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At least 289 records · Page 16Linked to original sources
PubMed1985

Changes in ventricular fibrillation threshold with stimulation of cardiac sympathetic nerves of the developing dog.

The effect of stimulation of the developing cardiac sympathetic nerves on the vulnerability to ventricular fibrillation was investigated in 50 puppies 1 to 6 weeks of age. Ventricular fibrillation thresholds were obtained before and during sympathetic nerve stimulation. Stimulation of either stellate ganglion increased ventricular fibrillation threshold, possibly due to diffuse functional innervation in pups. The effect of the left stellate increased progressively with age, whereas the effect of the right, although initially greater than that of the left, did not increase further with age. In contrast, stimulation of the left ventrolateral cardiac nerve, which is locally distributed, resulted in decreased ventricular fibrillation threshold. This decrease was progressively greater with age. The fact that activation of the left stellate ganglion and the left ventrolateral cardiac nerve affects ventricular fibrillation threshold in opposite directions suggests different sympathetically mediated changes on ventricular vulnerability in early life. The differing temporal patterns of maturation and the localized nature of the major distal branch distributions could provide a mechanism for promotion of arrhythmiogenesis under some conditions in early life.

Animals↗
PubMed2002

Continuous blockade of L-type Ca2+ channels suppresses activation of calcineurin and development of cardiac hypertrophy in spontaneously hypertensive rats.

We examined whether Ca2+ channel blockers inhibit the activation of the Ca2+-dependent phosphatase calcineurin and the development of cardiac hypertrophy in spontaneously hypertensive rats (SHR). We randomly divided 12-week-old SHR into three groups, one each receiving vehicle, bolus injection or continuous infusion of nifedipine (10 mg/kg/day) from 12 to 24 weeks of age. Systolic blood pressure (BP) and heart rate were measured every week after the treatment using the tail-cuff plethysmography method. After 4, 8 and 12 weeks of treatment, 6 rats of each group were subjected to examinations that included an assay for calcineurin activity in the heart, magnetic resonance imaging (MRI), histology and Northern blot analysis. Continuous infusion of nifedipine consistently reduced BP, whereas bolus injection resulted in a fluctuation of BP. Continuous infusion of nifedipine not only reduced left ventricular mass but also decreased the transverse diameter of cardiomyocytes, interstitial fibrosis and the expression of the atrial natriuretic peptide and brain natriuretic peptide genes in the heart, while bolus injection of nifedipine did not significantly attenuate any of these hypertrophic responses in SHR. The activity of calcineurin in the heart was strongly suppressed by continuous but not bolus infusion of nifedipine in SHR. The results indicate that continuous blockade of Ca2+ channels with nifedipine effectively suppresses the development of cardiac hypertrophy in SHR, possibly through inhibition of the calcineurin activity.

Animals↗
PubMed2003

Novel 3D culture system for study of cardiac myocyte development.

Insufficient myocardial repair after pathological processes contributes to cardiovascular disease, which is a major health concern. Understanding the molecular mechanisms that regulate the proliferation and differentiation of cardiac myocytes will aid in designing therapies for myocardial repair. Models are needed to delineate these molecular mechanisms. Here we report the development of a model system that recapitulates many aspects of cardiac myocyte differentiation that occur during early cardiac development. A key component of this model is a novel three-dimensional tubular scaffold engineered from aligned type I collagen strands. In this model embryonic ventricular myocytes undergo a transition from a hyperplastic to a quiescent phenotype, display significant myofibrillogenesis, and form critical cell-cell connections. In addition, embryonic cardiac myocytes grown on the tubular substrate have an aligned phenotype that closely resembles in vivo neonatal ventricular myocytes. We propose that embryonic cardiac myocytes grown on the tube substrate develop into neonatal cardiac myocytes via normal in vivo mechanisms. This model will aid in the elucidation of the molecular mechanisms that regulate cardiac myocyte proliferation and differentiation, which will provide important insights into myocardial development.

Actin Cytoskeleton↗
PubMed2002

Development of cardiac rhythms in birds.

Heart rate (HR) in avian embryos developing inside an eggshell has been measured by various means while maintaining adequate gas exchange through the eggshell. This is an important requirement in order to avoid adverse effects of impeding gas exchange on the cardiac rhythms of developing embryos. The present report is a review of our ontogenetic study on embryonic HR, which was measured with fulfillment of the above requirement and also hatchling HR measured non-invasively. Firstly, we reviewed measurements of daily changes (developmental patterns) in embryonic mean heart rate (MHR), which were determined from a short-term measurement of HR once a day, in 34 species of altricial and precocial birds. The allometric relationship between the MHR during pipping in altricial birds and their fresh egg masses was the same as that between the MHR at 80% of incubation duration and fresh egg masses in pre-cocial birds. Secondly, we presented the developmental patterns of MHR in chick embryos and hatchlings, which were determined from long-term, continuous measurement of HR before, during and after hatching. The ultradian and circadian rhythms of HR were clearly shown in embryos and hatchlings, respectively. Thirdly, we summarized instantaneous HR fluctuations: HR variability and HR irregularities, in chick embryos and hatchlings. The distinctive patterns were shown in pre-pipped and pipped embryos and newly hatched chicks, individually, which were partly related to autonomic nervous functions and physiological functions.

Analysis of Variance↗
PubMed1998

The bHLH factors, dHAND and eHAND, specify pulmonary and systemic cardiac ventricles independent of left-right sidedness.

dHAND and eHAND are basic helix-loop-helix transcription factors that play critical roles in cardiac development. The HAND genes have a complementary left-right cardiac asymmetry of expression with dHAND predominantly on the right side and eHAND on the left side of the looped heart tube. Here we show that although eHAND is asymmetrically expressed along the anterior-posterior and dorsal-ventral embryonic axes, it is symmetrically expressed along the left-right axis at early stages of embryonic and cardiac development. After cardiac looping, dHAND and eHAND are expressed in the right (pulmonary) and left (systemic) ventricles, respectively. The left-right (LR) sidedness of dHAND and eHAND expression is demonstrated to be anatomically reversed in situs inversus (inv/inv) mouse embryos; however, dHAND expression persists in the pulmonary ventricle and eHAND in the systemic ventricle regardless of anatomic position, indicating chamber specificity of expression. Previously we showed that dHAND-null mice fail to form a right-sided pulmonary ventricle. Here mice homozygous for the dHAND and inv mutations are demonstrated to have only a right-sided ventricle which is morphologically a left (systemic) ventricle. These data suggest that the HAND genes are involved in development of segments of the heart tube which give rise to specific chambers of the heart during cardiogenesis, rather than controlling the direction of cardiac looping by interpreting the cascade of LR embryonic signals.

Animals↗
PubMed1989

Analysis of the endocardium and cardiac jelly in truncal development in the cardiac lethal mutant axolotl Ambystoma mexicanum.

Recessive mutant gene c in axolotls results in a failure of the heart to function because of abnormal embryonic induction processes. The myocardium in this mutant lacks organized sarcomeric myofibrils. The present study was undertaken to determine if developmental abnormalities were evident in other areas of the heart besides the myocardium. A detailed comparative survey of the structure of developing normal and mutant hearts, including the endocardium, its cellular derivatives, and the extracellular matrix, known as cardiac jelly, showed that in the mutant there are fewer than the normal number of endocardial cells lining the heart lumen, the number of mesenchyme cells is reduced, and the cardiac jelly area is greatly enlarged in the posterior part of the truncus adjacent to the ventricle.

Ambystoma↗
PubMed2004

Gender modulates cardiac phenotype development in genetically modified mice.

Recent research using genetically modified mice has revealed significant sex differences in cardiac phenotypes. In the majority of strains, females display a lower mortality, less severe hypertrophy, better preserved function and mitigated cardiac pathology compared with male counterparts. Thus, gender is an independent determinant for the development of cardiac phenotype in murine models. While there is strong evidence for estrogen as a cardiac protector, emerging evidence indicates adverse actions of testicular hormones that might be responsible in part for the sex differences. Studies using mouse models have also revealed novel information on signalling mechanisms mediating the sex difference.

Animals↗
PubMed1990

Signal transduction of a tissue interaction during embryonic heart development.

During early cardiac development, progenitors of the valves and septa of the heart are formed by an epithelial-mesenchymal cell transformation of endothelial cells of the atrioventricular (AV) canal. We have previously shown that this event is due to an interaction between the endothelium and products of the myocardium found within the extracellular matrix. The present study examines signal transduction mechanisms governing this differentiation of AV canal endothelium. Activators of protein kinase C (PKC), phorbol myristate acetate (PMA) and mezerein, both produced an incomplete phenotypic transformation of endothelial cells in an in vitro bioassay for transformation. On the other hand, inhibitors of PKC (H-7 and staurosporine) and tyrosine kinase (genistein) blocked cellular transformation in response to the native myocardium or a myocardially-conditioned medium. Intracellular free calcium concentration ([Ca2+]i) was measured in single endothelial cells by microscopic digital analysis of fura 2 fluorescence. Addition of a myocardial conditioned medium containing the transforming stimulus produced a specific increase in [Ca2+]i in "competent" AV canal, but not ventricular, endothelial cells. Epithelial-mesenchymal cell transformation was inhibited by pertussis toxin but not cholera toxin. These data lead to the hypothesis that signal transduction of this tissue interaction is mediated by a G protein and one or more kinase activities. In response to receptor activation, competent AV canal endothelial cells demonstrate an increase in [Ca2+]i. Together, the data provide direct evidence for a regional and temporal regulation of signal transduction processes which mediate a specific extracellular matrix-mediated tissue interaction in the embryo.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2002

Developing a cardiac rehabilitation education resource for rural health workers in Queensland: reviewing the process and outcomes.

The provision of cardiac rehabilitation services to people living in rural and remote areas is often limited to the nearest large hospital situated in urban coastal centres, leaving a gap in the rehabilitation of cardiac patients. This paper discusses the development, composition and the results of a process evaluation of a cardiac rehabilitation education resource for rural health workers. The development of the structure and content of the manual were informed by a review of current rehabilitation literature, the results of focus groups with 60 rural health workers in five Queensland rural centres, and survey results of 135 rural cardiac patients admitted to five Queensland hospitals. The draft manual was trialled by health workers in seven rural centres throughout Queensland by the National Heart Foundation (Queensland Division). The results of the process evaluation provided valuable feedback on the efficacy of the manual as an educational resource for rural health workers in the cardiac rehabilitation of their patients. Specific content in the educational resource was strengthened as a result of this evaluation. The limitations of the evaluation and suggestions for its improvement are also discussed. The paper highlights the importance of this level of evaluation in the development of health promotion education resources.

Australia↗
PubMed1984

The role of alkaline protease in the development of cardiac lesions in myopathic hamsters: effect of verapamil treatment.

The role of alkaline protease in the development of myocardial lesions in myopathic hamsters was studied. There was abnormal elevation of alkaline protease in the myopathic heart at 1 month of age, preceding the development of cardiac lesions. In vivo treatments of verapamil were carried out in 1-month-old myopathic animals for 30 days. Results indicated that the drug treatment was effective in preventing the occurrence of the severe myocardial lesions found in the untreated animals at 2 months of age. Reduced lesion development was associated concomitantly with lowered levels of alkaline protease activity. Withdrawal of drug treatment caused the return of severe lesions and high levels of alkaline protease. The study of the alkaline protease activity in the skeletal muscle of the myopathic hamster also showed a parallel relationship between the enzyme levels and severity of lesions. The results are discussed in light of possible involvement of a serine protease and a Ca2+-activated protease in producing the cardiac lesions.

Aging↗
PubMedDate not supplied

Prolonged cytomegalovirus infection with viremia is associated with development of cardiac allograft vasculopathy.

Several reports have suggested an association between cytomegalovirus infection and the subsequent development of cardiac allograft vasculopathy. The difficulties in interpreting these studies include the variety of methods used for the diagnosis of cytomegalovirus infection and variable criteria for the diagnosis of cardiac allograft vasculopathy. To determine whether specific aspects of cytomegalovirus infection are risk factors for cardiac allograft vasculopathy, the patient population of the Oregon Cardiac Transplant Program was analyzed for the following variables: cytomegalovirus infection, primary cytomegalovirus infection, and persistent cytomegalovirus infection for 4 or 6 months documented by either blood or urine cultures and persistent cytomegalovirus viremia for 4 months. In the 129 patients available for analysis, there was no higher incidence of cardiac allograft vasculopathy in patients with or without cytomegalovirus infection, nor was there a higher incidence of cardiac allograft vasculopathy in primary cytomegalovirus infection. There was a nonstatistically significant trend toward an increased incidence of cardiac allograft vasculopathy in patients with persistent cytomegalovirus infection as assessed by cultures positive for infection in either blood or urine. There was, however, a significant increase in the incidence of cardiac allograft vasculopathy in patients who had persistent viremia for at least 4 months compared with those without this finding (47% vs 18%, respectively; p = 0.012). In our population persistent cytomegalovirus viremia and presumably long-term exposure of the allograft coronary tree to cytomegalovirus is associated with cardiac allograft vasculopathy.

Coronary Disease↗
PubMed2006

Influence of pre-existing donor atherosclerosis on the development of cardiac allograft vasculopathy and outcomes in heart transplant recipients.

OBJECTIVES: This study sought to evaluate the influence of donor lesions on the development of cardiac allograft vasculopathy and outcomes in heart transplant recipients. BACKGROUND: After orthotopic heart transplantation (OHT), coronary artery narrowing occurs as a combination of pre-existing donor lesions and new lesions that develop as a result of cardiac allograft vasculopathy. METHODS: Intravascular ultrasound (IVUS) studies were performed in 301 recipients at 1.3 +/- 0.6 months and again at 12.2 +/- 0.8 months after OHT. Additional IVUS studies were performed in 90 patients at two and three years of follow-up. Sites at baseline with maximum intimal thickness > or =0.5 mm were defined as pre-existing donor lesions. The angiographic diagnosis of transplant coronary artery disease (TCAD) was defined as a new > or =50% diameter narrowing of a major epicardial vessel. RESULTS: Donor lesions were present in 30% of the hearts. By IVUS, sites with donor lesions did not have a greater increase in intimal area compared with sites without donor lesions. Angiographically, the incidence of TCAD up to three years after transplantation was higher in recipients with donor lesions than in recipients without donor lesions (25% vs. 4%, p < 0.001). However, the three-year mortality rate was similar between recipients with or without donor lesions (4.5% vs. 5.2%, p = 1.0). CONCLUSIONS: Pre-existing donor lesions do not act as a nidus for accelerating the progression of intimal hyperplasia. However, patients with donor lesions have a higher incidence of angiographic TCAD. Donor lesions do not affect the long-term survival of patients with OHT up to three years.

Adult↗
PubMedDate not supplied

Further evidence that NK cells may contribute to the development of cardiac allograft vasculopathy.

In prior experiments, we found that recipients, even though specifically tolerant of donor antigens, will develop striking cardiac allograft vasculopathy (CAV) in allogeneic mouse heart transplants. This suggested that innate immune responses, in addition to conventional adaptive immunity, may be involved in the development of CAV. We accordingly performed transplants in the parental-to-F1 combination seeking supportive evidence of NK cell activity directed against the vessels of parental donor transplants as a manifestation of "hybrid resistance." When such lesions were indeed found, we investigated their pathogenesis employing immunopathological analysis, in vitro measurements of NK cytotoxicity, and donor-specific T-cell activity in F1 recipients of parental donor hearts. We present evidence that NK cells can promote cardiac allograft vasculopathy. Since NK cell activity is not well targeted by current immunosuppressive therapy, its control may offer a valuable new possibility for improving the long-term outcome of transplanted organs.

Animals↗
PubMed1991

[Chylothorax developed after cardiac surgery in children: a report of three cases].

Two children developed chylothorax after median sternotomy and a third child developed chylothorax after a Blalock-Taussig operation under the left thoracotomy. The first patient had a closure of ASD and a pulmonary valvotomy and then later developed chylothorax. The thoracic duct was ligated 10 cm just above the diaphragm at 28 days after the first operation because of unsuccessful conservative treatment. The second patient had a Blalock-Taussig operation and the third patient had radical operation for ECD and both developed chylothorax. The latter two patients were cured with conservative treatments such as the administration of Medium Chain Triglyceride or total parenteral nutrition with thoracic drainage. Children who developed chylothorax after cardiac surgery should be treated conservatively for at least the early postoperative period when circulatory and/or respiratory conditions are still unstable.

Child, Preschool↗
PubMed1976

The role of myocardial membrane lipids in the development of cardiac necrosis.

1. The fatty acid composition of cardiac membrane lipids is influenced by age, sex, diet and other factors. 2. The relative amounts of various polyunsaturated fatty acids in cardiac lipids influence markedly the development of myocardial necrosis and mortality following overstimulation with isoproterenol. 3. The availability and metabolism of arachidonic acid may play an important role in regulation of cardiac metabolism.

Adenosine Triphosphate↗
PubMed1986

Normal development of cardiac beta adrenoceptors in mice exposed to ethanol in utero.

Abnormalities of cardiac physiology and anatomy may occur in children with the fetal alcohol syndrome. To understand the basis of these abnormalities, research has been performed which shows that in mice exposed to ethanol from gestation day 8 to birth via a liquid diet regime with pairfed controls there are ultrastructural changes in the cardiac myocytes. To determine if the exposure to ethanol also affects the development of the cardiac noradrenergic system, which in turn could cause developmental abnormalities, beta adrenoreceptor binding was characterized by Scatchard analyses of concentration dependent binding curves in newborn mice exposed to ethanol in utero. Although body and heart weight were lower in newborns from both the pairfed and ethanol groups compared to a normally fed group, no differences in the densities of the beta adrenoceptors or in the Kd values for binding were seen due to the ethanol or the liquid diet regime. Therefore, at least one component of the development of the cardiac sympathetic system was not altered by ethanol exposure or a reduced caloric intake.

Animals↗
PubMed2004

Cross-bridge versus thin filament contributions to the level and rate of force development in cardiac muscle.

In striated muscle thin filament activation is initiated by Ca(2+) binding to troponin C and augmented by strong myosin binding to actin (cross-bridge formation). Several lines of evidence have led us to hypothesize that thin filament properties may limit the level and rate of force development in cardiac muscle at all levels of Ca(2+) activation. As a test of this hypothesis we varied the cross-bridge contribution to thin filament activation by substituting 2 deoxy-ATP (dATP; a strong cross-bridge augmenter) for ATP as the contractile substrate and compared steady-state force and stiffness, and the rate of force redevelopment (k(tr)) in demembranated rat cardiac trabeculae as [Ca(2+)] was varied. We also tested whether thin filament dynamics limits force development kinetics during maximal Ca(2+) activation by comparing the rate of force development (k(Ca)) after a step increase in [Ca(2+)] with photorelease of Ca(2+) from NP-EGTA to maximal k(tr), where Ca(2+) binding to thin filaments should be in (near) equilibrium during force redevelopment. dATP enhanced steady-state force and stiffness at all levels of Ca(2+) activation. At similar submaximal levels of steady-state force there was no increase in k(tr) with dATP, but k(tr) was enhanced at higher Ca(2+) concentrations, resulting in an extension (not elevation) of the k(tr)-force relationship. Interestingly, we found that maximal k(tr) was faster than k(Ca), and that dATP increased both by a similar amount. Our data suggest the dynamics of Ca(2+)-mediated thin filament activation limits the rate that force develops in rat cardiac muscle, even at saturating levels of Ca(2+).

Adenosine Triphosphate↗
PubMed1992

The development of cardiac transplantation.

The history of cardiac transplantation provides an excellent prototype for the development of a therapeutic technique. The first observations on cardiac transplantation were made in animal models in the early 20th century. Surgical problems were solved through a series of technologic advances, and problems associated with immune-mediated rejection were discovered and successfully addressed. By the late 1960s, cardiac transplantation in humans had become feasible. Since the first successful transplantation of a heart in a human in 1967, the management of rejection and infection has steadily progressed, and the long-term outcome after cardiac transplantation has improved dramatically. The success of cardiac transplantation has led to an expansion of the potential recipient pool to include children and adults in the eighth decade of life. Unfortunately, the growth of cardiac transplantation has resulted in an inadequate supply of suitable donor hearts. The limited supply of donor hearts has provided the impetus for further research in xenotopic cardiac transplantation and for the development of implantable circulatory assist devices.

Animals↗