Methods and Reliability of Tissue Doppler Imaging for Assessment of Left Ventricular Radial Wall Motion in Horses

Background: Noninvasive assessment of left ventricular (LV) function is incompletely studied in horses.
Objectives: The goals of this study were to investigate the feasibility, techniques, and reliability of tissue Doppler imaging (TDI) for characterization of LV radial wall motion in healthy horses.
Animals: Three Standardbreds, 3 Thoroughbreds; age 8–14 years; body weight 517–606 kg.
Methods: Repeated echocardiographic examinations were performed by 2 observers in unsedated horses using TDI. Test reliability was determined by estimating measurement variability, within-day interobserver variability, and between-day interobserver and intraobserver variability of all echocardiographic variables. Variability was expressed as coefficient of variation (CV) and the absolute value below which the difference between 2 measurements will lie with 95% probability.
Results: Assessment of LV radial wall motion by TDI was feasible in all horses. Measurement variabilities were very low (CV < 5%) to low (CV 5–15%) for most variables. Within-day interobserver variability as well as between-day interobserver and intraobserver variabilities were low to moderate (CV 16–25%) for most variables. All pulsed-wave TDI variables of systolic LV function showed very low to low variability, whereas some of the variables of LV diastolic and LA function showed moderate to high (CV > 25%) variability. Pulsed-wave TDI variables appeared more reliable than color TDI variables.
Conclusions and Clinical Importance: Measurement of TDI indices of LV function is feasible and reliable in adult Standardbred and Thoroughbred horses. The clinical relevance of LV function assessment by TDI remains to be determined.     

Right ventricular rupture after lateral thoracotomy for removal of rib-associated telangiectatic osteosarcoma in a dog

Objective – To describe a case of a focal right ventricular rupture following removal of a rib-associated telangiectatic osteosarcoma (TOS) in a dog.
Case Summary – A 2-year-old spayed female mixed-breed dog, weighing 20 kg, was presented in compensated hypovolemic shock due to active bleeding into the thoracic cavity. The dog was stabilized with appropriate fluid administration. Subsequent computed tomographic examination revealed a large mineralized mass originating from the body of a rib and displacing the heart. Two days after surgical removal of this mass, focal right ventricular rupture occurred and the dog died. The mass was later identified as a TOS.
New or Unique Information Provided – Although hemothorax secondary to TOS has been described previously, this report describes for the first time, spontaneous focal right ventricular rupture as a rare complication of thoracotomy and rib resection for the removal of a rib-associated, intrathoracic TOS.     

QUANTIFICATION OF LEFT VENTRICULAR MASS USING CARDIAC MAGNETIC RESONANCE IMAGING COMPARED WITH ECHOCARDIOGRAPHY IN DOMESTIC CATS

The hypotheses were that cardiac magnetic resonance imaging (cMRI) would accurately determine LV mass in domestic cats and would do so more accurately than echocardiography (ECHO). ECHO was performed on seven sedated cats. LV mass was calculated using the truncated ellipse formula from a right parasternal long-axis view. T1 weighted gradient echo cMRI was acquired from anesthetized cats during multiple phases of the cardiac cycle. Short-axis images were obtained by acquiring 3 mm thick contiguous slices perpendicular to the cardiac long axis. LV mass was determined using Simpson's rule. Endocardial and epicardial borders were traced on each slice at end-systole, end-diastole, and mid-cycle and the difference in areas was myocardial area. Myocardial area was multiplied by slice thickness to calculate myocardial volume. Total (summated) myocardial volume was multiplied by myocardial density (1.05) to obtain LV mass at three measured phases of the cardiac cycle. Cats were euthanized and the LV was dissected and weighed to determine true mass. CMRI at end-systole most accurately quantified LV mass and was more accurate than echocardiography (P = 0.0078). Actual LV mass ranged from 6.5 to 10.5 g (mean = 8.5 g, SD = 1.6 g) compared with MRI LV mass at end-systole, which ranged from 6.7 to 11.1 g (mean = 8.7 g, SD = 1.7 g) and echocardiographic LV mass at enddiastole, which ranged from 5.2 to 9.1 g (mean= 7.1 g, SD = 1.8 g). Inter- and intraobserver variability for cMRI was 2%. CMRI obtained at end-systole accurately and reliably quantifies LV mass in domestic cats. It is more accurate than the echocardiographic method used in this study.     

Nitric oxide opens the second window of protection in ischemic preconditioning via induction of heat shock protein 72

AIM:To examine the inhibition of nitric oxide (NO) synthesis during ischemic preconditioning (IP) on the induction of heat shock protein 72 (HSP72) and infarct size-limiting effect of the second window of protection. METHODS:Rabbits were subjected to 4 cycles of 5 min of coronary artery occlusion separated by 10 min reperfusion, or received a sham operation. During this procedure, N^G-nitro-L-arginine methyl ester (L-NAME, an inhibitor of NO synthase) was injected intravenously 5 min before IP followed by its continuous infusion. Twenty-four hours later, the hearts were rapidly excised for assaying HSP72 expression or were subjected to 30 min coronary artery occlusion followed by 120 min reperfusion and then measured infarct size (IS). RESULTS:Twenty-four hours later, immunoblotting revealed an increase in HSP72 protein levels in the IP group, and this was blocked by L-NAME. IS of the IP rabbits was reduced as compared with the control (29.8%±3.7% vs 50.8%±4.3%, P＜0.01). IS in the IP rabbits was elevtated as a result of L-NAME treatment (46.0%±5.1%). Administration of L-arginine reversed the effects of L-NAME on the induction of HSP72 and IS (33.5%±4.0%). The intravenous administration of S-nitroso-N-acetylpenicillamine (SNAP, a NO donor) increased the induction of HSP72 and reduced IS (31.3%±5.7%, P＜0.01vs control) 24 h later. CONCLUSION:These findings suggest that NO may be involved in the induction of HSP72 and the opening of the second window of protection of IP.     

海洋双吲哚化合物FGFC1对心血管血栓模型大鼠血浆FDP、D-D、Plg的影响

建立大鼠心血管血栓模型及观察海洋双吲哚生物碱FGFC1溶解大鼠心血管血栓的纤溶特性。采用异硫氰酸荧光素(Fluorescein 5-isothiocyanate, FITC)标记的纤维蛋白诱导法建立大鼠心血管血栓模型。低场核磁、冰冻切片荧光扫描和苏木精-伊红染色(Hematoxylin-eosin staining, H.E)成像观察大鼠心血管血栓模型建立情况。荧光分析方法检测空白组、对照组、u-PA阳性对照组、FGFC1低、中、高剂量给药组大鼠的血浆荧光强度,ELISA法测定各组大鼠血浆纤维蛋白降解产物(Fibrin degradation product, FDP)含量、D-二聚体(D-Dimer, D-D)含量以及纤溶酶原(Plasminogen, Plg)活性。FITC标记的纤维蛋白原(Fibrinogen, FIB)在还原性SDS-PAGE显示为FITC-α、FITC-β、FITC-γ 3条肽链,FITC-fibrin荧光显微镜下显示绿色荧光,表明标记成功。低场核磁成像显示造模组大鼠心脏组织密度升高,冰冻切片荧光扫描显示心脏血管存在荧光物质斑块,表明心血管血栓模型建成,同时H...     

心肌缺血后处理对急性ST段抬高型心肌梗死再灌注心律失常的影响

目的探讨缺血后处理对STEMI心肌再灌注心律失常的影响.方法 2006年10月—2009年1月在北华大学附属医院心内科住院的STEMI患者且于12 h内行直接PCI者共64例,随机分为两组：对照组（34例）和缺血后处理组（30例）.对照组给予单纯再灌注治疗,缺血后处理组采用再灌注30 s/再缺30 s,交替3次后再持续灌注的方法.对比观察再灌注心律失常的发生频率.结果与对照组相比,缺血后处理组再灌注心律失常的发生率显著减少.结论急性心肌缺血后处理能够显著减少再灌注心律失常的发生.     

兔肺静脉心肌袖与心律紊乱相关的形态学研究

目的观察肺静脉心肌袖的组织学形态特性,以了解异位兴奋和局灶性房颤起源于肺静脉的形态学基础。方法取20只健康家兔的左心房和肺静脉,通过HE染色、Masson染色进行组织学研究,并用图像分析比较形态学差异。结果肺静脉心肌袖心肌纤维集合成束,走行不规则、方向各异;心肌袖组织中可观察到染色浅淡的苍白样细胞,与P细胞相似,成群或成对孤立存在;横切面肺静脉心肌袖心肌细胞的胞浆面积小、核面积小、核浆比值小、核圆形度大、核周长短,与左心房心肌细胞比较,差异有统计学意义(P<0.01)。结论肺静脉根部存在心房肌的延伸即心肌袖,其心肌纤维分布不均匀,走行方向各异,可能是电传导不均一、各向异性的原因;苍白样细胞的存在可能是引发异位兴奋和局灶自律性升高的形态学基础;肺静脉心肌袖心肌细胞体积较小,胞核较圆。     

Effect of administering dexmedetomidine with or without atropine on cardiac troponin I level in isoflurane-anesthetized dogs

We aimed to determine whether dexmedetomidine administration with or without atropine increases cardiac troponin I (cTnI) level in healthy dogs. We hypothesized that 10 µg/kg dexmedetomidine + atropine increases the cTnI level, whereas 5 µg/kg dexmedetomidine + atropine does not. Eighteen healthy, pet dogs that underwent an orthopedic surgery or ovariohysterectomy were included in this study. The dogs were randomly assigned to atropine (0.02 mg/kg)–dexmedetomidine (10 µg/kg), saline–dexmedetomidine (10 µg/kg), and atropine (0.02 mg/kg)–dexmedetomidine (5 µg/kg) groups. Each dog was premedicated with atropine or saline intramuscularly (IM). After 10 min, they were IM injected with dexmedetomidine (10 or 5 µg/kg)–morphine (0.5 mg/kg)–midazolam (0.2 mg/kg). Following this, anesthesia was induced after 10 min with propofol and maintained with isoflurane in 100% oxygen. The median plasma cTnI level at 6, 12 and 24 hr after premedication was significantly higher than that at baseline. The cTnI level in the atropine–dexmedetomidine (10 µg/kg) group was significantly higher than that in the saline–dexmedetomidine (10 µg/kg) and atropine–dexmedetomidine (5 µg/kg) groups at 6 and 12 hr after premedication. The cTnI level returned to normal within 72 hr after premedication in all groups. The administration of atropine in combination with 10 µg/kg dexmedetomidine increased the cTnI level, indicating subclinical myocardial damage.     

Wistar rats from different suppliers have a different response in an acute myocardial infarction model

The Wistar rat is a commonly used strain for experimental animal models. Recently it was shown that results vary between studies using Wistar rats of different suppliers. Therefore we studied whether Wistar rats obtained from Harlan Laboratories (Ha, n = 24) and Charles River (CR, n = 22) had a different outcome in an acute myocardial infarction (AMI) model. AMI was induced in both Ha and CR Wistar rats by one operator. This resulted in a significantly higher survival rate for Ha (79.2 ± 10.2%) compared with CR rats (54.2 ± 10.2%, p < 0.05). Furthermore, CR rats had lost significantly more weight after 7 days (−5.9 ± 3.1%) compared with Ha rats (−0.8 ± 1.7%; p < 0.001), indicating a worse health status of the CR rats. Paradoxically, the induced infarct was smaller in CR rats (7.3 ± 3.6% of the heart) compared with Ha rats (12.1 ± 4.7%, p < 0.05). This indicates that CR rats were less sensitive for the cardiomyocyte damage subsequent to AMI induction, but remarkably showed more clinical side effects indicating that Wistar rats from two suppliers had a different response within the same AMI model.     

山羊胚胎心肌细胞分化发育的超微结构研究

利用透射电镜观察了山羊胚胎心肌细胞分化发育过程中超微结构的变化。结果表明 :2 6日龄的山羊胚胎心肌细胞内肌节初步形成。随着胚胎发育 ,心肌细胞的肌节逐步完善 ,心肌细胞内的线粒体数量逐渐增多 ,排列规则 ,线粒体嵴逐渐变密 ,心肌细胞之间的连接也随着胚胎的生长发育逐渐形成和加强 ;2 6日龄山羊胚胎心肌内可见粗面内质网 ;34日龄的山羊胚胎心肌细胞胞浆内可见肌浆网、肌膜下池、横小管和二联管已形成 ;山羊胚胎心肌细胞内糖原颗粒丰富 ,随着胚胎日龄的增长 ,胞质内散布的糖原颗粒呈减少的趋势 ,而肌丝之间的糖原颗粒呈增加趋势 ;2 6日龄的山羊胚胎心房肌内出现少量特殊颗粒