高血压大鼠心肌肾素-血管紧张素系统的日变化

目的：探讨高血压大鼠心肌肾素-血管紧张素系统（RAS）元件基因（ATNG、AT1R、AT2R）的昼夜节律表达与高血压左心室肥厚的相关性.方法：建立肾性高血压大鼠的模型.取自发性高血压大鼠（SHR）,肾性高血压大鼠（RHR）以及正常SD大鼠,在 12 h 光暗交替的环境中饲养2周后,每隔 4 h 取心脏,测心重指数等各项指标,用RT-PCR的方法检测高血压大鼠心肌组织与正常大鼠心肌组织中血管紧张素原（ATNG）,血管紧张素Ⅱ受体1型（AT1R）与血管紧张素Ⅱ受体2型（AT2R）表达的变化.结果：SHR和RHR的左心重与全心重比值及全心重与体重比值较对照组明显增大;SHR和RHR组心脏RAS元件基因表达较对照组增高.RAS元件基因的mRNA的表达都表现出昼夜节律,SHR和RHR组昼夜变化的幅度较对照组明显.结论：RAS元件基因的过表达和其波动的增加在心肌肥厚的发病过程中可能起到了一定的作用.     

Clinical validation of technetium-99m MIBI-gated single-photon emission computed tomography (SPECT) for avoiding false positive results in patients with left bundle-branch block: comparison with stress-rest nongated SPECT

BACKGROUND: Septal perfusion defects are common on myocardial perfusion single-photon emission computed tomography (SPECT) slices in patients with left bundle-branch block (LBBB) in the absence of coronary artery disease. HYPOTHESIS: The use of gated myocardial perfusion SPECT imaging in such patients should be clinically validated. The aims of this study were, therefore, to validate clinically the use of gated myocardial SPECT imaging to avoid false positive septal perfusion defects in patients with LBBB and to compare nongated and gated SPECT imaging techniques in the same patients in the same imaging session. METHODS: We performed stress-rest myocardial perfusion SPECT and resting gated SPECT using Technetium-99m MIBI in 25 patients with LBBB and in 6 control subjects. Stress-rest SPECT images and end-diastolic and end-systolic gated SPECT slices were assessed visually and quantitatively (septum/lateral wall count ratio). Coronary angiography was performed in 15 patients with LBBB and in all 6 control subjects. RESULTS: Stress-rest (nongated) SPECT slices and end-diastolic and end-systolic gated SPECT images were normal in all control subjects. Stress-rest (nongated) SPECT imaging revealed septal perfusion defect in 20 (11 reversible, 9 irreversible) patients with LBBB, whereas the figures were 15 and 5 for end-systolic and end-diastolic gated SPECT images, respectively. Coronary angiography results were normal in all control subjects and in 15 patients with LBBB. Quantitative analysis of gated SPECT images revealed no statistically significant difference between patients with LBBB and control subjects in end-diastolic mean septum/lateral wall count values (0.86 +/- 0.19 in LBBB vs. 0.98 +/- 0.15 in normal subjects, p > 0.05), but the difference was statistically significant for end-systolic, stress, and rest values (p < 0.001 for all). CONCLUSION: Gated SPECT imaging, particularly end-diastolic images, revealed fewer false positive results and thus can be used to avoid false positive septal perfusion defects commonly seen in stress-rest (nongated) myocardial perfusion SPECT in patients with LBBB.     

Role of the sarcoplasmic reticulum in altered action potential and contraction of myopathic human and hamster ventricle

1. The present experiments were performed in order to study the role of the sarcoplasmic reticulum (SR) in the altered action potential and contraction of ventricular myocardium obtained from myopathic Syrian hamster and explanted human hearts (n = 8). The hamsters included age-matched healthy hamsters (F1B; n = 18), young myopathic hamsters (Bio 14.6; n = 8; aged 17-27 weeks) and older myopathic hamsters (n = 10; aged 39-43 weeks). 2. Action potentials were recorded by means of a microelectrode technique and force was recorded using a transducer. Post-rest potentiation of contraction (PRPC), a measure of the SR Ca2+-pumping activity, was determined after different rest intervals (2-60 s). Furthermore, cyclopiazonic acid (10 micro mol/L), a specific blocker of SR Ca2+-ATPase, was used to unmask abnormalities in the function of the SR. 3. The relationship between PRPC and rest interval was similar in younger healthy and myopathic hamsters, but the curve of the older myopathic muscle was obviously shifted downwards. Cyclopiazonic acid decreased predominantly the ascending part of the curve in both the healthy and myopathic hamster myocardium and could induce spontaneous action potentials during drug exposure or after washout. 4. In human myopathic myocardium, the curve of the PRPC-rest interval peaked at longer intervals (40-60 s) compared with that of the hamsters (10-20 s). Cyclopiazonic acid markedly depressed the relationship and increased the diastolic force (contracture) at high driving frequency, but did not induce action potentials during the rest interval. 5. We conclude that an impaired function of the SR contributes to the progressive deterioration of ventricular function in dilated cardiomyopathy and that the electromechanical behaviour of the ventricular myocardium of patients affected by dilated cardiomyopathy shows similarity and differences with the myopathic Syrian hamster model.     

Dynamic contrast-enhanced myocardial perfusion imaging using saturation-prepared TrueFISP

PURPOSE: To develop and test a saturation-recovery TrueFISP (SR-TrueFISP) pulse sequence for first-pass myocardial perfusion imaging. MATERIALS AND METHODS: First-pass magnetic resonance imaging (MRI) of Gd-DTPA (2 mL) kinetics in the heart was performed using an SR-TrueFISP pulse sequence (TR/TE/alpha = 2.6 msec/1.4 msec/55 degrees ) with saturation preparation TD = 30 msec before the TrueFISP readout. Measurements were also performed with a conventional saturation-recovery TurboFLASH (SRTF) pulse sequence for comparison. RESULTS: SR-TrueFISP images were of excellent quality and demonstrated contrast agent wash-in more clearly than SRTF images. The signal increase in myocardium was higher in SR-TrueFISP than in SRTF data. Precontrast SNR and peak CNR were not significantly different between both sequences despite 57% improved spatial resolution for SR-TrueFISP. CONCLUSION: SR-TrueFISP first-pass MRI of myocardial perfusion leads to a substantial improvement of image quality and spatial resolution. It is well suited for first-pass myocardial perfusion studies at cardiovascular MR systems with improved gradient hardware.     

Preconditioning - endogenous defence mechanisms of the heart

The term 'preconditioning' refers to the paradoxical phenomenon that pretreatment with a potential noxious stress-stimulus can increase cellular tolerance to subsequent noxious stress-stimuli. This was first described in an experimental model in dogs in which short-lasting periods of myocardial ischemia resulted in reduced infarction during a subsequent long-lasting coronary artery occlusion. Similar observations have also been made in other species and in other organs. During the last few years, the term preconditioning has been expanded to include pretreatment with other physical stress-stimuli or pharmacological agents that can increase cellular resistance to injury. The phenomenon probably represents a general adaptive response to cellular stress, but mechanisms involved are not fully clarified. This review focuses on preconditioning in the heart. Firstly, we want to address the observation that activation of endogenous defence mechanisms can increase cellular tolerance to several potentially noxious stimuli. Based on results from experimental research, we will give an overview of intracellular mechanisms that is currently in focus. Secondly, we want to address the potential role of preconditioning in clinical practice. We will present results from studies in patients with coronary artery disease and discuss possible clinical implications. Results show that the phenomenon probably exists in the human myocardium. In the future, this might be exploited in patients with acute coronary syndromes, especially since advanced techniques are now available for acute revascularization. Additionally, identification of possible mechanisms involved may influence the choice of medical treatment in high-risk patients with stable coronary artery disease. Preconditioning can also be exploited during elective surgical procedures. This should be of great interest, as the extent of elective surgery in patients at high-risk for coronary events is increasing. In this respect it is important to note that opioid-receptors are probably involved in preconditioning in humans. The last part of this review will address the possible relation between preconditioning and different anesthetic agents and sedatives.     

左旋四氢巴马汀对单个豚鼠心室肌细胞钙电流的阻滞作用(英文)

目的:研究左旋四氢巴马汀(l-THP)对L-钙电流的作用。方法:用全细胞膜片箝记录心室肌细胞的L-钙电流。结果:l-THP 1-100μmol·L~(-1)将I_(Ca~(2 )-max)从(999±93)PA分别减少到(700±111)pA(582±66)pA和(420±112)pA(n=6,P<0.01)。l-THP对钙通道有紧张性阻滞作用及使用依赖性。l-THP可将钙通道的恢复时间从(94±39)ms延长到(170±42)ms(n=6,P<0.01)。结论:l-THP对L-钙通道有阻滞作用。     

新型心肌灌注显像剂99mTc-Q3的标记方法学研究

为获得高质量的心肌灌注显像剂,作者进行了99m Tc-N,N′-亚乙基-二(乙酰丙酮亚胺)二[三(3-甲氧基-1-丙基)膦](99m Tc-Q3)的制备方法学研究.采用多元正交试验法进行了制备99mTc-Q 3最佳配方的筛选;用氯化亚锡化学还原法制备99mTC-Q3;用柱沉析法进行99m TC-Q3的分离和纯化、质量控制及体外稳定性试验;完成了无菌、热原、安全试验及家兔显像验证.制备99mTC-Q3的最佳配方为"A2B2C2"( 即:氢氧化钾、Sn2+及配体分别处于二水平的结果).药物标记率和放化纯大于99%.药物体外稳定性好,标记后4小时测得其标记率仍然大于92%(92%～99.37%).兔显像发现:注射 99 mTC-Q3后5分钟心肌便显影,至3小时心肌影像仍清晰可见.注射1小时后,血、肺中的放射性接近本底.提示:该方法可获得高质量的99mTC-Q3,而且为所有 9 9mTC-显像剂的制备建立了标准化流程,在此基础上可进一步研制99mTc-Q 3的一步法药盒.     

心复康对体外培养乳鼠心肌细胞缺氧损伤酶及超微结构影响的实验研究

目的:观察心复康对心肌细胞缺血样损伤的保护作用,探讨其保护机理。方法:采用培养的大白鼠乳鼠心肌细胞,通过暂时停止供应心肌细胞生存必需的糖和氧,造成心肌细胞缺血样损伤,观察心复康对体外培养心肌细胞心肌酶及超微结构的影响。结果:心复康可明显降低培养液中心肌酶的活性,改善心肌结构的缺血样损伤。结论:心复康对心肌细胞的缺血样损伤具有保护作用。     

晶体停搏液中钙离子浓度对幼兔未成熟心肌的保护作用

OBJECTIVE: To determine the myocardial protective effect of St. Thomas II cardioplegia at different calcium concentration on immature myocardium. METHODS: Isolated perfused neonatal rabbit hearts from three groups (the calcium concentration of St. Thomas II cardioplegia was modified: [Ca2+] 0.6 mmol/L; [Ca2+]1.2 mmol/L; [Ca2+]2.4 mmol/L) were subjected to 20 degrees C hypothermia, 90 minutes of global ischemia followed by 30 minutes reperfusion in Langendorff mode. RESULTS: Although the recovery of LVDP, +/- dp/dtmax at calcium content of 2.4 mmol/L after 10 minutes of reperfusion was significantly higher than that at 0.6 and 1.2 mmol/L calcium (P < 0.05, P < 0.01, respectively), the declined tendency of left ventricular hemodynamics in this group was detected after 20 minutes of reperfusion. By the end of 30-minute reperfusion, the left ventricular hemodynamic recovery at 2.4 mmol/L calcium did not differ from those at 0.6 mmol/L and 1.2 mmol/L calcium. Conversely, postischemic left ventricular functions at 0.6 and 1.2 mmol/L calcium were gradually improved during the 30 minutes reperfusion. Ca(2+)-ATPase activity at 2.4 mmol/L calcium showed significant increase (P < 0.01, P < 0.001), whereas ATP content was lower than that of other groups. CONCLUSION: Calcium accumulated in extracellular space during ischemia enters myocardial cell via Ca2+ channel and Ca2+/Na+ exchange after reperfusion, activates Ca(2+)-ATPase, and finally accelerates adenosinetriphosphate (ATP) consumption induced by calcium, which would be responsible for the results of our study. We conclude that, from the point of view of myocardial cell energy metabolism, St. Thomas II cardioplegia at high calcium concentration can not provide immature myocardium with optimal myocardial protection.     

参芪扶正注射液对小鼠心肌缺血再灌注损伤诱发心肌细胞凋亡的保护作用初探

目的：探讨参芪扶正注射液对小鼠心肌缺血再灌注损伤诱发的心肌细胞凋亡的保护作用。方法：40只小鼠随机分为4组，治疗组用参芪扶正注射液灌胃，阳性对照组用硝酸异山梨酯灌胃，模型组和空白对照组用生理盐水灌胃，对照观察小鼠缺血再灌注模型心肌细胞凋亡指数和凋亡相关蛋白Bcl-2、Bax表达。结果：参芪扶正注射液可通过上调Bcl-2、下调Bax的表达，明显抑制心肌细胞的凋亡。结论：参芪扶正注射液对小鼠心肌缺血再灌注损伤的心肌细胞有很好的保护作用。