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PubMed1991

Spatial distribution of "tissue-specific" antigens in the developing human heart and skeletal muscle. II. An immunohistochemical analysis of myosin heavy chain isoform expression patterns in the embryonic heart.

The spatial distribution of alpha- and beta-myosin heavy chain isoforms (MHCs) was investigated immunohistochemically in the embryonic human heart between the 4th and the 8th week of development. The development of the overall MHC isoform expression pattern can be outlined as follows: (1) In all stages examined, beta-MHC is the predominant isoform in the ventricles and outflow tract (OFT), while alpha-MHC is the main isoform in the atria. In addition, alpha-MHC is also expressed in the ventricles at stage 14 and in the OFT from stage 14 to stage 19. This expression pattern is very reminiscent of that found in chicken and rat. (2) In the early embryonic stages the entire atrioventricular canal (AVC) wall expresses alpha-MHC whereas only the lower part expresses beta-MHC. The separation of atria and ventricles by the fibrous annulus takes place at the ventricular margin of the AVC wall. Hence, the beta-MHC expressing part of the AVC wall, including the right atrioventricular ring bundle, is eventually incorporated in the atria. (3) In the late embryonic stages (approx. 8 weeks of development) areas of alpha-MHC reappear in the ventricular myocardium, in particular in the subendocardial region at the top of the interventricular septum. These coexpressing cells are topographically related to the developing ventricular conduction system. (4) In the sinoatrial junction of all hearts examined alpha- and beta-MHC coexpressing cells are observed. In the older stages these cells are characteristically localized at the periphery of the SA node.

Adult↗
PubMed2005

T-box genes coordinate regional rates of proliferation and regional specification during cardiogenesis.

Mutations in T-box genes are the cause of several congenital diseases and are implicated in cancer. Tbx20-null mice exhibit severely hypoplastic hearts and express Tbx2, which is normally restricted to outflow tract and atrioventricular canal, throughout the heart. Tbx20 mutant hearts closely resemble those seen in mice overexpressing Tbx2 in myocardium, suggesting that upregulation of Tbx2 can largely account for the cardiac phenotype in Tbx20-null mice. We provide evidence that Tbx2 is a direct target for repression by Tbx20 in developing heart. We have also found that Tbx2 directly binds to the Nmyc1 promoter in developing heart, and can repress expression of the Nmyc1 promoter in transient transfection studies. Repression of Nmyc1 (N-myc) by aberrantly regulated Tbx2 can account in part for the observed cardiac hypoplasia in Tbx20 mutants. Nmyc1 is required for growth and development of multiple organs, including the heart, and overexpression of Nmyc1 is associated with childhood tumors. Despite its clinical relevance, the factors that regulate Nmyc1 expression during development are unknown. Our data present a paradigm by which T-box proteins regulate regional differences in Nmyc1 expression and proliferation to effect organ morphogenesis. We present a model whereby Tbx2 directly represses Nmyc1 in outflow tract and atrioventricular canal of the developing heart, resulting in relatively low proliferation. In chamber myocardium, Tbx20 represses Tbx2, preventing repression of Nmyc1 and resulting in relatively high proliferation. In addition to its role in regulating regional proliferation, we have found that Tbx20 regulates expression of a number of genes that specify regional identity within the heart, thereby coordinating these two important aspects of organ development.

Animals↗
PubMed2000

Immunolocalization of the transcription factor Slug in the developing avian heart.

Slug is a transcription factor involved in processes such as the formation of mesoderm and neural crest, two developmental events that imply a transition from an epithelial to a mesenchymal phenotype. During late cardiac morphogenesis, mesenchymal cells originate from two epithelia--epicardial mesothelium and cushion endocardium. We aimed to check if Slug is expressed in these systems of epithelial-mesenchymal transition. We have immuno-located the Slug protein in the heart of quail embryos between Hamburger and Hamilton stages HH16 and HH30. In the proepicardium (the epicardial primordium), Slug was detected in most cells, mesothelial as well as mesenchymal. Slug immunoreactivity was strong in the mesenchyme of the endocardial cushions and subepicardium from its inception until HH24, but the immunoreactivity disappeared in later embryos. Only a small portion of the endocardial cells located in the areas of epithelial-mesenchymal transition (atrioventricular groove and outflow tract) were immuno-labelled, mainly between HH16 and HH20. Endocardial cells from other cardiac segments were always negative, except for a transient, weak immunoreactivity that coincided with the development of the intertrabecular sinusoids of the ventricle. In contrast, virtually all cells of the epicardial mesothelium were immunoreactive until stage HH24. The mesenchymal cells that migrate to the heart through the spina vestibuli were also conspicuously immunoreactive. The myocardium was not labelled in the stages studied. Our results stress the involvement of Slug in the epithelial to mesenchymal transition. We suggest that Slug can constitute a reliable marker of the cardiac epithelial cells that are competent to transform into mesenchyme as well as a transient marker of the epithelial-derived mesenchymal cells in the developing heart.

Animals↗
PubMed2000

Evidence for the expression of neonatal skeletal myosin heavy chain in primary myocardium and cardiac conduction tissue in the developing chick heart.

We isolated a neonatal skeletal myosin heavy chain (MHC) cDNA clone, CV11E1, from a cDNA library of embryonic chick ventricle. At early cardiogenesis, diffuse expression of neonatal skeletal MHC mRNA was first detected in the heart tube at stage 10. During subsequent embryonic stages, the expression of the mRNA in the atrium was upregulated until shortly after birth. It then diminished, dramatically, and disappeared in the adult. On the other hand, in the ventricle, only a trace of the expression was detected throughout embryonic life and in the adult. However, transient expression of mRNA in the ventricle was observed, post-hatching. At the protein level, during the embryonic stage, the atrial myocardium was stained diffusely with monoclonal antibody 2E9, specific for chick neonatal skeletal MHC, whereas the ventricles showed weak reactivity with 2E9. At the late embryonic and newly hatched stages, 2E9-positive cells were located clearly in the subendocardial layer, and around the blood vessels of the atrial and ventricular myocardium. These results provide the first evidence that the neonatal skeletal MHC gene is expressed in developing chick hearts. This MHC appears during early cardiogenesis and is then localized in cardiac conduction cells. Dev Dyn 2000;217:37-49.

Amino Acid Sequence↗
PubMed1993

The function of ATP/ADP translocator in the regulation of mitochondrial respiration during development of heart ischemic injury.

Inhibitor titration studies were carried out in order to quantify the amount of control exerted by ATP/ADP translocator on the rate of succinate, palmitoylcarnitine + malate and pyruvate + malate oxidation in ischemia-damaged heart mitochondria. It was shown that after 30 min of total ischemia in vitro the maximal value of the control coefficient of the translocator was as high as in the control: 0.5-0.72 (succinate), 0.8-0.87 (palmitoylcarnitine + malate), 0.83-0.95 (pyruvate+malate). However, the translocator-controlled range of respiratory rates of ischemic mitochondria was narrower than that of normal mitochondria. The control coefficient of the translocator close to State 3 and State 4 was equal to 0-0.15. After 45 min ischemia the maximal value of the translocator control coefficient decreased by 25-30% in comparison with normal mitochondria with all substrates investigated. This value was preserved within a wide range of mitochondrial respiratory rates including the maximal rate in State 3. It was found that the amount of ATP/ADP translocator in mitochondria decreased by 20% after only 45 min ischemia. Our data show that the ATP/ADP translocator is one of the most important steps in regulation of oxidative phosphorylation in isolated mitochondria during development of heart ischemic injury.

Animals↗
PubMed2006

Fgf8 is required for anterior heart field development.

In the mouse embryo, the splanchnic mesodermal cells of the anterior heart field (AHF) migrate from the pharynx to contribute to the early myocardium of the outflow tract (OT) and right ventricle (RV). Recent studies have attempted to distinguish the AHF from other precardiac populations, and to determine the genetic and molecular mechanisms that regulate its development. Here, we have used an Fgf8lacZ allele to demonstrate that Fgf8 is expressed within the developing AHF. In addition, we use both a hypomorphic Fgf8 allele (Fgf8neo) and Cre-mediated gene ablation to show that Fgf8 is essential for the survival and proliferation of the AHF. Nkx2.5Cre is expressed in the AHF, primary heart tube and pharyngeal endoderm, while TnT-Cre is expressed only within the specified heart tube myocardium. Deletion of Fgf8 by Nkx2.5Cre results in a significant loss of the Nkx2.5Cre lineage and severe OT and RV truncations by E9.5, while the remaining heart chambers (left ventricle and atria) are grossly normal. These defects result from significant decreases in cell proliferation and aberrant cell death in both the pharyngeal endoderm and splanchnic mesoderm. By contrast, ablation of Fgf8 in the TnT-Cre domain does not result in OT or RV defects, providing strong evidence that Fgf8 expression is crucial in the pharyngeal endoderm and/or overlying splanchnic mesoderm of the AHF at a stage prior to heart tube elongation. Analysis of downstream signaling components, such as phosphorylated-Erk and Pea3, identifies the AHF splanchnic mesoderm itself as a target for Fgf8 signaling.

Animals↗
PubMed2002

Exercise training normalizes altered calcium-handling proteins during development of heart failure.

The cardiac sarcoplasmic reticulum calcium-ATPase (SERCA2a), Na+/Ca2+ exchanger (NCX1), and ryanodine receptor (RyR2) are proteins involved in the regulation of myocyte calcium. We tested whether exercise training (ET) alters those proteins during development of chronic heart failure (CHF). Ten dogs were chronically instrumented to permit hemodynamic measurements. Five dogs underwent 4 wk of cardiac pacing (210 beats/min for 3 wk and 240 beats/min for the 4th wk), whereas five dogs underwent the same pacing regimen plus daily ET (5.1 +/- 0.3 km/h, 2 h/day). Paced animals developed CHF characterized by hemodynamic abnormalities and reduced ejection fraction. ET preserved resting hemodynamics and ejection fraction. Left ventricular samples were obtained from all dogs and another five normal dogs for mRNA (Northern analysis, band intensities normalized to glyceraldehyde-3-phosphate dehydrogenase) and protein level (Western analysis, band intensities normalized to tubulin) measurements. In failing hearts, SERCA2a was decreased by 33% (P < 0.05) and 65% (P < 0.05) in mRNA and protein level, respectively, compared with normal hearts; there was only an 8.6% reduction in mRNA and a 32% reduction in protein in exercised animals (P < 0.05 from CHF). mRNA expression of NCX1 increased by 44% in paced-only dogs compared with normal (P < 0.05) but only by 22% in trained dogs (P < 0.05 vs. CHF); protein level of NCX1 was elevated in paced-only dogs (71%, P < 0.05) but partially normalized by ET (33%, P < 0.05 from CHF). RyR2 was not altered in any of the dogs. In conclusion, long-term ET may ameliorate cardiac deterioration during development of CHF, in part via normalization of myocardial calcium-handling proteins.

Animals↗
PubMed1992

Expression of the sarcomeric actin isogenes in the rat heart with development and senescence.

Sarcomeric actin genes, alpha-cardiac and alpha-skeletal, are coexpressed in neonatal rodent hearts and are regulated in response to hormonal and hemodynamic stimuli; however, their precise developmental pattern of expression has not been determined, and it is unknown whether they are coexpressed during senescence. We have, therefore, investigated the accumulation of sarcomeric actin transcripts in rat heart during fetal and postnatal development and with senescence by two different techniques: primer extension analysis with an oligonucleotide common to both sarcomeric actins and RNA hybridization with specific cardiac alpha-actin cRNA probes. We found that at 17-19 days in utero both isogenes are coexpressed and alpha-skeletal actin mRNAs represent 28.0 +/- 0.8% of the sarcomeric actin mRNA total. Skeletal actin mRNAs increase to 40% of the total 1 week after birth (NS, p = 0.15), remain constant for 3 weeks, and decrease to less than 20% of the total in ventricles and atria of 1-month-old rats. The alpha-skeletal actin transcripts further decline to less than 5% of the total at 2 months of age and do not reaccumulate in senescent animals. There was no significant difference between male and female rat ventricles. By comparison with the known accumulations of alpha- and beta-myosin heavy chain mRNAs, our results demonstrate that whatever the developmental stage the kinetics of expression for the sarcomeric myosin and actin multigene families are independent.

Actins↗
PubMed1984

Hexose transport modification of rat hearts during development of chronic diabetes.

Transport of 3-o-methylglucose into hearts of chronic diabetic rats was studied to determine if loss of transporter activity could be accounted for by higher concentrations of citrate and triglyceride and to determine if 7 days post alloxan was a representative time period for study of myocardial changes in chronic diabetes. Chronic diabetes was induced in rats by rapid i.v. injection of alloxan (37.5 mg/kg body weight), and the rats were studied 1 to 5 weeks afterward. Basal sugar transport rate in isolated perfused hearts declined after 2 weeks of diabetes and was nearly undetectable at 3 to 5 weeks. Stimulation of transport by insulin was also very low. Triglyceride concentrations were 50% of normal and G6P concentrations were elevated, but citrate concentrations were not different from control. Results of these studies showed that tissue triglyceride and citrate concentrations were not correlated with transport inhibition in chronic diabetic rat hearts. Loss of basal transport activity and lowered insulin sensitivity in these hearts is more likely due to a loss of transporters from the sarcolemma. These studies also show that transport rate and metabolite concentrations continue to change over 5 weeks of diabetes, and, therefore, one time point cannot be defined as representative of chronic diabetes.

Animals↗
PubMed2002

Development of heart rate responses to acoustic stimuli in Muscovy duck embryos.

Heart rate (HR) of Muscovy duck embryos (Cairina moschata f. domestica) was continuously recorded from the 21st day of incubation (E21) until hatching (E35). During that period, embryos were exposed to different acoustic stimuli (species-specific maternal and duckling calls, music, rectangular and sine waves, white noise). Sudden HR changes occurred at the onset of acoustic stimulation (on-response), as well as spontaneously. From E27 onwards, the response rate was significantly higher than the rate of spontaneous HR changes. The on-response rate increased further until E30. Most responses were elicited by maternal calls and music, but rarely by duckling calls. On-responses could be classified into: HR increase (36.4%), HR decrease (37.9%) and an increase in instantaneous HR variability (23.2%). The increase in HR variability occurred only in response to sounds, but not spontaneously. HR increases were mainly observed when the baseline HR was lower than the long-term HR trend. On-response duration was no longer than 3 min in 90% of all observations. The hourly mean HR and standard deviation did not change, even during phonoperiods composed of several sound patterns and lasting several hours. We conclude that Muscovy duck embryos are able to perceive exogenous acoustic stimuli, and that the acousto-sensory-->cardiac axis is functional from E27.

Acoustic Stimulation↗
PubMed1998

Versican expression is associated with chamber specification, septation, and valvulogenesis in the developing mouse heart.

The versican (PG-M) gene encodes a chondroitin sulfate proteoglycan that is nonpermissive for cell migration and appears in association with slow cell proliferation and cytodifferentiation. Using the techniques of in situ hybridization and immunocytochemistry on sectioned mouse embryos, we found that the mRNA and protein for versican show similar distributions and are expressed in a dynamic pattern during development of the heart. Versican exhibits generalized expression in the tubular heart but becomes rapidly downregulated in the atrium and exhibits higher transcript levels on the right side of the ventricular chamber than the left, before the onset of ventricular septation. Versican is expressed strongly in the trabeculated ventricular myocardium, whereas the compact proliferative zone has lower transcript abundance. It is expressed in the outer layers and on the crest of the ventricular septum and is prominent on the mesenchymal cap of the primary atrial septum. Versican is particularly strongly expressed in the endocardial cushions of the atrioventricular and outflow tract regions and in the atrioventricular, semilunar, and venous valves. This study raises the possibility that versican may be involved in specification of the ventricular chambers, in growth and fusion of the atrial and ventricular septa, and in the transformation from epithelium to mesenchyme that characterizes development of the endocardial cushions. Versican may be a key participant in cardiogenesis, responding to the many diffusible signals that mediate interactions between the developing endocardium and myocardium.

Animals↗
PubMed2005

Nephropathy, but not retinopathy, is associated with the development of heart disease in Type 1 diabetes: a 12-year observation study of 462 patients.

AIMS: To study the occurrence of heart disease and death in Type 1 diabetic patients and evaluate whether presence of microangiopathy, i.e. nephropathy and retinopathy, was associated with the outcome. METHODS: A 12-year observation study of 462 Type 1 diabetic patients without a previous history of heart disease at baseline who were treated under routine care in a hospital out-patient clinic. RESULTS: A total of 85 patients developed signs of heart disease, i.e. myocardial infarction (n = 41), angina (n = 23), and heart failure (n = 17) and 56 patients died. The mortality for patients without signs of heart disease during the observation period was 7.6% compared with 51% in patients with myocardial infarction (P < 0.001), 26% in patients with angina (P < 0.01) and 65% in patients with heart failure (P < 0.001). The relative risk for death was 9.0 (P < 0.001) and 2.5 (P < 0.05) times higher in patients with macroalbuminuria and microalbuminuria, respectively. The risk for cardiovascular death was 18.3 times (P < 0.001) higher in patients with macroalbuminuria compared with patients with normoalbuminuria. In patients with sight-threatening retinopathy, the relative risk for death was 7.0 times higher (P < 0.01) and the risk for coronary heart disease events 4.4 times higher (P < 0.05) compared with patients with no retinopathy. However, when retinopathy was adjusted for presence of macroalbuminuria, this association disappeared. CONCLUSION: This study shows a high incidence of heart disease in patients with Type 1 diabetes. The worse prognosis was seen in patients with sight-threatening retinopathy and macroalbuminuria and microalbuminuria at baseline. Macroalbuminuria and microalbuminuria were independently associated with a high risk for heart disease and death while the association with sight-threatening retinopathy only occurred in the presence of nephropathy.

Adult↗
PubMed2003

Autoimmune cardiomyopathy and heart block develop spontaneously in HLA-DQ8 transgenic IAbeta knockout NOD mice.

A line of nonobese diabetic (NOD) mice expressing the human diabetes-associated HLA-DQ8 transgene in the absence of mouse IAbeta failed to show spontaneous insulitis or diabetes, but rather developed dilated cardiomyopathy, leading to early death from heart failure. Pathology in these animals results from an organ- and cell-specific autoimmune response against normal cardiomyoctes in the atrial and ventricular walls, as well as against very similar myocytes present in the outermost muscle layer surrounding the pulmonary veins. Progression of the autoimmune process could be followed by serial ECG measurements; irradiation of young animals significantly delayed disease progression, and this effect could be reversed by adoptive transfer of splenocytes taken from older animals with complete heart block. Disease progression could also be blocked by cyclosporin A treatment, but was accelerated by injection of complete Fruend's adjuvant. The constellation of findings of spontaneously arising destructive focal lymphocytic infiltrates within the myocardium, rising titers of circulating anticardiac autoantibodies, dilation of the cardiac chambers, and gradual progression to end-stage heart failure bears a striking resemblance to what is seen in humans with idiopathic dilated cardiomyopathy, a serious and often life-threatening medical condition. This transgenic strain provides a highly relevant animal model for human autoimmune myocarditis and postinflammatory dilated cardiomyopathy.

Animals↗
PubMed2006

Dosage-dependent transcriptional regulation by the calcineurin/NFAT signaling in developing myocardium transition.

Thin spongy myocardium is critical at early embryonic stage [before embryonic day (E) 13.5 in mice] to allow diffusion of oxygen and nutrients to the developing cardiomyocytes. However, establishment of compact myocardium at later stage ( approximately E16.5) during development is necessary to prepare for the increase in demand for blood circulation. Elucidating molecular targets of the spongy-compact myocardium transition between E13.5 and E16.5 in heart development is thus important. Previous studies demonstrated that multiple transcription factors and signaling pathways are involved in the regulation and function of the myocardium in heart development. Disruption of certain transcription factors or critical components of signaling pathways frequently causes structural malformation in heart and persistence of "thin spongy myocardium". We have recently demonstrated activation of the calcineurin/NFAT signaling pathway at E14.5 in developing myocardium. Constitutive inhibition of the calcineurin/NFAT signaling pathway caused embryonic lethality. Molecular targets downstream of the calcineurin/NFAT signaling pathway, however, remains elusive. Here, we report transcription targets, independently and dependently, regulated by the calcineurin/NFAT signaling during the E13.5-E16.5 myocardium transition. We have uncovered that expression of one-third of the induced genes during myocardium transition is calcineurin/NFAT-dependent. Among these calcineurin/NFAT-dependent transcription targets, there is a dosage-dependent regulation. Molecular studies indicate that formation of distinct NFAT:DNA complex, in part, accounts for the dosage-dependent regulation. Thus, in addition to temporal and spatial regulation, dosage-dependent threshold requirement provides another mechanism to modulate transcription response mediated by the calcineurin/NFAT signaling during heart development.

Animals↗
PubMed1986

Sarcolemmal Na-Ca exchange and sarcoplasmic reticulum calcium uptake in developing chick heart.

Ontogenetic changes in calcium transport mediated by the sarcolemmal Na-Ca exchanger and by the sarcoplasmic reticulum calcium pump were studied in crude membranes from chick heart. Transport activities were evaluated per mass of membrane protein and heart tissue. Relative to unit heart mass Na-Ca exchange activity increases linearly from embryonic day 4 to day 10 of newborn stage. The overall increase is about 20-fold. An excellent correlation exists between activity of sodium gradient-induced calcium uptake and ouabain-sensitive (Na,K)-ATPase in crude membranes of embryonic, newborn and adult hearts. In the same membrane preparations active calcium uptake into vesicles of sarcoplasmic reticulum increases about 3-fold from embryonic day 4 to embryonic day 7, and then increases continuously until day 20. This is followed by a 3-fold elevation in reticular calcium accumulation at hatching on day 21. Maximal sarcoplasmic reticulum calcium transport activity reached at day 10 after hatching is 40- to 50-fold greater than activity values at embryonic day 4. In adult hearts the activities of both Na-Ca exchange and reticular calcium uptake drop to levels characteristic for the late embryonic period. This comparative study of sarcolemmal sodium gradient-dependent calcium flux and reticular calcium sequestration demonstrates that during chick heart differentiation the two calcium transport systems do not develop in parallel. Na-Ca exchange appears to play a greater role in calcium control of embryonic as compared to newborn and adult hearts. By contrast, the contribution of sarcoplasmic reticulum calcium transport to cardiac calcium movements becomes more predominant during and after hatching.

Animals↗
PubMedDate not supplied

Lymphocytic subsets and histopathologic changes associated with the development of heart transplant arteriosclerosis.

Transplantation of vascularized organ allografts is associated with the development of arteriosclerosis in the vessels of the donor graft. We have recently examined the distribution of lymphocytic/mononuclear inflammatory cell subsets and histopathologic changes seen in the sequential development of transplant arteriosclerosis in cardiac allografts exchanged between inbred rat strain combinations (LEW-to-F344) that differ for weak histocompatibility loci. The donor grafts were harvested at 7, 14, 21, 28, 50 to 65, and 90 days after transplantation, and the vascular lesions were characterized for the immunopathologic changes associated with the chronic rejection of the grafts. The inflammatory cell infiltration of the graft myocardium was present as early as 7 days after transplantation (53.37 +/- 9.06 inflammatory cells/high-power field), and the accumulation of cells increased at 3 and 4 weeks after transplantation (112.12 +/- 16.58 and 130.40 +/- 21.24 cells/high-power field, respectively). The infiltrating inflammatory cells in the grafts at 4 weeks after transplantation were predominantly ED-1+ macrophages (63.39%), with a substantial number of OX19+ T lymphocytes (28%), OX8+ Tc/s cells (25.4%), 3.2.3+ natural killer cells (16.89%), W3/25+ Th cells (20.2%), and a small number of OX33+ B lymphocytes (1.13%) and interleukin-2 receptor+ T lymphocytes (2.6%). Among the T-cell population, most (87.6%) were positive (R73+) for T-cell receptors. The arteriosclerotic lesions present in the cardiac grafts exhibited a gradual increase in severity of the vascular intimal proliferation and a similar pattern of increased intensity of cellular infiltration. The lesions were infiltrated with inflammatory cells beginning in the first week and increasing for the first month after transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Suppression of atrial myosin gene expression occurs independently in the left and right ventricles of the developing mouse heart.

Many cardiac genes are broadly expressed in the early heart and become restricted to the atria or ventricles as development proceeds. Additional transcriptional differences between left and right compartments of the embryonic heart have been described recently, in particular for a number of transgenes containing cardiac regulatory elements. We now demonstrate that three myosin genes which become transcriptionally restricted to the atria between embryonic day (E) 12.5 and birth, alpha-myosin heavy chain (MHC), myosin light chain (MLC) 1A and MLC2A, are coordinately downregulated in the compact myocardium of the left ventricle before that of the right ventricle. alpha-MHC protein also accumulates in the right, but not left, compact ventricular myocardium during this period, suggesting that this transient regionalization contributes to fktal heart function. dHAND and eHAND, basic helix-loop-helix transcription factors known to be expressed in the right and left ventricles respectively at E10. 5, remain regionalized between E12.5 and E14.5. Downregulation of alpha-MHC, MLC1A, and MLC2A in iv/iv embryos, which have defective left/right patterning, initiates in the morphological left (systemic) ventricle regardless of its anatomical position on the right or left hand side of the heart. This points to the importance of left/right ventricular differences in sarcomeric gene expression patterns during fktal cardiogenesis and indicates that these differences originate in the embryo in response to anterior-posterior patterning of the heart tube rather than as a result of cardiac looping. Dev Dyn 2000;217:75-85.

Animals↗
PubMedDate not supplied

[Diastolic and systolic ventricles function at the early stage of the development of heart failure in patients with ischemic heart disease].

It was established that diastolic function of the left ventricle is realized as the process of filling, so any damage to it can be detected at the early stage not by any changes of systolic characteristics of the ventricle but from its diastolic ones. The signs of the development of biventricle dysfunction as an important part of heart failure progression can be seen at the early stage of this process. The formation of pulmonary hypertension and changes from right chambers of the heart comes secondly. The development of diastolic dysfunction of right ventricle becomes evident at still preserved its systolic function.

Cardiac Output, Low↗