MAGNETIC RESONANCE IMAGING OF CEREBRAL CORTICAL NECROSIS (POLIOENCEPHALOMALACIA) IN A DOG

A 3-year-old neutered female mixed breed dog was examined because of severe, generalized seizure activity, tetraparesis, and encephalopathic signs. Cerebrospinal fluid (CSF) evaluation was unremarkable except for a mild increase in protein. Serum and CSF titers for infectious diseases were negative. Magnetic resonance (MR) imaging examination of the brain was performed and lesions were found within the cerebral gray matter of the temporal and parietal lobes. The lesions had increased signal intensity on T1, T2, and proton density-weighted images. There was mild inhomogeneous enhancement following intravenous contrast medium administration. Neurologic status improved and the seizures were well controlled, but the dog never regained normal mentation and euthanasia was performed 10 weeks after initial evaluation. At necropsy, severe cerebral cortical necrosis was found in the regions corresponding to the lesions seen on MR imaging examination. Large numbers of fat-containing macrophages (gitter cells) were found within these areas, and are thought to be responsible for the characteristic hyperintensity seen on the MR images.     

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AIM: To investigate the contribution of angiotensin-converting enzyme inhibitor (ACEI) to the regulation of calpain system in infarcted myocardium. METHODS: Rat myocardial infarction (MI) model was established by permanent ligation of the left coronary artery. The treatment with the ACEI inhibitor rampril (1 mg·kg-1·d-1) was started 7 days prior to surgery. On day 1, 3, 7 and 14 after MI, protein levels of calpainⅠ, Ⅱ and calpastatin were determined in left ventricular free wall (LVFW), interventricular septum (IS) and right ventricule. RESULTS: CalpainⅠprotein level was increased in IS 14 d post MI, whereas the protein level of calpainⅡ was maximally increased in LVFW 3 d post MI. Rampril decreased protein up-regulation of calpainⅠ and Ⅱ, and reduced infarct size and interstitial fibrosis. Calpastatin protein expression was not affected by ACEI. CONCLUSIONS: CalpainⅠ is involved in cardiac remodelling in the late and calpainⅡ contributes to cardiac tissue damage in the early phase of MI. The heart protective effect of ACEI may be related to the inhibition of calpain system in the pathogenesis of myocardial infarction.     

MAGNETIC RESONANCE IMAGING FINDINGS OF PRESUMED CEREBELLAR CEREBROVASCULAR ACCIDENT IN TWELVE DOGS

The magnetic resonance imaging (MRI) findings of presumed cerebrovascular accident in 12 dogs are described. Fourteen lesions were seen, commonly (11 of 14) within the gray matter of the cerebellar hemispheres or vermis. Thirteen lesions were hyperintense on T2-weighted images (in 11 dogs) and one was hypointense. Eleven of 14 lesions were within the region supplied by the rostral cerebellar artery or one of its main branches and there was no, or minimal, mass effect. Contrast enhancement was only seen in six lesions and was mild in all. Gradient-echo images provided additional information in two dogs. The appearance of infarction in dogs with diffusion-weighted images (DWI) is similar to that in humans, and provided supportive evidence for the diagnosis of infarction in five dogs. The use of gradient-echo and DWI is recommended for the evaluation of suspected cerebrovascular accidents in dogs. Six of the 12 affected animals were spaniels or spaniel crosses, suggesting a possible breed predisposition.     

Effects of carvedilol,cilazapril and their combination on left ventricular remodeling after acute myocardial infarction in rats

AIM:To compare the effects of carvedilol, cilazapril and their combination on left ventricular remodeling(LVRM) after acute myocardial infarction(AMI) in rats. METHODS: Twenty-four hours after AMI operation, 100 surviving rats were randomly assigned to: ①AMI control(n= 25), ②AMI+carvedilol(1 mg·kg^-1 ·d^-1, n= 25)(C1), ③AMI+cilazapril(1 mg·kg^-1 ·d^-1, n= 25)(Z1), and ④ AMI+combination(n= 25) groups. Sham-operated group(n= 17) were selected randomly. After 4 weeks of therapy with the drugs gastric gavage, hemodynamic and pathological studies were performed. RESULTS: There were no significant differences in MI size among the four AMI groups(all P> 0.05) Left ventricular(LV) end diastolic pressure(LVEDP), volume(LVV), weight(LVW) and septal thickness(STh) were all higher and left ventricular pressure maximal rate of rise and fall(±d p /d t) were lower(all P< 0.01) in AMI group than sham-operated group. The LVEDP, LVV, LVW and STh were all lower and ±dp /dt were higher in Z1, C1, and combination groups than those in AMI group(P< 0.05, P< 0.01), with LVEDP and STh were more lower in the combination group than in the two monotherapy group(P< 0.05, P< 0.01), but there were no significant differences in other variables among the three therapy groups. CONCLUSION: Carvedilol, cilazapril and their combination all can prevent from LVRM after AMI in rats, improve hemodynamics and LV function, with the combination superior.     

Changes of potassium currents in rabbit ventricle with healed myocardial infarction

AIM: To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), and to investigate the changes of action potential duration (APD),transient outward potassium current (I_to), delayed rectifier potassium current (I_K) and inward rectifier potassium current (I_K1) of left ventricular myocytes in noninfarcted zone of HMI. METHODS: 12 rabbits were randomly assigned in two groups: HMI group (thoracotomy and ligation of the circumflex coronary); sham-operated group (thoracotomy but no conorary ligation). 3 months after operation, whole cell patch clamp technique was used to record APD, I_to, I_K and I_K1 of ventricular myocytes in non-infarcted zone. RESULTS: Membrane capacitance was larger in HMI group than that in sham-operated group. Action potential duration was lengthened significantly in HMI group and early after depolarization (EAD) appeared in HMI group. The densities of I_to, I_K,tail and I_K1 were reduced significantly in HMI group (P<0.01), from (6.72±0.42) pA/pF, (1.54±0.13) pA/pF and (25.6±2.6) pA/pF in Sham-operated group to (4.03±0.33) pA/pF, (1.14±0.11) pA/pF and (17.6±2.3) pA/pF, respectively. CONCLUSION: The reduced densities of I_to, I_K,tail and I_K1 in ventricular myocytes of non-infarcted zone in HMI are responsible for the prolongation of APD and the presentation of EAD, which play important roles in the malignant arrhythmia of HMI.     

Long-term effects of TCV116 on left ventricular remodeling and heart function after myocardial infarction in rats

AIM: To investigate the effects of long-term TCV116 on left ventricular remodeling and heart function after myocardial infarction. METHODS: Myocardial infarction (MI) was caused by ligation of the left anterior descending coronary artery in rats. One week after the surgical performance, the surviving rats were randomly assigned to the following treatment protocols: (1) MI rats with no therapy; (2) MI rats treated with TCV116 2 mg/kg per day; (3) Sham-operated control; (4) Sham-operated rats, treated with TCV116 2 mg/kg per day. At 22 weeks, cardiac hemodynamic parameters such as MAP, LVSP, dp/dt_max and LVEDP, and histomorphometric parameters such as LVW/BW and LVCA/BW were measured, mRNA of cardiac genes such as βMHC, BNP, TGF-β₁, collagen I and III were quantified, and survival rates were calculated. RESULTS: Compared with sham-operated rats, MI rats without therapy showed significant increases in histomorphometric parameters as well as in mRAN expressions of cardiac genes (P<0.01); While their hemodynamic parameters were significantly impaired (P<0.01), and survival duration shortened (P<0.05). Compared with MI rats without therapy, MI rats treated with TCV116 showed significant attenuation of mRAN expression of cardiac genes (P<0.01); While their hemodynamic parameters were significantly improved (P<0.05 or P＜0.01), and survival duration extended (P<0.05). CONCLUSION: Treatment with long-term angiotensin II type 1 receptor antagonist may improve left ventricular remodeling and cardiac function after MI in rats.     

Effects of non-excitatory electric stimulation on cardiac function in normal and infarcted heart rabbits and it's regional effect on myocardium

AIM: To investigate the influences of electric stimulation applied during the absolute refractory period (ARP) on the cardiac function of normal rabbits and rabbits after myocardial infarction (MI) and to observe the regional effects of this electric stimulation. METHODS: 64 rabbits were randomly assigned to normal and MI groups and each group was then divided into the anterior and posterior groups. A thoracotomy was performed 4 weeks after MI in rabbits. One set of electrodes was inserted into the anterior and posterior wall of left ventricle of the anterior and posterior groups, respectively. Current pulses were delivered during the ARP (called CCM) during sinus rhythm in rabbits. The left ventricular systolic pressure (LVSP) and the left ventricular end diastolic pressure(LVEDP) as well as maximum positive and negative left ventricular pressure change (±dp/dt_max) were observed. RESULTS: In the normal and MI groups, LVSP, +dp/dt_max significantly increased, and LVEDP, -dp/dt_max were reduced during CCM stimulation compared with the baseline (P<0.05). In the normal rabbits, electric stimulation in the anterior group improved the cardiac function more significantly than that in the posterior group (P<0.05). In the MI rabbits, there was no difference between the anterior and the posterior groups (P>0.05). CONCLUSION: Electric stimulation delivered during the ARP significantly enhances the contractility and the relaxation of myocardium in normal rabbits and rabbits after MI, and the effects of CCM stimulation on heart are regional.     

Effects of noninvasive delayed limb ischemic preconditioning on prognosis of myocardial infarction

AIM: To study the effects of noninvasive delayed limb ischemia preconditioning (NDLIP) on animal cardiac function, myocardial morphology and myocardial apoptosis after myocardial infarction (MI). METHODS: Healthy SD male rats[n=45, weighing (250±10) g] were randomly divided into 3 groups:MI group:the animal model of MI was established by surgical ligation of left anterior descending artery (LAD) after 2 weeks; NDLIP group:after the success of the MI animal model, NDLIP was carried out every other day until the 4th, 6th and 8th weeks; sham group:as the negative control group, the animals were taken heart LAD threading but no ligation. All rats were fed conventionally. At the end of the 4th, 6th and 8th weeks, all rats were made ventricular intubation, and then the hemodynamic parameters were recorded. The blood samples were withdrawn from the abdominal aorta and the serum was separated via centrifugation. The serum contents of Bcl-2 and Bax were measured by ELISA. Left ventricular anterior wall was homogenized. The mitochondrial respiratory chain complexes Ⅰ, Ⅱ, Ⅲ and Ⅳ in the myocardial tissues were detected by ELISA. RESULTS: At the end of the 4th, 6th and 8th weeks, compared with MI group, left ventricular systolic pressure in NDLIP group was significantly increased, while left ventricular end-diastolic pressure in NDLIP group was significantly decreased (both P<0.05). Mitochondrial respiratory chain complexesⅠ, Ⅱ, Ⅲ and Ⅳ in NDLIP group were significantly increased (P<0.05). The serum level of Bcl-2 in NDLIP group was significantly increased and Bax level was reduced remarkably (both P<0.01). CONCLUSION: NDLIP improves the hemodynamic indexes, promotes the mitochondrial respiratory function and inhibits cell apoptosis, thus improving the prognosis of MI.     

血浆D-二聚体和超敏C反应蛋白检测在急性脑梗死中的临床价值

目的探讨血浆D-二聚体(D-dimer,D-D)及超敏C反应蛋白(high-sensitivity C-reactive protein,hs-CRP)水平与急性脑梗死(acute cerebral infarct,ACI)的关系。方法采用免疫透射比浊法检测102例ACI患者和50例正常对照者血浆D-D和hs-CRP水平。根据梗死灶大小102例ACI患者分为大梗死灶组、中梗死灶组和小梗死灶组,并进行相关统计分析。结果 ACI组患者血浆D-D和hs-CRP水平显著高于正常对照组(P0.01);大梗死灶组D-D和hs-CRP水平明显高于中、小梗死灶,而中梗死灶组D-D和hs-CRP水平高于小梗死灶组。结论监测血浆D-D和hs-CRP能为ACI的临床诊断、病情判断提供重要的参考依据。