Influence of caffeine, Ca2+, and Mg2+ on ryanodine depression of the tension transient in skinned myocardial fibers of the rabbit

1992 ◽  
Vol 421 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Judy Y. Su
Keyword(s):  
Tension Transient ◽  
Myocardial Fibers

Mitochondria in Cardiomyopathy: Alterations in Size, Number and Internal Structures

1968 ◽  
Vol 26 ◽  
pp. 126-127
Author(s):  
George Hug ◽  
William K. Schubert
Keyword(s):  
Heart Failure ◽  
Biochemical Analysis ◽  
Left Ventricular ◽  
Size Number ◽  
Internal Structures ◽  
Left Ventricular Outflow ◽  
Chest X Ray ◽  
Myocardial Fibers ◽  
Muscle Biopsies ◽  
Needle Liver Biopsy

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.

Reconstruction of the Architecture of Ventricular Myocardial Fibers in Ex Vivo Human Hearts

2009 ◽  
Vol 12 (4) ◽  
pp. E225-E229 ◽  
Author(s):  
Changqing Gao ◽  
Kun Lu ◽  
Weihua Ye ◽  
Libing Li ◽  
Liuquan Cheng
Keyword(s):  
Ex Vivo ◽  
Myocardial Fibers

scholarly journals Heart transplantation in an adult patient with isolated noncompaction of the left ventricular myocardium

Medicina ◽  
2010 ◽  
Vol 46 (3) ◽  
pp. 193 ◽  
Author(s):  
Sigita Glaveckaitė ◽  
Kęstutis Ručinskas ◽  
Jelena Čelutkienė ◽  
Vytė Maneikienė ◽  
Diana Zakarkaitė ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Adult Patient ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Important Process ◽  
Ventricular Noncompaction ◽  
Myocardial Development ◽  
Myocardial Fibers ◽  
Heart Lesions

Isolated noncompaction of the ventricular myocardium is defined as a rare cardiomyopathy caused by intrauterine arrest of compaction of the myocardial fibers and meshwork, an important process in myocardial development, in absence of any coexisting congenital heart lesions. A lot of controversies exist about diagnostic criteria, nomenclature, origin, pathogenesis, and prognosis of this disease. Here, we describe an adult patient with isolated left ventricular noncompaction who presented with worsening congestive heart failure and was successfully treated with heart transplantation.

scholarly journals Protective Effect of Citrulline on the Hearts of Rats with Sepsis Induced by Cecal Ligation and Puncture

2018 ◽  
Vol 2018 ◽  
pp. 1-10
Author(s):  
Ji-qiu Zhou ◽  
Xiong Xu ◽  
Wei-wei Zhen ◽  
Yu-long Luo ◽  
Bin Cai ◽  
...  
Keyword(s):  
Protective Effect ◽  
Inflammatory Cell ◽  
Cecal Ligation ◽  
Blood Cell Count ◽  
Sod Activity ◽  
Cardiac Tissues ◽  
Blood Tests ◽  
Blood Biochemical ◽  
Neutrophil Percentage ◽  
Myocardial Fibers

Purpose. To investigate the protective effect of citrulline (Cit) on the hearts of rats with sepsis. Methods. Wistar rats were divided into the normal, sham-operated, CLP, Cit, and CLP+Cit groups. Routine blood tests were performed, and the blood biochemical indexes were measured. Pathological changes in the cardiac tissues were observed. The levels of NO and iNOS in blood and SOD activity and MDA levels in the heart were measured. Results. Less inflammatory cell infiltration of the myocardial fibers and significantly decreased white blood cell count, absolute neutrophil count, neutrophil percentage, CK, HBDH, and NO (all P<0.05) were detected in the CLP+Cit group compared with the CLP group. In addition, SOD activity and MDA levels in heart tissues were, respectively, higher and lower in the CLP+Cit group than in the CLP group (both P<0.05). Conclusions. Cit reduces pathological damage in the heart and enhances the heart’s antioxidant capacity, thereby protecting cardiomyocytes.

Diabetes increases stiffness of live cardiomyocytes measured by atomic force microscopy nanoindentation

2014 ◽  
Vol 307 (10) ◽  
pp. C910-C919 ◽  
Author(s):  
Juan C. Benech ◽  
Nicolás Benech ◽  
Ana I. Zambrana ◽  
Inés Rauschert ◽  
Verónica Bervejillo ◽  
...  
Keyword(s):  
Atomic Force Microscopy ◽  
Physiological Condition ◽  
Diabetic Mice ◽  
Cell Nuclei ◽  
Buffer Solution ◽  
Isolated Cardiomyocytes ◽  
Force Microscopy ◽  
Atomic Force ◽  
Myocardial Fibers

Stiffness of live cardiomyocytes isolated from control and diabetic mice was measured using the atomic force microscopy nanoindentation method. Type 1 diabetes was induced in mice by streptozotocin administration. Histological images of myocardium from mice that were diabetic for 3 mo showed disorderly lineup of myocardial cells, irregularly sized cell nuclei, and fragmented and disordered myocardial fibers with interstitial collagen accumulation. Phalloidin-stained cardiomyocytes isolated from diabetic mice showed altered (i.e., more irregular and diffuse) actin filament organization compared with cardiomyocytes from control mice. Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2a) pump expression was reduced in homogenates obtained from the left ventricle of diabetic animals compared with age-matched controls. The apparent elastic modulus (AEM) for live control or diabetic isolated cardiomyocytes was measured using the atomic force microscopy nanoindentation method in Tyrode buffer solution containing 1.8 mM Ca2+ and 5.4 mM KCl (physiological condition), 100 nM Ca2+ and 5.4 mM KCl (low extracellular Ca2+ condition), or 1.8 mM Ca2+ and 140 mM KCl (contraction condition). In the physiological condition, the mean AEM was 112% higher for live diabetic than control isolated cardiomyocytes (91 ± 14 vs. 43 ± 7 kPa). The AEM was also significantly higher in diabetic than control cardiomyocytes in the low extracellular Ca2+ and contraction conditions. These findings suggest that the material properties of live cardiomyocytes were affected by diabetes, resulting in stiffer cells, which very likely contribute to high diastolic LV stiffness, which has been observed in vivo in some diabetes mellitus patients.

scholarly journals Left ventricular noncompaction: Clinical-echocardiographic study

2012 ◽  
Vol 69 (1) ◽  
pp. 32-36 ◽  
Author(s):  
Aleksandra Nikolic ◽  
Ljiljana Jovovic ◽  
Slobodan Tomic ◽  
Milan Vukovic
Keyword(s):  
Heart Failure ◽  
Clinical Presentation ◽  
Color Doppler ◽  
Neuromuscular Diseases ◽  
Left Ventricular ◽  
Left Ventricular Noncompaction ◽  
Ventricular Noncompaction ◽  
Mortality And Morbidity ◽  
Echocardiographic Examination ◽  
Myocardial Fibers

Background/Aim. Left ventricular noncompaction (LVNC) is a disorder in endomyocardial morphogenesis, seen either isolated (in the absence of other cardiac anomalies) or in association with congenital heart disease and some neuromuscular diseases. Intrauterine arrest of the compaction of myocardial fibers is postulated to be the reason of LVNC. Recognition of this condition is extremely important due to its high mortality and morbidity that lead to progressive heart failure, ventricular arrhythmias and thromboembolic events. The aim of this study was to determine the prevalence and clinical presentation of LVNC among consecutive outpatients according to clinical and echocardiographyic findings. Methode. A total of 3,854 consecutive patients examined at the Institute for Cardiovascular Diseases within a period January 2006 - January 2007 were included in the study. All the patients underwent echocardiographic examination using the same equipment (Vivid 7, GE Medical System). Echocardiographic parameters and clinical presentation in patients with echocardiographic criteria for LVNC were analyzed. Results. Analyzing 3,854 consecutive outpatients, using two-dimensional Color Doppler echocardiography from January 2006 to January 2007, 12 patients met the criteria for LVNC. Seven of them were male. The mean age at diagnosis was 45 ? 15 years. Analyzing clinical manifestation of LVNC it was found that seven patients had signs of heart failure, six had arrhythmias with no embolic events. Conclusion. Our results suggest that the real prevalence of LVNC may be higher than expected. New studies have to be done to solve this problem.

scholarly journals Myocardial involvement in diabetes mellitus: echocardiography data

1996 ◽  
Vol 42 (2) ◽  
pp. 15-17
Author(s):  
Ye. I. Sokolov ◽  
A. P. Zayev ◽  
R. P. Olkha ◽  
T. P. Morozova ◽  
S. A. Zhizhina ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Peripheral Resistance ◽  
Posterior Wall ◽  
Minute Volume ◽  
Left Ventricular ◽  
Specific Power ◽  
Control Group ◽  
End Diastolic Volume ◽  
Myocardial Fibers ◽  
Hyperdynamic Syndrome

Echocardiographic parameters of the central and intracardiac hemodynamics were analyzed in 67 patients with compensated diabetes mellitus of types I and II of 2 to 6 years standing. The control group consisted of 30 subjects. The increase of the minute volume, stroke volume, specific power of the left ventricle, and reduction of total peripheral resistance were revealed in both groups of patients. These shifts are characteristic of a hyperkinetic type of central hemodynamics. The hyperdynamic syndrome was due to left-ventricular hypertrophy in patients with noninsulin-dependent diabetes and due to increased heart rate and the rate of circulatory shortening of myocardial fibers in patients with the insulin-dependent condition. Impaired diastolic function presenting as an increase of the end diastolic volume and a reduced rate of relaxation of the left-ventricular posterior wall myocardium were observed in all the patients, no matter what the type of the condition. The above shifts are predictors of a reduction of myocardial contractility, responsible for the grave and atypical course of coronary disease in diabetics.

scholarly journals Investigating the Histological Changes in Heart, Lung, Liver and Kidney of Male Albino Mice Treated with Ivabradine

2019 ◽  
Vol 16 (3(Suppl.)) ◽  
pp. 0719
Author(s):  
Hadeel Kamil Khaleel
Keyword(s):  
Pulmonary Congestion ◽  
Male Mice ◽  
Histological Changes ◽  
Cardiac Atrophy ◽  
Vascular Congestion ◽  
Myocardial Degeneration ◽  
Liver And Kidney ◽  
Tissue Changes ◽  
Myocardial Fibers ◽  
Hepatocyte Necrosis

            The present study aimed to investigate the histological changes of heart, lung, liver and kidney which caused by different concentrations (10, 20 and 40 mg/kg) of Ivabradine. Results of the study revealed some histological changes represented by aggregation of the lymphocytes around respiratory bronchioles of the lung. In the liver, the drug caused hepatocyte necrosis and infiltration of the lymphocytes. In Kidney, there are no histopathological modifications in the tissue after the animals treated with 10 mg\kg of Ivabradine. When the animals treated with Ivabradine drug at 20mg/kg of bw, dose showed vascular congestion between myocardial fibers of heart. Emphysematous changes of the alveoli and infiltration of lymphocytes around respiratory bronchioles of lung. In the liver there were dilated blood sinusoids. Also, there are vascular congestion and congestion of capillaries in the glomerular of kidney. Male mice treated with Ivabradine drug at 40 mg/kg of bw cause increase spaces between myocardial fibers, cardiac atrophy and myocardial degeneration in the heart. In addition, there are infiltration of lymphocytes around respiratory bronchioles, pulmonary congestion and emphysematous changes of the alveoli in lung. In the liver, the drug cause amyloid deposition and degeneration of hepatocytes. Furthermore, the drug caused vascular congestion in the kidney. Conclusion: From the current study, we conclude that the different concentrations of Ivabradine caused tissue changes in the heart, lung, liver and kidneys. The study should continue using different drugs and concentrations.

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