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PubMed1997

Hyperplasia and hypertrophy of chicken cardiac myocytes during posthatching development.

For characterization of the growth pattern of cardiac myocytes during posthatching development, cardiac myocytes were enzymatically isolated from the ventricles of 1-, 15-, 29-, and 42-day-old chickens for measurement of myocyte nucleation, length, width, volume, and number, and for immunolabeling of cytoskeletal proteins. Ventricular myocyte number increased 156% from day 1 to day 42. Average cell volume increased more than 400%, and myocytes lengthened 125%, but cell width only increased 53% during this period. All myocytes were mononucleated at day 1. At day 15, 18% of myocytes became binucleated with < 1% of myocytes containing more than two nuclei. Interestingly, binucleated myocytes were able to divide with two nuclei going through mitosis at the same time. As demonstrated by staining with tubulin and alpha-actinin antibodies, two mitotic spindles and two cleavage furrows were formed in dividing binucleated myocytes. At day 42, binucleated myocytes increased to 44% with 11% of myocytes containing more than two nuclei. Sarcomeric alpha-actinin was partially disassembled in prometaphase and was reorganized into regular Z lines of sarcomeres in telophase. Desmin was disassembled in prophase and was reassembled during late telophase. These results suggest that chicken myocytes undergo hypertrophy and continue to proliferate during posthatching maturation, although it is currently believed that myocytes of all vertebrates withdraw from the cell cycle shortly after birth. We provide direct evidence for the first time of in vivo myocyte division in 6-wk-old chicken hearts.

Aging↗
PubMed1994

[2 cases of the tension pneumopericardium following blunt chest trauma resulting in the cardiac tamponade].

A 63-year-old man (case 1) was brought to our emergency unit following a high speed collision. He developed fatal cardiopulmonary arrest shortly after arrival despite resuscitation efforts. Tension pneumopericardium was revealed by chest X-ray and CT examination. An 18-year-old man (case 2) was admitted after a motorcycle accident. Pneumopericardium was noted on admission chest X-ray and CT examination. He developed cardiac tamponade after the examination. He was intubated and mechanically ventilated after the subxiphoid pericardial drainage. Pneumopericardium following blunt chest trauma is realized with tracheobronchial, pulmonary or esophageal injury. The clinical significance of pneumopericardium is the development of tension pneumopericardium resulting into cardiac tamponade. In a patient with traumatic pneumopericardium who requires mechanical ventilatory support, continuous pericardial drainage should be considered. In addition, tension pneumopericardium may occur in patients with breathing spontaneously as in our cases. In these cases, careful observation and immediate subxiphoid pericardial drainage are required.

Accidents, Traffic↗
PubMed2000

Cardiac hypertrophy and cardiac renin-angiotensin system in Dahl rats on high salt intake.

OBJECTIVE: On high salt intake, Dahl salt-sensitive rats develop cardiac hypertrophy disproportionate to the degree of hypertension. In the present studies, we assessed whether the cardiac hypertrophy induced by high salt depends on the development of hypertension per se, and leads to over-activity of the cardiac renin-angiotensin system (RAS). METHODS: Cardiac angiotensin converting enzyme (ACE) mRNA and activity, cardiac and plasma angiotensin I and II (AngI, II), as well as plasma renin activity (PRA) were assessed in Dahl salt-sensitive (Dahl S) and salt-resistant (Dahl R) rats on high (1370 micromol/g food) or regular salt (120 micromol/g food) diet for 2-5 weeks. Cardiac ACE and hypertrophic response in Dahl S on high salt were also assessed after central blockade of sympathetic hyperactivity and hypertension. RESULTS: In Dahl S rats, ACE mRNA and activity of the left ventricle (LV) increased markedly after 4-5 weeks of high salt diet compared with Dahl S on the control diet and Dahl R on either diet Chronic intra-cerebroventricular treatment with Fab fragments blocking brain 'ouabain' prevented the hypertension by high salt in Dahl S rats but did not affect the salt-induced increases in LV weight or in LV ACE mRNA and activity. On regular salt diet, Dahl S rats demonstrated significantly lower cardiac AngI and AngII than Dahl R rats. However, high salt intake did not cause significant changes in cardiac AngI and II in either strain. On regular salt diet, PRA, plasma AngI and II were all significantly lower in Dahl S versus R. In Dahl S rats, high salt did not cause further decreases of the already low PRA or plasma AngI and II. CONCLUSIONS: These data indicate a low activity of both circulatory and cardiac RAS in Dahl S versus R rats. The marked cardiac hypertrophy and increase in cardiac ACE mRNA and activity induced by high salt in Dahl S do not depend on the increase in blood pressure. High salt intake did not increase cardiac AngII in Dahl S, suggesting that the increase in ACE mRNA and activity may be relevant for non-angiotensinergic mechanisms involved in cardiac hypertrophy.

Angiotensin I↗
PubMed2003

Developmental anatomy of the heart: a tale of mice and man.

Because of the increasing availability of tools for genetic manipulation, the mouse has become the most popular animal model for studying normal and abnormal cardiac development. However, despite the enormous advances in mouse genetics, which have led to the production of numerous mutants with cardiac abnormalities resembling those seen in human congenital heart disease, relatively little comparative work has been published to demonstrate the similarities and differences in the developmental cardiac anatomy in both species. In this review we discuss some aspects of the comparative anatomy, with emphasis on the atrial anatomy, the valvuloseptal complex, and ventricular myocardial development. From the data presented it can be concluded that, apart from the obvious differences in size, the mouse and human heart are anatomically remarkably similar throughout development. The partitioning of the cardiac chambers (septation) follows the same sequence of events, while also the maturation of the cardiac valves and myocardium is quite similar in both species. The major anatomical differences are seen in the venous pole of the heart. We conclude that, taking note of the few anatomical "variations," the use of the mouse as a model system for the human heart is warranted. Thus the analysis of mouse mutants with impaired septation will provide valuable information on cellular mechanisms involved in valvuloseptal morphogenesis (a process often disrupted in congenital heart disease), while the study of embryonic lethal mouse mutants that present with lack of compaction of ventricular trabeculae will ultimately provide clues on the etiology of this abnormality in humans.

Anatomy, Comparative↗
PubMed1997

The cardiac transcription factors Nkx2-5 and GATA-4 are mutual cofactors.

The tissue-restricted GATA-4 transcription factor and Nkx2-5 homeodomain protein are two early markers of precardiac cells. Both are essential for heart formation, but neither can initiate cardiogenesis. Overexpression of GATA-4 or Nkx2-5 enhances cardiac development in committed precursors, suggesting each interacts with a cardiac cofactor. We tested whether GATA-4 and Nkx2-5 are cofactors for each other by using transcription and binding assays with the cardiac atrial natriuretic factor (ANF) promoter_the only known target for Nkx2-5. Co-expression of GATA-4 and Nkx2-5 resulted in synergistic activation of the ANF promoter in heterologous cells. The synergy involves physical Nkx2-5-GATA-4 interaction, seen in vitro and in vivo, which maps to the C-terminal zinc finger of GATA-4 and a C-terminus extension; similarly, a C-terminally extended homeodomain of Nkx2-5 is required for GATA-4 binding. Structure/function studies suggest that binding of GATA-4 to the C-terminus autorepressive domain of Nkx2-5 may induce a conformational change that unmasks Nkx2-5 activation domains. GATA-6 cannot substitute for GATA-4 for interaction with Nkx2-5. This interaction may impart functional specificity to GATA factors and provide cooperative crosstalk between two pathways critical for early cardiogenesis. Given the co-expression of GATA proteins and NK2 class members in other tissues, the GATA/Nkx partnership may represent a paradigm for transcription factor interaction during organogenesis.

Animals↗
PubMed2004

The effect of vascular endothelial growth factor on in vitro embryonic heart development in rats.

In vitro effects of vascular endothelial growth factor (VEGF) on heart development and total embryonic growth were investigated in 84 rat embryos (obtained from nine pregnant females) at 9.5 days of gestation that were cultured in whole rat serum (WRS), in <30 kDa + >50 kDa serum fractions [retenate (R)], and in R + VEGF. After 24-h culture, the embryos from each group were harvested and divided into two groups. One group was analysed morphologically and biochemically to obtain embryo protein content, the second group was serially sectioned and examined by light microscopy. Morphological score, embryo protein content, somite number and crown-rump length of embryos indicated that embryos cultured in R had significant embryonic retardation, whereas the addition of VEGF to R increased embryonic growth and development. The morphological scores for WRS, R and R + VEGF were 57.7 +/- 0.87, 46.6 +/- 1.90 and 52.1 +/- 0.97, somite numbers were 26.5 +/- 0.47, 20.1 +/- 0.63 and 24.4 +/- 0.46, crown-rump lengths were 3 +/- 0.07, 2.4 +/- 0.06 and 2.7 +/- 0.06 mm, and embryo protein contents were 160.5 +/- 7.41, 98.2 +/- 4.81 and 141.1 +/- 10.96 mug per embryo, respectively. The results of histological examination of heart development were similar. The hearts of embryos grown in R were unseptated and tubular. The atrioventricular endocardial cushions were incompletely developed. The addition of VEGF to R improved heart development. There were no gross morphological differences in the cardiac development between embryos grown in WRS and R + VEGF. In both groups, development of the muscular interventricular septum had begun. Development of the atrioventricular cushions was also similar in both groups and had caused narrowing of the atrioventricular canals, but the atrial septation was not observed.

Animals↗
PubMed1997

Indicators of delayed maturation of rat heart treated prenatally with dexamethasone.

We investigated the effects of prenatal dexamethasone treatment on indicators of cardiac maturation: heart weight/body weight ratios, myosin heavy chain (MHC) expression, cell proliferation, and extracellular matrix. We administered dexamethasone, a synthetic glucocorticoid (approximately 48 microg/d, 3-wk slow release pellets), to pregnant rats (n = 8) beginning at 17 d postconception. Control dams were unmanipulated (n = 8). After approximately 4-5 d of dexamethasone exposure, hearts were collected from neonatal rats (12-24 h after birth). The prenatal dexamethasone treatment produced smaller pups with larger heart/body weight ratios, accompanied by a higher proliferative index and a reduction in extracellular matrix in the ventricles (with lowest values in the septal region) compared with control pups. We also report that, although there were no sex differences in body mass or heart and heart/body weight ratios, females had a greater proportion of cells synthesizing DNA in the heart. In addition, ventricles of male pups treated with dexamethasone contained lower levels of alpha-MHC mRNA, as reflected in a sex by treatment interaction. The changes in each parameter are consistent with delayed maturation. Our findings suggest that exposure to excess glucocorticoids in utero can affect cardiac development in potentially detrimental ways and that assessment of cardiac function should be closely monitored when such circumstances arise.

Animals↗
PubMed1999

Cardiac arrhythmias and the athlete.

Athletes, although the healthiest segment of society, can develop cardiac arrhythmias. Benign bradycardias and atrial and ventricular premature contractions are common and seldom require treatment. Supraventricular tachycardias are less common and are usually not life-threatening, but do require treatment. Ventricular arrhythmias, although uncommon, are life-threatening and require treatment. Most athletes with ventricular arrhythmias have structural cardiac abnormalities, and further competitive play is usually prohibited. Commotio cordis, which is a recently described syndrome of sudden death caused by low-energy chest wall impact, may account for a significant percentage of the sudden deaths in athletes.

Arrhythmias, Cardiac↗
PubMed1975

Electrical alternans in cardiac tamponade.

Of nine patients with pericardial effusion due to various causes, four developed cardiac tamponade. Electrical alternans was present in all four, being total in three and ventricular in one. The alternans corresponded very well with the clinical diagnosis of cardiac tamponade and the radiological signs of a large pericardial effusion. In two patients alternans was present even with heart rates below 100 per minute. Apart from the exact (1 : 1) type of electrical alternans, three new types are described, a 2 : 1, 3 : 1, and a varying type. It is concluded that (a) electrical alternans associated with pericardial effusion is strongly suggestive of impending or established cardiac tamponade, and (b) electrical alternans is produced when the heart is oscillating within the pericardial sac distended by fluid with a frequency equal to one-half (exact alternans), one-third (2 : 1 alternans), and one-quarter (3 : 1 alternans) of the heart rate. The aetiology and mechanism of electrical alternans are discussed.

Adult↗
PubMed1992

Fate of the atrioventricular endocardial cushions in the developing chick heart.

To determine the fate of the atrioventricular endocardial cushions in cardiac development, we used staining methods for extracellular fibronectin, which is abundant in the endocardial cushions, and actin, which is abundant in the myocytes. White Leghorn chick embryo hearts were harvested at Hamburger and Hamilton stages 26 to 36, and serial sections of the atrioventricular valve region were stained. Before atrioventricular valve formation, fibronectin and actin staining reveal separation between the fibronectin-rich endocardial cushions and the actin-rich myocardial layer. The developing mitral valve leaflets at all of the observed stages contain a fibronectin-rich matrix but no actin-rich myocytes. In contrast, the tricuspid band includes both fibronectin matrix and actin-rich cells. We conclude that the mitral valve leaflets in the chick form predominantly from the endocardial cushion tissue, and the tricuspid band receives contributions from both the endocardial cushions and surrounding myocardium.

Actins↗
PubMed2003

Preservation of base-line hemodynamic function and loss of inducible cardioprotection in adult mice lacking protein kinase C epsilon.

Signaling pathways involving protein kinase C isozymes are modulators of cardiovascular development and response to injury. Protein kinase C epsilon activation in cardiac myocytes reduces necrosis caused by coronary artery disease. However, it is unclear whether protein kinase C epsilon function is required for normal cardiac development or inducible protection against oxidative stress. Protein kinase C delta activation is also observed during cardiac preconditioning. However, its role as a promoter or inhibitor of injury is controversial. We examined hearts from protein kinase C epsilon knock-out mice under physiological conditions and during acute ischemia reperfusion. Null-mutant and wild-type mice displayed equivalent base-line morphology and hemodynamic function. Targeted disruption of the protein kinase C epsilon gene blocked cardioprotection caused by ischemic preconditioning and alpha(1)-adrenergic receptor stimulation. Protein kinase C delta activation increased in protein kinase C epsilon knock-out myocytes without altering resistance to injury. These observations support protein kinase C epsilon activation as an essential component of cardioprotective signaling. Our results favor protein kinase C delta activation as a mediator of normal growth. This study advances the understanding of cellular mechanisms responsible for preservation of myocardial integrity as potential targets for prevention and treatment of ischemic heart disease.

Animals↗
PubMed1987

A method for recording isometric tension development by isolated cardiac myocytes: transducer attachment with fibrin glue.

The purpose of this study was to develop a method for attachment of single isolated cardiac myocytes to a transducer for recording isometric tension development. Cardiac myocytes were isolated from the hearts of the toad, Bufo marinus or ferrets by enzymatic digestion with collagenase. The method that we used provided a 60-80% yield of Ca++-tolerant cells. A suspension of cells was placed into a superfusion chamber coated with bovine thrombin. Two glass microtools - each attached to a micromanipulator - were brought into proximity with the ends of a single myocyte; one of the microtools was attached to the element of a low-level force transducer. Human fibrinogen was loaded into a fine-tipped glass micropipette mounted on a micromanipulator. Small amounts of fibrinogen were pressure-ejected from the pipette at each junction between the microtool and the end of the myocyte. The fibrin that formed produced a stable attachment of the ends of the myocyte to the microtools. The myocyte could subsequently be stretched and a length-tension curve recorded. We have used this method to record concentration-dependent tension development in response to the Ca++-ionophore, A23187, and potassium depolarization. Our results indicate that fibrin glue may facilitate the study of the mechanical properties of isolated myocytes.

Animals↗
PubMed1993

Residual strain in the ventricle of the stage 16-24 chick embryo.

Residual stress and strain, i.e., the stress and strain remaining in a solid when all external loads are removed, may be produced in biological tissues by differential growth. During cardiac development, residual stress and strain may play a role in cardiac morphogenesis by affecting ventricular wall stress. After a transmural radial cut, a passive ventricular cross section opens into a sector, and the size of the opening angle provides a measure of the circumferential residual strain. Residual strains were characterized in this manner for the apical region of the diastolic embryonic chick heart for Hamburger-Hamilton stages 16, 18, 21, and 24 (approximately 2.5, 3.5, 4.0, and 4.5 days, respectively, of a 21-day incubation period). The average opening angle at these stages was 107 +/- 10 degrees, 79 +/- 10 degrees, 73 +/- 11 degrees, and 74 +/- 7 degrees, respectively (n > or = 5 for each stage). These measured angles were correlated with changes in ventricular morphology. Scanning electron micrographs of the apex revealed that the wall of the ventricle is smooth at stage 16. Then at stage 18, myocardial trabeculae develop, forming ridges with primarily a circumferential orientation. By stage 21, the trabeculae develop into a mesh, giving the ventricular wall a spongelike appearance, and the preferred orientation is lost by stage 24. The large decrease in opening angle between stages 16 and 18 corresponded to the onset of trabeculation, which is the greatest change in form during the studied stages. We speculate that residual strain is an important biomechanical factor during cardiac morphogenesis.

Animals↗
PubMed2001

Electric field stimulation of cardiac myocytes during postnatal development.

Studies on cardiac cell response to electric field stimulation are important for understanding basic phenomena underlying cardiac defibrillation. In this work, we used a model of a prolate spheroidal cell in a uniform external field (Klee and Plonsey, 1976) to predict the threshold electric field (ET) for stimulation of isolated ventricular myocytes of rats at different ages. The model assumes that ET is primarily determined by cell shape and dimensions, which markedly change during postnatal development. Neonatal cells showed very high ET, which progressively decreased with maturation (experimental mean values were 29, 21, 13, and 5.9 and 6.3 V/cm for 3-6, 13-16, 20-21, 28-35, and 120-180 day-old rats, respectively, P < 0.001; theoretical values were 24, 18, 11, 9, and 6 V/cm, respectively). Estimated maximum membrane depolarization at threshold (deltaVT approximately equals 35 mV, under our experimental conditions) was reasonably constant during development, except for cells from 1-mo-old animals, in which deltaVT was lower than at other ages. We conclude that the model reasonably correlates ET with cell geometry and size in most cases. Our results might be relevant for the development of efficient procedures for defibrillation of pediatric patients.

Analysis of Variance↗
PubMed1993

Backtransplantation of chick cardiac neural crest cells cultured in LIF rescues heart development.

The cardiac neural crest is essential for normal development of the cardiovascular system. Cardiac neural crest cells are derived from the neural folds located between the mid-otic placodes and the caudal limit of somite 3. These crest cells can differentiate into a variety of mesenchymal cell types that support cardiovascular development, in addition to neurogenic cells. When cultured, many express alpha-smooth muscle actin or neurofilaments and lose their undifferentiated neural crest phenotype as shown by a decrease in HNK-1 reactivity. We wanted to determine whether cultured cardiac neural crest cells maintained the potency to support normal heart development when backtransplanted into embryos lacking their native cardiac neural crest. Under usual circumstances removal of the cardiac neural crest results in 80-100% incidence of persistent truncus arteriosus. The present study reports a system in which cardiac neural folds are cultured for 3 days and the cells backtransplanted into chick embryos after laser-induced ablation of the intrinsic cardiac neural folds. Rescue of heart development was improved 50% when cultured cells were backtransplanted and almost 200% when the backtransplanted cells had been cultured in leukemia inhibitory factor (LIF). To determine whether the cultured cells are capable of following normal migratory routes, cultured homospecific cardiac neural crest cells were tagged with DiI. Initially, fluorescent cells were found concentrated around the neural tube. By the second day following backtransplantation, the cells had migrated to the circumpharyngeal crest, populated the pharyngeal arches and aortic arch arteries, and were in the region of the cardiac outflow tract. By the third day, the labeled cells had dispersed, but could be found around the neural tube, esophagus, cardiac outflow tract, and within the dorsal root ganglia. Interestingly, a cranial migration to the periphery of the eyes was also noted. With the exception of the cranial migration to the eyes, cultured and backtransplanted cardiac neural crest cells followed normal migratory pathways to the cardiac outflow tract. LIF is used for the in vitro maintenance of the pluripotential phenotype of embryonic stem cells. In an effort to understand why LIF improves the ability of cultured neural crest cells to support normal heart development, we have examined the relationship of neural crest expression of HNK-1 antigen, alpha-smooth muscle actin, and neurofilament protein in neural crest cells cultured in LIF. LIF treatment resulted in an expanded period of expression of HNK-1 antigen, associated with a decrease in expression of alpha-smooth muscle actin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Development of isoproterenol-induced cardiac hypertrophy.

The development of cardiac hypertrophy was studied in adult female Wistar rats following daily subcutaneous injections of isoproterenol (ISO) (0.3 mg/kg body weight). A time course was established for the change in tissue mass, RNA and DNA content, as well as hydroxyproline content. Heart weight increased 44% after 8 days of treatment with a half time of 3.4 days. Ventricular RNA content was elevated 26% after 24 h of a single injection and reached a maximal level following 8 days of therapy. The half time for RNA accumulation was 2.0 days. The total content of hydroxyproline remained stable during the first 2 days of treatment but increased 46% after 4 days of therapy. Ventricular DNA content was unchanged during the early stage (1-4 days) of hypertrophic growth but increased to a new steady-state level 19% above the controls after 8 days of treatment. Intraventricular pressures and coronary flow measures were similar for control and experimental animals following 4 days of developed hypertrophy. However, dP/dt in the ISO-treated hearts was slightly but significantly (P less than 0.05) elevated. These data indicate that the adaptive response to ISO shows an early hypertrophic phase (1-4 days) characterized by a substantial increase in RNA content and cardiac mass in the absence of changes in DNA. However, prolonged stimulation (8-12 days) appears to represent a complex integration of both cellular hypertrophy and hyperplasia within the heart.

Animals↗