基于热致液晶弹性体的仿生心脏泵的设计

为设计一款仿生心脏功能较佳的心室泵,采用柔性、热致伸缩的热致形变弹性体代替心肌,根据螺旋心室心肌带理论,选择心肌带的左心室段,并选取了Hilbert平面填充曲线作为热致导体在热致形变弹性体中的走行方式,设计出与真实心脏类似的心室泵结构.通过试验测量了所设计的心室泵的射血分数与心率,结果显示该心室泵的搏出量高于自然心脏,而其心率远低于自然心脏.相对于机械泵,所设计的心室泵结构与真实心脏类似,具有收缩能力强,射血分数高的优点,且不易破坏血细胞,生物相容性较好.不足之处在于,热致动液晶弹性体变形响应慢,暂时还未能达到正常心脏的心率.论证了构建双稳态结构,提高仿生心室泵效率的可能性,以及对于心肌纤维走向较为复杂的其他心肌带段,双轴拉伸机械雕刻对其仿生的可能性.此研究可为容积心脏泵的研发提供新的思路,也可以对右心衰竭等心脏疾病起到辅助治疗的作用.     

外源性磷酸肌酸停跳液对儿童心肌保护作用的临床观察

目的:观察外源性磷酸肌酸对儿童心肌保护作用。方法:将30例心脏手术患儿随机分为实验组和对照组,每组15例。实验组采用含磷酸肌酸(CP)的st.Thomas 号停跳液,对照组采用st.Thomas 号停跳液,分别以手术中心脏停跳液用量、心脏停搏情况、心脏复跳情况、术后心律失常的发生率、血中肌钙蛋白T(Tn T)评价两种诱导停跳液的心肌保护作用。结果:(1)实验组停跳液能达到与对照组停跳液同样好的停跳效果;(2 )心脏自动复跳率、复跳后ST段改变、术后心律失常的发生率,两组间差异无显著性(P>0 .0 5 ) ;(3)实验组术中、术后6、2 4、4 8h的血Tn T水平均明显低于对照组(P<0 .0 1)。结论:磷酸肌酸停跳液较单纯晶体停跳液具有更好的心肌保护作用。     

I、aVL、V5、V6导联Q波消失对急性下壁伴右室心肌梗死的诊断价值

目的探讨I、AVL、V5、V6导联Q波消失对急性下壁伴右室心肌梗死的诊断价值.方法观察73例急性下壁心肌梗死患者的心电图.结果 35例急性下壁伴右室梗死患者中有18例I、AVL、V5、V6导联Q波同时消失,占51.42%,而38例不伴右室梗死患者,仅有1例I、AVL、V5、V6导联Q波消失,占2.63%,差异有非常显著性 (P<0.01).以I、AVL、V5、V6导联Q波消失作为急性下壁伴右室梗死的诊断指标的敏感性为51.42%,特异性为97.36%.结论I、AVL、V5、V6导联Q波同时消失对急性下壁伴右室梗死具有较高的诊断价值.     

中西医结合治疗缓慢型心律失常34例疗效观察

目的观察中西医结合治疗缓慢型心律失常疗效．方法治疗组采用中西医结合治疗,静脉滴注生脉注射液、西咪替丁等,对照组使用阿托品等治疗缓慢型心律失常．结果两组结果经统计学处理,痊愈率有高度差异性（P〈0．01）,总有效率有统计学意义（P〈0．01）．结论用中西医结合治疗缓慢型心律失常疗效显著．     

人参皂苷Rb3及Rb2组合物对大鼠实验性心肌梗死的保护作用

目的研究人参皂苷Rb,及Rb,组合物对大鼠急性心肌梗死的保护作用。方法采用大鼠结扎左冠状动脉前降支制备急性心肌梗死模型,计算急性心肌梗死24h后的心肌梗死面积（MIS）,测定血清肌酸磷酸激酶（CK）、乳酸脱氢酶（LDH）、天门冬氨酸氨基转换酶（AST）、超氧物歧化酶（SOD）及谷胱甘肽过氧化物酶（GSH—Px）活力,丙二醛（MAD）及一氧化氮（NO）含量。结果人参皂苷Rb,及Rb：组合物5、10、20mg／kg均可明显缩小急性心肌梗死大鼠的MIS,降低血清CK、LDH、AST活性及MAD含量,提高血清SOD、GSH—Px活性及NO含量。结论人参皂苷Rb,及Rb：组合物对大鼠急性心肌梗死具有明显保护作用,可能与其增强抗氧化酶活性,减少氧自由基对心肌的损伤等机制有关。     

Effect of hydrogen sulfide on myocardial fibrosis and PPARγ and NF-κB expression in rat model of diabetes

AIM: To explore the effects of hydrogen sulfide (H₂S) on the myocardial fibrosis in a rat model of diabetes and its mechanism.METHODS: Single intraperitoneal injection of streptozotocin (STZ) was utilized to establish a rat model of diabetes. Sodium hydrosulfide was used as an exogenous donor of hydrogen sulfide. Male SD rats were randomly divided into control group, STZ group, STZ+H₂S group and H₂S group. Eight weeks later, HE and VG staining methods were used to observe the collagen distribution and collagen volume fraction was measured by image analysis. The expression levels of type I collagen, PPARγ and NF-κB in the cardiac tissues were determined by Western blotting.RESULTS: Compared with control group, collagen distribution and the expression levels of type I collagen and NF-κB in the cardiac tissues were markedly increased (P<0.05), while PPARγ was significantly decreased in STZ group (P<0.05), but these indexes were reversed significantly in STZ+H₂S group (P<0.05). The expression levels of type I collagen, PPARγ and NF-κB had no significant difference between H₂S group and control group.CONCLUSION: Hydrogen sulfide attenuates cardiac fibrosis in diabetic rats, and its mechanism may be related to PPARγ-NF-κB signaling pathway.     

Evaluation of cardiac performance of the dog after induction of portal hypertension and gastric ischemia

Objective: To determine changes in hemodynamic and cardiac energetic parameters in dogs after induction of portal hypertension and gastric ischemia. These blood flow alterations are similar to changes seen in splanchnic blood flow in dogs with gastric dilatation volvulus syndrome (GDV). Design: Original experimental study. Setting: Veterinary teaching hospital. Animals: Seven purpose‐bred, intact male dogs. Interventions: Standard midline laparotomy and median sternotomy were performed under general anesthesia. Dogs were instrumented to obtain arterial blood pressure, aortic flow, cardiac chamber pressures, central venous pressure, portal flow, and portal pressure. Colored microsphere technology was used for the determination of myocardial blood flow. Measurements and samples were obtained at baseline, following induction of portal hypertension, and after induction of portal hypertension and gastric ischemia. Measurements and main results: Left ventricular myocardial blood flow was increased from 81.8±20.1 mL/100 g/min at baseline to 127.7±57.2 mL/100 g/min (P=0.02) after induction of portal hypertension and gastric ischemia. Myocardial oxygen consumption increased from 142.2±27.4 J/min/100 g at baseline to 219.1±33.4 J/min/100 g (P=0.003) after induction of portal hypertension and gastric ischemia, but cardiac external work remained unchanged (13.67±6.2 to 13.27±9.6 J/min; P=0.78; power=0.79). Cardiac efficiency decreased from 11.6±6.1% at baseline to 7.6±5.1% (P=0.017) after induction of portal hypertension and gastric ischemia. Conclusions: Transfer of energy within the myocardium was less efficient after induction of portal hypertension and ischemia of the stomach wall. On the basis of these results, alterations in cardiac function associated with GDV may result from deterioration of cardiac efficiency.     

Hydrogen sulfide inhibits inflammatory responses induced by acute myocardial ischemia in isolated rat hearts

AIM：To investigate whether hydrogen sulfide (H2S) protects the hearts against inflammatory responses induced by acute myocardial ischemia in isolated rat hearts. METHODS：Rat acute myocardial ischemia injury was induced by ligation of the left anterior descending coronary artery for 4 h, and the normal perfusate was replaced with NaHS (5 μmol/L, 10 μmol/L and 20 μmol/L) perfusate accordingly in NaHS groups 2 h after ischemia. The changes of cardiac function in the myocardial ischemic injury rats were observed. The mRNA expression of TNF-α, IL-1β, IL-6, IL-10 and ICAM-1 was detected by real-time PCR. The protein level of nuclear factor-κB (NF-κB) in the myocardial tissues was detected by Western blotting. RESULTS：The cardiac function in ischemia group was lower than that in sham group (P<0.01). Compared with ischemia group, perfusion of NaHS resulted in the improvement of the cardiac function (P<0.05 or P<0.01). Compared with sham group, the mRNA expression of TNF-α, IL-1β, IL-6 and ICAM-1 in the cardiac tissues was significantly increased, and the mRNA expression of IL-10 in the cardiac tissues was significantly decreased in ischemia group (P<0.01). Compared with ischemia group, the perfusion of NaHS significantly decreased the mRNA expression of TNF-α, IL-1β, IL-6 and ICAM-1 (P<0.05 or P<0.01). The perfusion of NaHS at concentrations of 10 μmol/L and 20 μmol/L significantly increased the mRNA expression of IL-10 (P<0.01). The protein level of NF-κB in ischemia group was markedly higher than that in sham group (P<0.01). Compared with ischemia group, the perfusion of NaHS at concentrations of 10 μmol/L and 20 μmol/L significantly decreased the expression of NF-κB (P<0.05 or P<0.01). CONCLUSION：H2S protects the hearts against acute ischemia injury through inhibition of NF-κB activation and subsequent down-regulation of NF-κB-dependent inflammatory gene expression.     

Resolvin D1, a Metabolite of Omega-3 Polyunsaturated Fatty Acid,Decreases Post-Myocardial Infarct Depression

We hypothesized that inflammation induced by myocardial ischemia plays a central role in depression-like behavior after myocardial infarction (MI). Several experimental approaches that reduce inflammation also result in attenuation of depressive symptoms. We have demonstrated that Resolvin D1 (RvD1), a metabolite of omega-3 polyunsaturated fatty acids (PUFA) derived from docosahexaenoic acid, diminishes infarct size and neutrophil accumulation in the ischemic myocardium. The aim of this study is to determine if a single RvD1 injection could alleviate depressive symptoms in a rat model of MI. MI was induced in rats by occlusion of the left anterior descending coronary artery for 40 min. Five minutes before ischemia or after reperfusion, 0.1 μg of RvD1 or vehicle was injected in the left ventricle cavity. Fourteen days after MI, behavioral tests (forced swim test and socialization) were conducted to evaluate depression-like symptoms. RvD1 reduced infarct size in the treated vs. the vehicle group. Animals receiving RvD1 also showed better performance in the forced swim and social interaction tests vs. vehicle controls. These results indicate that a single RvD1 dose, given 5 min before occlusion or 5 min after the onset of reperfusion, decreases infarct size and attenuates depression-like symptoms.