶原容积分数进行检测.结果表明:①单纯运动组（EG）大鼠主动脉收缩压、左室内压峰值、±dp/dt_max（左室内压最大上升速率/下降速率）显著升高（P < 0.01）,舒张压、AT₁R蛋白表达显著降低（P < 0.01）,w（HYP）、w（CC）（心肌胶原浓度）、PVCA（血管周围胶原面积）、CVF（心肌胶原容积分数）及ρ（AngⅡ）有升高趋势（P>0.01）;②单纯SO₂污染组（SRG）大鼠左室末期舒张压显著升高（P < 0.01）,左室内压±dp/dt_max显著降低（P < 0.01）;w（HYP）、w（CC）、PVCA、CVF、ρ（AngⅡ）及AT₁R蛋白表达水平均显著升高（P < 0.01）;③SO₂污染+运动组（SEG）大鼠左室末期舒张压显著升高（P < 0.01）,主动脉收缩压、左室内压峰值、左室内压±dp/dt_max显著降低（P < 0.01）,w（HYP）、w（CC）、PVCA、CVF、ρ（AngⅡ）及AT₁R蛋白表达水平均显著升高（P < 0.01）,并且较SRG大鼠升高更显著（P < 0.01）.研究显示,SO₂污染导致运动大鼠心肌胶原纤维形态结构发生异常重塑,最终使大鼠的心功能产生显著的负性变力性效应,其机制可能与心脏局部RAS系统的激活有关.      

尿激酶溶栓治疗急性心肌梗塞的观察与护理

运用尿激酶溶栓治疗急性心肌梗塞，运用现代护理程序，对病人实施整体护理．在严密监测精心护理下，病人病情恢复快，均好转出院。     

PM2.5暴露导致老年小鼠可逆性心肌肥大

采用10月龄C57BL/6雌性小鼠作为实验模型,将小鼠分为对照和PM_(2.5)染毒组两组.将染毒组小鼠采用3 mg·kg~(-1)PM_(2.5)暴露4周后,分别在最后一次暴露后1 d、1周和2周处死小鼠.采用苏木素-伊红染色(HE)对小鼠心脏组织进行观察;采用荧光定量PCR技术检测心肌肥大相关因子ANP和β-MHC及基质金属蛋白酶MMP2和MMP9的mRNA水平;并采用Western Blot技术检测TGFβ1和MMP2的蛋白表达水平.结果发现,与对照组相比,经PM_(2.5)暴露4周后,小鼠心肌细胞核质比显著降低,心脏组织中ANP、β-MHC、MMP2和MMP9的mRNA表达水平及TGFβ1和MMP2的蛋白表达水平显著上升.停止暴露恢复1周后,小鼠心肌细胞核质比降低仍有显著差异,TGFβ1和MMP2蛋白表达水平仍显著上升,而各基因mRNA表达水平与对照组相比无显著变化.停止暴露恢复2周后,小鼠心肌细胞核质比、上述基因的mRNA和蛋白表达均无显著性差异.实验表明PM_(2.5)暴露可导致小鼠可逆性心肌肥大,提示PM_(2.5)所造成的心肌肥大损伤效应是可逆的,在暴露停止后机体可以通过自我修复等过程逐渐恢复正常.     

Ecological Analysis of Spleen Hypertrophy in Cyclomorphic Rodents Taking into Account the Type of Ontogeny

The functional approach at the level of physiological functional groups (PFGs) reflecting two types of ontogeny was used to analyze spleen hypertrophy in five species of rodents. In addition to a wide variation of spleen weight, its hypertrophy was observed: in bank voles (Clethrionomys glareolus), the spleen weight was as great as 3.5 g versus the normal value of 100–150 mg. The variation range of the relative spleen weight was estimated. For example, in the dominant species, C. glareolus, this range was considerable (from 2 to 125). A distinct relationship with the types of animal ontogeny was revealed. The genus specificity of the phenomenon—its occurrence in three species of Clethrionomys voles and absence in Microtus voles and mice—was determined in the study region. The animals with normal and hypertrophied spleens did not differ from each other significantly in their vital activity (at least, with respect to the parameters studied). The voles with hypertrophied spleens normally reproduced, and the hypertrophy was asymptomatic. These findings suggest that the populations have adapted to a damaging factor (or factors) in the course of a prolonged coevolution. This parameter is regarded as the indicator of the presence of a damaging factor in the population.