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PubMed1980

[Early morphological changes during the development of cardiac hypertrophy (author's transl)].

The development of a cardiac hypertrophy depends on modulation of two parameters, such as the amount of increased work load imposed on the heart and the rapidity with which the work load is applied. A gradual development of cardiac hypertrophy is usually observed in humans; at variance, the induction of cardiac hypertrophy is quite a rapid process in animal experiments. The enlargement of cardiac muscle cells during hypertrophy is due not only to an increased synthesis of contractile proteins but also to an accumulation of other cell constituents parallelly involved in the hypertrophy process. The mechanism whereby new sarcomeres are formed during cardiac hypertrophy is not yet completely clarified. Once the stimulus producing overload is removed, cardiac hypertrophy can regress completely. The possible role of biological regulators in inducing cardiac hypertrophy was also discussed.

Aging↗
PubMed2005

Sequential development of hematopoietic and cardiac mesoderm during embryonic stem cell differentiation.

The ability to generate a wide spectrum of differentiated cell types from ES cells in culture offers a powerful approach for studying lineage induction and specification and a promising source of progenitors for cell replacement therapy. Although significant efforts are being made to optimize culture conditions for the generation of different cell populations from ES cells, the identification and efficient isolation of specific progenitors for many lineages within these cultures remains a major challenge. By specifically tracking hematopoietic and cardiac development, we demonstrate here that these two lineages arise from distinct mesoderm subpopulations that develop in sequential waves from pre-mesoderm cells. Access to these populations provides a unique approach to isolate and characterize the earliest progenitors of these lineages.

Animals↗
PubMed2002

Autotransplantation of the heart for primary cardiac malignancy: development and surgical technique.

Primary cardiac malignancy presents an unusual and difficult surgical challenge. Malignant tumors of the left atrium have proved problematic due to their posterior location and difficulty of surgical exposure. The technique of cardiac explantation, ex vivo resection and cardiac reconstruction, and reimplantation--the cardiac autotransplantation procedure--was developed to solve this anatomic problem. Herein, we discuss the development of this approach and describe the surgical technique.

Cardiopulmonary Bypass↗
PubMed2001

Visualization and functional characterization of the developing murine cardiac conduction system.

The cardiac conduction system is a complex network of cells that together orchestrate the rhythmic and coordinated depolarization of the heart. The molecular mechanisms regulating the specification and patterning of cells that form this conductive network are largely unknown. Studies in avian models have suggested that components of the cardiac conduction system arise from progressive recruitment of cardiomyogenic progenitors, potentially influenced by inductive effects from the neighboring coronary vasculature. However, relatively little is known about the process of conduction system development in mammalian species, especially in the mouse, where even the histological identification of the conductive network remains problematic. We have identified a line of transgenic mice where lacZ reporter gene expression delineates the developing and mature murine cardiac conduction system, extending proximally from the sinoatrial node to the distal Purkinje fibers. Optical mapping of cardiac electrical activity using a voltage-sensitive dye confirms that cells identified by the lacZ reporter gene are indeed components of the specialized conduction system. Analysis of lacZ expression during sequential stages of cardiogenesis provides a detailed view of the maturation of the conductive network and demonstrates that patterning occurs surprisingly early in embryogenesis. Moreover, optical mapping studies of embryonic hearts demonstrate that a murine His-Purkinje system is functioning well before septation has completed. Thus, these studies describe a novel marker of the murine cardiac conduction system that identifies this specialized network of cells throughout cardiac development. Analysis of lacZ expression and optical mapping data highlight important differences between murine and avian conduction system development. Finally, this line of transgenic mice provides a novel tool for exploring the molecular circuitry controlling mammalian conduction system development and should be invaluable in studies of developmental mutants with potential structural or functional conduction system defects.

Animals↗
PubMed1998

Distinct molecular phenotypes in murine cardiac muscle development, growth, and hypertrophy.

The onset of cardiac hypertrophy is associated with characteristic changes in myocardial gene expression that are thought to recapitulate a developmental gene program. We report here the first gene expression profile of the murine myocardium, using a rapid method of quantitative expression analysis based on real-time analytical RT-PCR. This assay was used to measure expression levels of 29 genes in (1) late stage development as represented by day 1 neonatal ventricles, (2) normal cardiac growth in 3 and 18 month old mice, and (3) cardiac hypertrophy following pressure overload by aortic constriction. For males and females normal growth is not associated with differential expression although there is elevated expression of skeletal and smooth muscle actin mRNA's in males compared to females. Using normal adult ventricles as a reference, there are many qualitative and quantitative differences between the day 1 neonatal myocardium and experimental cardiac hypertrophy. These data suggest that the response to POL involves a subset of re-expressed developmental genes together with altered expression of genes not necessarily associated with cardiac development.

Animals↗
PubMed2004

New developments in cardiac surgery.

In cardiac surgery new developments in the current area are mainly directed towards minimally invasive surgery techniques. New anastomotic devices for CABG are clinically available and will facilitate partial and total endoscopic CABG techniques. In valve surgery percutaneous techniques are already available for AVR and PVR. Single percutaneous mitral valve repair is not a too far away procedure. Tissue engineering will offer biocompatible heart valves. New developments for heart failure therapy are booming. The major drawback for the achievements of this amazing progress is the financial cost. An open debate between all the parties concerned in healthcare is urgently needed in order to maintain the quality of surgical care for the decades to come.

Coronary Artery Bypass↗
PubMed1998

New developments in cardiac magnetic resonance imaging.

Technical developments have increased the speed and versatility of cardiac magnetic resonance imaging (MRI). Numerous studies show that cardiac MRI is as accurate as more conventional alternatives for diagnosis of many cardiac conditions. This review looks at the current state of cardiac MRI, indicates those areas where MRI has become established as a reliable diagnostic technique and discusses future developments.

Aorta, Thoracic↗
PubMed1976

[Mechanisms of development of cardiac insufficiency in old age].

Tests conducted with adult (8--10 months) and old (26--28 months) rats brought evidence that in ageing the cardiac ejection, dp/dt max, contractility index, the ATP concentration, that of creatinophosphate, glycogen, pyruvate decline, the phosphorylation coefficient, the lactate content increase, while the level of water-soluble proteins and collagen diminishes and that of water-insoluble ones decreases. In adult rats hemodynamics and myocardial contractility change but unsignificantly on the 4--6th day after coarctation of the aorta, whereas in the old ones there occur functional and metabolic alterations in the heart that are indicative of a developing cardiac insufficiency. The age-specific differences persist also on the 14--16th day following coarctation of the aorta. During these periods the weight of the heart, the content of the myofribrillary proteins and collagen are on the rise, whereas in the old ones the weight of the heart remains unchanged and the level of water-soluble protein drops. Changes in the properties of the actomyosin complex, disruption of the calcium pump, shifts in the system of the energy generation, limitation of potential possibilities incident to the systems of protein biosynthesis in the myocardial cell, all this leads to the development of cardiac incompetence following loading in old age.

Aging↗
PubMed2001

Molecular mechanism of cardiac hypertrophy and development.

Congestive heart failure is a major issues for cardiologists and to fully understand heart failure, it is important to understand the mechanism of the development of cardiac hypertrophy. Hemodynamic overload, namely mechanical stress, is a major cause of cardiac hypertrophy and to dissect the signaling pathways from mechanical stress to cardiac hypertrophy, an in-vitro device by which mechanical stress can be imposed on cardiac myocytes of neonatal rats cultured in serum-free conditions has been developed. Passively stretching cardiac myocytes cultured on silicone membranes induced various hypertrophic responses, such as activation of the phosphorylation cascades of many protein kinases, expression of specific genes and an increase in protein synthesis. During this process, secretion and production of vasoactive peptides, such as angiotensin II and endothelin-1, were increased and they played critical roles in the induction of these hypertrophic responses. Candidates for the 'mechanoreceptor' that receives the mechanical stress and converts it into intracellular biochemical signals have been recently demonstrated. Gene therapy and cell transplantation are hopeful strategies for the treatment of heart failure and require an understanding of how normal cardiac myocytes are differentiated. A key gene that plays a critical role in cardiac development has been isolated. The cardiac homeobox-containing gene Csx is expressed in the heart and the heart progenitor cells from the very early developmental stage, and targeted disruption of the murine Csx results in embryonic lethality because of the abnormal looping morphogenesis of the primary heart tube. With a cardiac zinc finger protein GATA4, Csx induces cardiomyocyte differentiation of teratocarcinoma cells as well as upregulation of cardiac genes. Mutations of human CSX cause various congenital heart diseases including atrial septal defect, ventricular septal defect, tricuspid valve abnormalities and atrioventricular block.

Animals↗
PubMed2002

Depletion of recipient CD4+ but not CD8+ T lymphocytes prevents the development of cardiac allograft vasculopathy.

BACKGROUND: We have described that chimeric rat hearts bearing recipient-type antigen-presenting cells (APCs) do not reject acutely, but develop cardiac allograft vasculopathy (CAV) in untreated recipients. This suggests that CAV is triggered either by CD8+ direct allorecognition or by CD4+ indirect allorecognition. To determine the allorecognition pathway responsible for CAV in this model, recipients of chimeric hearts underwent either CD8+ or CD4+ T cell depletion. METHODS: Chimeric hearts were created via bone marrow transplantation in two fully major histocompatibility-mismatched rat strain combinations. DA recipients were thymectomized and treated with Ox8 and Ox38 murine monoclonal antibodies, which deplete CD8+ and CD4+ T cells, respectively. Chimeric PVG hearts bearing DA APCs, abbreviated PVG(DA), were heterotopically transplanted into recipients undergoing thymectomy alone or recipients undergoing thymectomy plus either CD4+ or CD8+ T cell depletion. RESULTS: PVG(DA) allografts survived 100 days, but developed CAV in thymectomized recipients and in those permanently depleted of CD8+ T cells. In contrast, chimeric hearts transplanted into permanently CD4+ T cell-depleted recipients survived 100 days and demonstrated no evidence of CAV. CONCLUSIONS: In this specific strain combination, recipient CD8+ T cells are neither necessary nor sufficient for the development of CAV, whereas recipient CD4+ T cells are required for the development of CAV. These findings suggest that CAV is dependent on CD4+ indirect allorecognition and that CD8+ direct allorecognition stimulated by nonprofessional APCs plays a minor role.

Animals↗
PubMed2003

Development of electrical activity in cardiac myocyte aggregates derived from mouse embryonic stem cells.

Embryonic stem cells differentiate into cardiac myocytes, repeating in vitro the structural and molecular changes associated with cardiac development. Currently, it is not clear whether the electrophysiological properties of the multicellular cardiac structure follow cardiac maturation as well. In long-term recordings of extracellular field potentials with microelectrode arrays consisting of 60 substrate-integrated electrodes, we examined the electrophysiological properties during the ongoing differentiation process. The beating frequency of the growing preparations increased from 1 to 5 Hz concomitant to a decrease of the action potential duration and action potential rise time. A developmental increase of the conduction velocity could be attributed to an increased expression of connexin43 gap junction channels. Whereas isoprenalin elicited a positive chronotropic response from the first day of spontaneous beating onward, a concentration-dependent negative chronotropic effect of carbachol only developed after approximately 4 days. The in vitro development of the three-dimensional cardiac preparation thus closely follows the development described for the mouse embryonic heart, making it an ideal model to monitor the differentiation of electrical activity in embryonic cardiomyocytes.

Adrenergic beta-Agonists↗
PubMed1988

Postnatal nutritional status influences development of cardiac adrenergic receptor binding sites.

Nutritional status in neonatal rats was manipulated by altering the litter size to produce overnourished (5-6 pups/litter) and undernourished animals (16-17 pups/litter) for comparison with standard nutritive status (10-11 pups/litter). Nutritionally deprived pups showed impaired body and cardiac growth and a slowing of development of cardiac membrane binding sites for alpha 1- and beta-receptor ligands. Overnourishment enhanced growth and receptor development. In all cases, restitution of receptor binding characteristics to normal occurred at the beginning of nutritional rehabilitation (i.e., at weaning), well before the return of body and organ weights. These results thus suggest that the ontogenetic pattern of receptor binding sites is dependent upon nutritional intake rather than on weight gains per se. Receptor deficits caused by neonatal malnutrition probably contribute to reduced responsiveness to adrenergic stimulation.

Adrenergic Fibers↗
PubMed1999

Angiotensin II receptor blockade during gestation attenuates collagen formation in the developing rat heart.

OBJECTIVE: Fetal cardiac development includes rapid formation of a three-dimensional collagen network, composed mainly of type I and III fibrillar collagens. Collagen fibrils have been found in cardiac jelly at very early stages of cardiac development and are thought to have structural and functional properties. In adult rat cardiac tissue, angiotensin II (AngII) via AT1 receptor binding and AngII-regulated expression of transforming growth factor beta-1 (TGF-beta 1) each upregulate collagen transcription. AT1 and AT2 receptor subtypes are developmentally regulated; both have been localized in fetal tissue where the AT2 receptor is considered a determinant of morphogenesis. We sought to determine whether blockade of either receptor would result in attenuation of collagen mRNA expression and fibrillar collagen accumulation and alter TGF-beta 1 mRNA expression in the developing fetal heart examined at birth. METHODS: Pregnant rats were treated either with an AT1 receptor antagonist losartan or an AT2 receptor antagonist PD123319 and compared with untreated age-matched controls. Offspring were studied within 24 h of birth. Type I and type III collagen mRNA expression, as well as TGF-beta 1 mRNA expression, were examined by in situ hybridization. Collagen concentration was determined spectrophotometrically by picrosirius red staining and type I and III collagens were detected by immunoblotting. RESULTS: We found: (1) comparable birth weights in control and PD123319-treated animals, but reduced body weight in newborn losartan-treated animals; (2) compared to untreated animals, type I collagen and TGF-beta 1 mRNA expression in cardiac tissue were each equally reduced in both losartan and PD123319-treated animals; (3) increased type III collagen mRNA expression in both PD123319- and losartan-treated groups; and (4) a significant decrease in total soluble cardiac collagen concentration in both losartan and PD123319-treated groups, confirmed by attenuated immunoreactivity of type I and III collagens in whole heart extracts by Western blotting. CONCLUSIONS: The results of these pharmacologic interventions suggest AngII receptors are expressed in cardiac tissue during gestation, where both AT1 and AT2 receptors are involved in the regulation of type I and III collagen expression and structural protein accumulation. These effects appear to be mediated, in part, by attenuated cardiac TGF-beta 1 levels. The marked decrease in newborn cardiac collagen content has yet undefined functional consequences.

Angiotensin II↗
PubMed2004

NF-kappaB activation is required for the development of cardiac hypertrophy in vivo.

In the present study, we examined whether NF-kappaB activation is required for cardiac hypertrophy in vivo. Cardiac hypertrophy in rats was induced by aortic banding for 1, 3, and 5 days and 1-6 wk, and age-matched sham-operated rats served as controls. In a separate group of rats, an IkappaB-alpha dominant negative mutant (IkappaB-alphaM), a superrepressor of NF-kappaB activation, or pyrrolidinedithiocarbamate (PDTC), an antioxidant that can inhibit NF-kappaB activation, was administered to aortic-banded rats for 3 wk. The heart weight-to-body weight ratio was significantly increased at 5 days after aortic banding, peaked at 4 wk, and remained elevated at 6 wk compared with age-matched sham controls. Atrial natriuretic peptide and brain natriuretic peptide mRNA expressions were significantly increased after 1 wk of aortic banding, reached a maximum between 2 and 3 wk, and remained increased at 6 wk compared with age-matched sham controls. NF-kappaB activity was significantly increased at 1 day, reached a peak at 3 wk, and remained elevated at 6 wk, and IKK-beta activity was significantly increased at 1 day, peaked at 5 days, and then decreased but remained elevated at 6 wk after aortic banding compared with age-matched sham controls. Inhibiting NF-kappaB activation in vivo by cardiac transfection of IkappaB-alphaM or by PDTC treatment significantly attenuated the development of cardiac hypertrophy in vivo with a concomitant decrease in NF-kappaB activity. Our results suggest that NF-kappaB activation is required for the development of cardiac hypertrophy in vivo and that NF-kappaB could be an important target for inhibiting the development of cardiac hypertrophy in vivo.

Adenoviridae↗
PubMed1994

[Perioperative management of a patient with myotonic dystrophy developing the cardiac symptoms initially prior to the neuromuscular symptoms].

The authors anesthetized a 48-year-old woman with endometrial cancer and a large ovarian cyst. She developed cardiac failure initially followed by the sick sinus syndrome and A-V block from hypertrophic cardiomyopathy, prior to neuromuscular symptoms. Epidural anesthesia assisted by general anesthesia was carried out safely without intravenous administration of any muscle relaxants. From this experience, it is considered that epidural anesthesia assisted with some other proper methods is suitable for surgery of lower abdomen.

Anesthesia, Epidural↗
PubMed1989

Altered sympathetic system and adrenoceptors during the development of cardiac hypertrophy.

Increasing experimental evidence suggests that the development of cardiac hypertrophy may involve the sympathetic system and associated receptor mechanisms. However, very little work has been done so far to understand changes in the sympathetic system and cardiac adrenoceptors soon after an increased work load is imposed on the heart. Accordingly rat hearts subjected to aortic banding-induced pressure overload were assessed 3, 7, and 14 days postoperatively. Sham-operated rats without aortic banding were used as a control group. Rats with aortic constriction had increases in heart rate, left ventricular systolic pressure, and total mechanical energy during the entire study period. The cardiac RNA level was increased without a significant increase in left ventricular mass on days 3 and 7 in aortic-banded animals; these results were associated with a decrease in the cardiac norepinephrine (NE) store and an increase in the plasma level of NE and dopamine beta-hydroxylase (DBH) activity. By day 14 a significant increase in left ventricular mass and the NE store were found; both plasma NE and DBH remained elevated. Catecholamines in other tissues such as the spleen and kidney were depleted in the banded group, whereas the dopamine level, particularly in the brain, was significantly higher during the entire study. Furthermore, the density of alpha-adrenoceptors was higher on day 3 of aortic banding, and a reciprocal correlation was evident between cardiac alpha- and beta-adrenoceptors on day 14; the density of beta-adrenoceptors was increased, whereas that of alpha-adrenoceptors was decreased in the banded group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Application of cDNA microarrays in determining molecular phenotype in cardiac growth, development, and response to injury.

BACKGROUND: Normal myocardial development and the tissue response to cardiac stress are accompanied by marked changes in gene expression; however, the extent of these changes and their significance remain to be fully explored. We used cDNA microarrays for gene expression profiling in rat cardiac tissue samples to study developmental transitions and the response to myocardial infarction (MI). METHODS AND RESULTS: Microarrays with rat cDNAs for 86 known genes and 989 anonymous cDNAs obtained by molecular subtraction (representational difference analysis) of mRNA from sham-operated and 6-week post-MI samples were used in 2-color hybridization experiments. Twelve known genes previously associated with myocardial development were identified together with 10 uncharacterized expressed sequence tags and 36 genes not previously associated with cardiac development. After MI, genes associated with myocardial stress and wound healing exhibited differences in magnitude and expression kinetics, and 14 genes not previously associated with MI were identified. In situ hybridization revealed mRNA localization characteristic of wound healing and vascular and cardiomyocyte reactivity. CONCLUSIONS: Tissue analysis of gene expression with cDNA microarrays provides a measure of transcriptional or posttranscriptional regulation and cellular recruitment. Our results demonstrate the complexity of gene regulation in the developing myocardium and show that cDNA microarrays can be used to monitor the evolution of the cardiac stress-inducible phenotype.

Animals↗
PubMed2005

[Role of MyD88-dependent nuclear factor-kappaB signaling pathway in the development of cardiac hypertrophy in vivo].

OBJECTIVE: To investigate the role of MyD88-dependent nuclear factor-kappaB (NF-(B) activation signaling pathway in the development of cardiac hypertrophy in vivo. METHODS: Dominant negative myeloid differentiation protein (dn-MyD) 88 fragment was inserted into pShuttle plasmid and then fused into adenovirus so as to construct Ad5-dn-MyD88. Some Sprague-Dawley (SD) rats underwent banding of aorta (aorta binding group) and some SD rats underwent sham operation (sham operation group). Part of the rats in the aorta banding group were transfected with Ad5-dn-MyD88 into the myocardium tissue (Ad5-dn-MyD88 transfection group) or adenovirus expressing dnMyD88 (Ad5-GFP) (control group) so as to determine the effect of blocking down stream of MyD88 signaling on the development of cardiac hypertrophy. Three days after the hearts of some rats from the 4 groups were collected and Western blotting was used to detect the expression of dn-MyD88 protein and fluorescent microscopy was used to detect the expression of GFP. Three weeks after the beginning of experiment the hearts were collected to calculate the heart weight/body weight (HW/BW) ratio and extract the plasma protein and nuclear protein. Electrophoretic mobility shift assay (EMSA) was used to determine the NFkappaB binding activity. Western blotting was used to examine the phosphorylation of IkappaBalpha and IKKalpha/beta with appropriate specific anti-phospho antibodies. RESULTS: Flag and dn-MyD88 were effectively expressed 3 days after the transfection of Ad5-dn-MyD88 into the myocardium. Three weeks after the HW/BW ratio was 0.47 +/- 0.01 in the aorta banding group, significantly higher, by 37.8%, than that of the sham operation group (0.34 +/- 0.01, P < 0.01), and was 0.41 +/- 0.02 in the Ad5-dn-MyD88 transfection group, significantly lower, by 11.58%, than that of the aorta banding group (P < 0.01); the myocardial ANP protein expression level of the aorta binding group was significantly higher, by 43.5%, than that of the sham operation group (P < 0.01) and 36.2% higher than that of the Ad5-dnMyD88 transfection group (P < 0.01); the ANP/GAPDH in the aorta binding group was significantly higher than that of the sham operation group (P < 0.01) and that of the Ad5-dn-MyD88 transfection group (P < 0.01); the NF-kappaB binding activity in the myocardium of the aorta banding group was 9.94 +/- 1.58, significantly higher, by 144.8%, than that of the sham operation group (4.06 +/- 0.52, P < 0.01) and significantly lower, by 41.8%, than that of the Ad5-dn-MyD88 transfection group (5.79 +/- 0.52, P < 0.05); the phospho-(p-) IkappaBalpha level and p-IkappaBalpha/IkappaBalpha of the aorta binding group were significantly higher than those of the sham operation group (P < 0.01) and significantly higher, by 26.7%, than that of the Ad5-dn-MyD88 transfection group (P < 0.05); the p-IKKalphabeta/IKKalphabeta in the myocardium of the aorta binding group was significantly higher, by 318.0%, than that of the sham operation group (P < 0.01), and significantly higher, by 77.4%, than that of the Ad5-dn-MyD88 transfection group (P < 0.01). CONCLUSION: MyD88-dependent NFkappaB signaling is a novel pathway for inducing the development of cardiac hypertrophy in vivo and blocking MyD88 mediated signaling pathway attenuates the development of cardiac hypertrophy.

Adaptor Proteins, Signal Transducing↗