Effect of heat shock precondition on reperfusion arrhythmia in rats

AIM:To investigate the effect of the heat shock response on the reperfusion arrhythmias(RAs) and the possible mechanism involved. METHODS:Fifty-five Sprague Dawley rats were randomly divided into 2 groups: the heat shock group (group H,n=29) and the control group (group C,n=26). The rats in group H were preconditioned with heat shock 24 hours before, and that in group C were not. The hearts of 16 rats in group H and 16 in group C were exercised and mounted on a non-circulating Langendorff perfusion apparatus and perfused retrogradely with modified K-H buffer and mimic ischemia/reperfusion was applied. Additionally, conventional intracellular microelectrode techniques were used for recording such electrophysiological parameters as resting potential(RP), action potential amplitude(APA), over shot(OS), maximum depolarization velocity(Vmax) of the hearts of other 13 rats in group H and 10 in group C. RESULTS:①Prior heat stress significantly decreased reperfusion arrhythmia. ②The amount of CK release in the effluent in group H was much less than that in group C. ③Myocardial HSP70 content was elevated significantly in group H. ④Heat stress significantly increased myocardial anti-oxydases activity and decreased lipid peroxydative products. Additionally, heat stress significantly reduced the Vmax of action potential. It indicated that rapid Na⁺ channel of papillary muscles may be inhibited by heat shock. The degree of change of Vmax after ischemia in H group was significantly less than that in group C. And the time of reperfusoin with Tyrode's solution till the action potential appeared as large as that before perfusion with mimic ischemic solution is shorter in group H than in group C. CONCLUSION:Heat shock pretreatment markedly reduces ischemia/reperfusion-induced injury of heart and ventricular arrhythmias in rats and this effect may be associated with the inhibition of rapid Na⁺ channel of papillary muscles by heat shock and the increase in myocardial HSP70 and anti-oxydase activity.     

Arrhythmogenic right ventricular cardiomyopathy in Bulldogs: Evaluation of clinical and histopathologic features,progression, and outcome in 71 dogs (2004–2016)

ObjectivesThis study aimed to characterize the clinical and histopathological features of arrhythmogenic right ventricular cardiomyopathy (ARVC) in English Bulldogs, American Bulldogs, and Bulldog-type mixed breed dogs and assess affected Bulldogs for a striatin gene mutation previously reported in Boxers with ARVC.AnimalsSeventy-one Bulldogs fit the inclusion criteria. Genetic analysis was performed on five dogs. Cardiac post-mortem evaluations were performed on two dogs.MethodsMedical records from a single veterinary cardiology group (CVCA) were retrospectively evaluated. Tissue and blood samples were submitted for histopathological analysis and genetic testing in select patients.ResultsPresenting complaints included syncope (38%), arrhythmia (81.7%), or murmur (34.2%) documented on examination. On presentation, congestive heart failure (CHF) was diagnosed in 22 (31%) dogs, and 58 (81.7%) had ventricular arrhythmias. On bivariable analyses, the two-dimensional (2D) left atrial-to-aortic root ratio (LA:Ao) was the only prognostic variable significantly associated with survival time. Dogs with 2D LA:Ao below the mean (1.41) had longer median survival to all-cause mortality (12 months; 95% confidence interval [CI] six–15 months) than those with 2D LA:Ao above the mean (four months; 95% CI two–six months; p=0.0384). Most dogs (54%) died from cardiac disease, with 42.1% experiencing sudden death. The median time from diagnosis to cardiac death was four months.ConclusionsArrhythmogenic right ventricular cardiomyopathy affects Bulldogs with both arrhythmogenic and dilated-type phenotypes. Despite variable arrhythmia severity and predominantly right-sided involvement in many dogs, an increase in left atrial size was the only significant predictor of mortality in this sample of dogs.     

Anaesthetic management for balloon dilation of cor triatriatum dexter in a dog

A three-month-old female Rottweiler puppy was referred for intravascular correction of a previously identified cor triatriatum dexter. Echocardiography confirmed the presence of a hyperechoic membrane that divided the right atrium into a cranial and caudal chamber. A foramen in this membrane allowed the blood to flow from the caudal to the cranial chamber. Balloon dilation of the defect under transthoracic echocardiographic guidance was scheduled for the following day. The dog was premedicated with 0.5 μg/kg sufentanil and 0.2 mg/kg midazolam administered intravenously. General anaesthesia was induced with 2 mg/kg propofol and maintained with inhaled isoflurane in oxygen; at the same time, a constant rate infusion of 0.5 μg/kg/h sufentanil was administered by means of an infusion pump. Uneventful ventricular and supraventricular tachyarrhythmias developed during the placement of catheters and balloon dilation. At the end of procedure, when the guide wire and balloon catheter were removed, normal sinus rhythm was observed. To the authors’ knowledge, no previous reports have described the anaesthetic management of a balloon dilation procedure for cor triatriatum dexter in dogs.     

肺癌术后并发心律失常的相关因素分析

目的：探讨诱发肺癌术后心律失常的相关因素,为其防治提供依据。方法：对2002年3月～2006年8月期间的肺癌手术患者212例进行回顾性分析,以可能诱发术后心律失常的相关因素分组,比较术后心律失常的发生率。结果：年龄≥60岁、术前肺功能差（FEV1/FVC〈70%）、全肺切除术、术中失血量≥400ml、术后未安装镇痛泵等病例术后心律失常的发生率较高（P〈0.05）。结论：年龄≥60岁、术前肺功能FEV1/FVC〈70%、全肺切除术、术中失血量≥400ml等可能是肺癌术后心律失常的危险因素;术前改善心肺功能,严格掌握手术适应症,术中减少出血、避免损伤自主神经,术后纠正低氧、镇痛等可能会有效减少术后心律失常发生。     

Pivotal role of microRNAs in cardiac development and heart diseases

MicroRNAs (miRNAs) are non-coding small RNAs, which bind to the 3'-UTR of target mRNAs and negatively regulate the gene expression. Accumulating evidence demonstrates that miRNAs are involved in many biological processes such as embryo development, cell proliferation, differentiation, apoptosis and tumorigenesis. Heart development and heart diseases are complex processes controlled by various signaling pathways. Recent researches indicate the importance of miRNAs in the process of cardiac development and heart diseases. In this review, the role of miRNAs in cardiac development and the pathogenesis of heart diseases are overviewed. The insight into the regulating miRNAs will significantly expand the cardiovascular therapeutic strategies beyond classical pharmacology.     

Postconditioning of zacopride depresses ischemia/reperfusion-induced arrhythmias in rats

ATM: To investigate the effects of postconditioning of zacopride, a specific agonist of inwardly rectifying potassium channel (K_ir), on ischemia/reperfusion-induced arrhythmias and the involved electrophysiological mechanisms. METHODS: Langendorff-perfused SD rat hearts or anesthetized rats were subjected to coronary artery occlusion for 15 min followed by 15 min of reperfusion to induce ischemia/reperfusion arrhythmias. Zacopride was applied 3 min before reperfusion. Various arrhythmias were monitored and compared in different groups. The single rat ventricular myocyte was isolated by collagenase digestion. The effects of zacopride on hypoxia/reoxygenation-induced delayed afterdepolarizations (DADs) and ATP-sensitive potassium channel (K_ATP) were observed by the technique of whole-cell patch clamping. RESULTS: Post-conditioning of 0.1~10 μmol/L zacopride significantly prevented the hearts from reperfusion arrhythmias. During reperfusion, 0.1 μmol/L zacopride showed the maximum effect, with decreasing the number of premature ventricular beats (PVB), reducing the incidences of ventricular tachycardia (VT) and ventricular fibrillation (VF), and shorte-ning the duration of VT and VF (P<0.01). The postconditioning effects were partly reversed by 1 μmol/L BaCl₂(P<0.01), suggesting that the antiarrhythmic effect of zacopride was mediated by K_ir. In the in vivo study, 1.5~5 μg/kg zacopride had positive effects on reperfusion-induced VT and VF and negative effect on PVB. At the dose of 1.5 μg/kg, zacopride showed the most potent antiarrhythmic effect, which compared favourably with that of a classical antiarrhythmic agent, lidocaine. Furthermore, zacopride significantly inhibited hypoxia/reoxygenation-induced DADs (P<0.01). Zacopride had no effect on K_ATP.CONCLUSION: The inhibitory effect of zacopride on ischemia/reperfusion-induced arrhythmias is mediated by the activation of K_ir. Augmentation of K_ir cuvrent, thus diminishing the DADs, might be the critical mechanisms underlying postconditioning of zacopride.