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PubMedDate not supplied

G proteins, adenylyl cyclase and related phosphoproteins in the developing rat heart.

The postnatal alterations of the composition of alpha subunit isoforms (Gi alpha c, Gi alpha 3, G(o) alpha, and Gq alpha) of G proteins, the adenylyl cyclase activity as well as of cAMP-regulated phosphoproteins e.g. troponin I and phospholamban were investigated in the ventricular tissue of 1, 7, 30 days old rats. Quantitative immunodetection revealed a 5.7-fold decrease in Gi alpha 3 at 30th postnatal day compared with the postnatal day 1 and up to 15-fold at 4 months. The amounts of Gq alpha and G(o) alpha as well as the G beta subunits were found to be higher in the earlier life period compared to the adult. In contrast, the content of Gs alpha was uneffected by the developmental state. Basal adenylyl cyclase activity (pmoles cAMP/min x mg protein) increased from 30.9 +/- 5.0, 36.8 +/- 5.0 to 63.9 +/- 5.9 at 1st, 7th and 30th postnatal day, respectively. Isoprenaline (100 microM) enhanced the activity of adenylyl cyclase from day 1, 7-30 from 46.2 +/- 7.0, 79.1 +/- 9.2 to 120.5 7.2, respectively. The effects of forskolin and NaF on adenylyl cyclase activity was found to be not influenced within the first postnatal month. Furthermore, a developmentally controlled expression of cardiac troponin I was observed (6-fold from the first to the 28th postnatal day) whereas the level of phospholamban was found to be age-independent. In conclusion, there is an increase in the efficiency of the beta-adrenergic signal transfer mainly caused by a reduction of the inhibitory G proteins and a dominance of the Gs alpha-linked pathway in the postnatal rat heart. Furthermore the developmentally controlled expression of troponin I might be of functional importance in the cAMP-supported relaxation. Additionally, altered Gq alpha, G(o) alpha and G beta pattern of the developing rat ventricle may play a role in the observed change of alpha-adrenerg-mediated heart contractility as well as in cardiac differentiation and growth processes.

Adenylyl Cyclases↗
PubMed1997

[The apolipoprotein AII gene is not a risk factor for development ischemic heart disease in the Moscow population].

Polymorphism of microsatellite (CA)n repeat in the second intron of the apolipoprotein AH gene--one of the major structural proteins of high-density lipoproteins--was performed in male coronary heart disease (CHD) patients and in a random sample of men from the Moscow population. No association between the polymorphism and the development of CHD was revealed. Therefore, apolipoprotein AII gene is not a factor of genetic risk of the development of atherosclerosis in the population studied.

Adult↗
PubMed1998

Immunoreactivity of the ets-1 transcription factor correlates with areas of epithelial-mesenchymal transition in the developing avian heart.

Cardiac morphogenesis involves substantial remodeling processes that include cell transdifferentiation and migration. The c-ets-1 protooncogene codes for a transcription factor that can transactivate a number of genes involved in developmental processes such as degradation of extracellular matrices and cell migration. We have immunolocated the ets-1 protein in the heart of quail and chick embryos between the Hamburger and Hamilton stages HH16 and HH37. In HH16-17 embryos, the ets-1 transcription factor was only detected in some endocardial cells and in most mesothelial and mesenchymal cells of the proepicardium. Ets-1 immunoreactivity increased markedly in the developing endocardial cushions, myocardium, epicardium and early subepicardial mesenchyme of HH18-19 embryos. By HH20-24 the immunoreactivity was found throughout the heart, with a stronger intensity in the areas of epithelial-mesenchymal transition of the endocardium and epicardium. In embryos between HH26 and HH33, ets-1 immunoreactivity increased in the cushion mesenchyme, atrioventricular endocardium, ventricular epicardium and subepicardial mesenchyme cells, but not in other areas of the heart. The immunoreactivity declined in the innermost part of the endocardial cushions. The subepicardial mesenchyme was particularly immunoreactive in these stages, coinciding with the development of the subepicardial vascular network. In fact, ets-1 colocalized with the quail vascular marker QH1 in the subepicardial mesenchymal cells. Ets-1-negative cells were abundant in the subepicardium and valvuloseptal tissue of the HH37 embryos. The results suggest that ets-1, probably through transactivation of genes such as urokinase-type plasminogen activator and matrix metalloproteinases, might play a crucial role in the differentiation of the cushion and subepicardial mesenchyme, the formation of the intratrabecular sinusoids and the early development of the cardiac vessels.

Animals↗
PubMed1997

Functional consequences of acute collagen degradation studied in crystalloid perfused rat hearts.

OBJECTIVES: The impact of acute collagen disruption by the disulfide donor, 5,5'-dithio-2-nitrobenzoic acid (DTNB) on ventricular properties was tested in rat hearts. METHODS: Collagen was degraded acutely in 13 isolated, isovolumically contracting rat hearts by perfusion with 1 mM DTNB added to Krebs-Henseleit solution for 1 hour followed by 2-hour perfusion with normal solution. Another 13 hearts were perfused with normal solution for 3 hours (Control). RESULTS: Collagen content was 3.5 +/- 0.5% of ventricular dry weight in control group compared with 2.1 +/- 0.4% in DTNB group (decrease by 40%, p < 0.01). Scanning electron micrographs revealed loss of the delicate collagen network surrounding muscle fibers in DTNB treated hearts. Developed pressure at a fixed volume decreased to 86 +/- 17% of the baseline value after 3-hour perfusion in the control group, whereas in DTNB treated hearts developed pressure fell to 68 +/- 13% (p < 0.01). End-diastolic pressure was set at 5 mmHg at the beginning of the experiment and rose to 15 +/- 8 mmHg in control and 30 +/- 13 mmHg (p < 0.01) in the treated hearts. Concomitantly, wet-to-dry weight ratio increased from 5.63 +/- 0.26 in control to 6.07 +/- 0.11 (p < 0.05) in the DTNB treated hearts. A separate set of experiments on isolated myocytes excluded the possibility of a direct effect of DTNB on myocyte contractile function. CONCLUSIONS: These data suggested that with 40% collagen disruption by DTNB there is a significant increase in tissue edema that results in a decrease in chamber capacitance; in addition, there is a significant decrease in systolic performance which reflects the combined effect of edema and loss of collagen.

Animals↗
PubMed1998

Heart and extra-embryonic mesodermal defects in mouse embryos lacking the bHLH transcription factor Hand1.

The basic helix-loop-helix (bHLH) transcription factors, Hand1 and Hand2 (refs 1,2), also called eHand/Hxt/Thing1 and dHand/Hed/Thing2 (refs 3,4), respectively, are expressed in the heart and certain neural-crest derivatives during embryogenesis. In addition, Hand1 is expressed in extraembryonic membranes, whereas Hand2 is expressed in the deciduum. Previous studies have demonstrated that Hand2 is required for formation of the right ventricle of the heart and the aortic arch arteries. We have generated a germline mutation in the mouse Hand1 gene by replacing the first coding exon with a beta-galactosidase reporter gene. Embryos homozygous for the Hand1 null allele died between embryonic days 8.5 and 9.5 and exhibited yolk sac abnormalities due to a deficiency in extraembryonic mesoderm. Heart development was also perturbed and did not progress beyond the cardiac-looping stage. Our results demonstrate important roles for Hand1 in extraembryonic mesodermal and heart development.

Animals↗
PubMed2001

Comparative studies on the expression patterns of three troponin T genes during mouse development.

In vertebrates, three troponin T (TnT) genes, cardiac TnT (cTnT), skeletal muscle fast-twitch TnT (fTnT), and slow-twitch TnT (sTnT), have evolved for the regulation of striated muscle contraction. To understand the mechanism for muscle fiber-specific expression of the TnT genes, we compared their expression patterns during mouse development. Our data revealed that the TnT expression in the developing embryo was not as restricted as that in the adult. In addition to a strong expression in the developing heart beginning at day 7.5 p.c (postcoitum), the cTnT transcript was detected at later stages in some skeletal muscles, where beginning at day 11.75 p.c. the fTnT and sTnT genes were also expressed. Only sTnT but not fTnT was found transiently in the developing heart. At day 13.5 p.c., expressions of all three genes were detected in the developing tongue and this co-expression continued to day 16.5 p.c. with the fTnT isoform being predominant. At this stage, overlapping and distinct expression patterns of both sTnT and fTnT genes were also evident in many developing skeletal muscles. These data suggest that different muscles during development undergo a complex change in TnT isoforms resulting in different contractile properties. Unexpectedly, the cTnT transcript was persistently found in the developing bladder, where presumably smooth muscle is present. In transgenic mice, expression of a LacZ gene driven by a rat cTnT promoter (-497 to +192 bp) was very similar to that of the endogenous cTnT gene, suggesting that this promoter contained regulatory elements sufficient for the control of tissue-specific cTnT expression during development.

Animals↗
PubMed1998

A review: trichloroethylene metabolites: potential cardiac teratogens.

This review is a a series of the authors' studies designed to test the hypothesis that administration of trichloroethylene (TCE), dichloroethylene (DCE), their metabolites, and related compounds are responsible for fetal cardiac teratogenesis when given to pregnant rats during organogenesis. Identification of teratogenic compounds will allow more accurate assessment of environmental contaminants and public health risks. Epidemiologic studies and previous teratogenic studies using chick embryos and fetal rats have reported an increased number of congenital cardiac defects when exposed to TCE or DCE during fetal development. Metabolites of TCE and DCE studied in the drinking-water exposure study include trichloroacetic acid TCAA), monochloroacetic acid, trichloroethanol, carboxymethylcysteine, trichloroacetaldehyde, dichloroacetaldehyde, and dichlorovinyl cysteine. Varying doses of each were given in drinking water to pregnant rats during the period of fetal heart development. Rats receiving 2730 ppm TCAA in drinking water were the only metabolite group demonstrating a significant increase in the number of cardiac defects in fetuses on a per-litter basis (p = 0.0004 Wilcoxon test and p =0.0015 exact permutation test). Maternal and fetal variables showed no statistically significant differences between treated and untreated groups. When treated with TCAA the increased cardiac defects, as compared to controls, do not preclude the involvement of other metabolites as cardiac teratogens, but indicates TCAA as a specific cardiac teratogen. Further studies of drinking-water exposure and potential mechanisms of action on the developing heart are proceeding.

Abnormalities, Drug-Induced↗
PubMed1992

Force-frequency relationship, contraction duration and recirculating fraction of calcium in postnatally developing rat heart ventricles: correlation with heart rate.

Heart rates (HR) of awake unrestrained animals, isometric contraction duration and force-frequency relationship of ventricular tissue were determined in adult and postnatally developing rats. Resting HR was lowest in newborns (256 beats min-1), reached maximum at the age of 2.5 weeks (506 beats min-1) and then declined to the level of adult rats (381 beats min-1). Duration of isometric contraction correlated negatively with HR. Time to peak tension (TPT) was 185 ms in newborns but fell rapidly during the first days of post-natal life. Minimum was attained at the age of 2.5 weeks (TPT = 98 ms), followed by a slight prolongation towards adulthood. Recirculating fraction of activator Ca2+ increased parallel with HR, being 6% in newborns, 33% in 11-day-old pre-weanlings, and 87% in adult rats. Similar developmental pattern of the parameters suggests that a post-natal increase in HR and a shortening of contraction duration are closely associated with a shift from extracellular to intracellular source of activator Ca2+. Force-frequency curves were similar at different developmental stages and consisted of three phases; a negative staircase between 0.05 and 1.0 Hz, a positive staircase between 1.0 and 4.0 Hz, and a secondary decline above 4.0 Hz. In adult rats the positive force staircase was weak or absent. Furthermore, our results show that negative staircase is not only a property of adult rat heart but is present, and even more pronounced, in pre-weanling and weanling rat heart. Therefore negative staircase is not solely explained by quantitative changes in the contribution of sarcoplasmic reticulum (SR) to contractile activation, but rather by the mechanisms which regulate loading and/or release of sarcoplasmic reticular Ca2+.

Animals↗
PubMed2005

Functional dissection of sequence-specific NKX2-5 DNA binding domain mutations associated with human heart septation defects using a yeast-based system.

Human heart development requires an orderly coordination of transcriptional programs, with the homeodomain protein NKX2-5 being one of the key transcription factors required for the differentiation of mesodermal progenitor cells. Indeed, lack of Nkx2-5 in mice arrests heart development prior to looping, resulting in embryonic lethality. There are 28 germline NKX2-5 mutations identified in humans that are associated with congenital heart disease, and we recently reported multiple somatic mutations in patients with complex cardiac malformations. To address the functional consequences of single and multiple mutations of NKX2-5, we developed a functional assay in the budding yeast Saccharomyces cerevisiae, which could determine transactivation capacity and specificity of expressed NKX2-5 alleles towards targeted response element (RE) sequences. We focused on mutants of the third helix, which provides DNA binding specificity, and characterized mutations that were highly associated with either ventricular (VSD) or atrioventricular (AVSD) septal defects. Individual mutants exhibited partial to complete loss of function and differences in transactivation capacity between the various REs. The mutants also exhibited gene dosage rather than dominant effects on transcription. Surprisingly, all AVSD patients (22/23) had a single K183E mutation in the DNA binding domain, which resulted in transcriptional inactivation. None of the VSD patients had this mutation; yet 14/29 had at least one mutation in the third helix leading to either inactivation or reduction of NKX2-5 transactivation. Therefore, mutations of somatic origin in the binding domains of NKX2-5 were associated specifically with AVSD or VSD and resulted in loss of protein function.

Base Sequence↗
PubMed1976

Incidence and clinical features of patent ductus arteriosus in low-birthweight infants: a prospective analysis of 150 consecutively born infants.

The incidence of persistent patency of the ductus arteriosus beyond the third day of life was prospectively determined in 100 preterm infants with birthweights of 2,000 gm or less and 50 infants with birthweights of 2,001 to 2,500 gm. The overall incidence was 21% and was inversely related to increasing gestational age and birthweight. The data suggest that immaturity is the major determinant of the persistent patency of the ductus arteriosus. Spontaneous delayed closure of the ductus occurred in 79% of patients that survived the immediate neonatal period. There was a high degree of association between the presence of a patent ductus arteriosus (PDA) and respiratory distress syndrome (RDS). Eight infants with severe RDS and PDA developed heart failure and four required surgical ligation of the ductus. None of the infants with birthweights greater than 2,000 gm who had PDA developed heart failure or required surgical ligation of the ductus arteriosus.

Birth Weight↗
PubMed1993

Production of a new monoclonal antibody recognizing alpha-actinin: analysis of the changes in subcellular expression in the developing chick heart.

A new monoclonal antibody that recognizes alpha-actinin in cardiac muscle cells was used in a quantitative study (fluorescence activated cell sorting and polyacrylamide gel electrophoresis) of the expression of this protein during chick embryo development, to determine the changes in cytoplasmic and cytoskeletal compartments. alpha-Actinin expression was weak in early stages of development (Hamburger and Hamilton stage 18) and increased steadily until Hamburger Hamilton stage 40. In all stages, the protein was more abundant in the cytoplasmic compartment. The monoclonal antibody cross-reacted with alpha-actinin in chicken smooth and striated muscle cells and also showed a faint cross-reaction with human cardiac muscle alpha-actinin.

Actinin↗
PubMed1995

Developmental regulation of connexin 40 gene expression in mouse heart correlates with the differentiation of the conduction system.

In adult mouse heart, CX40 is expressed in the atria and the proximal part of the ventricular conduction system (the His bundle and the upper parts of the bundle branches). This cardiac tissue is specialized in the conduction of the electrical impulse. CX40 is the only mouse connexin known to be expressed in these parts of the adult conductive tissue and is thus considered as a marker of the conduction system. In the present report, we investigated CX40 expression and distribution during mouse heart development. We first demonstrate that CX40 mRNA is regulated throughout development, as are other heart connexin transcripts, i.e., CX37, CX43, and CX45, with a decreasing abundance as development proceeds. We also show that the CX40 transcript and protein are similarly regulated, CX40 being expressed as two different phosphorylated and un-phosphorylated forms of 41 and 40 kDa, respectively. Surprisingly, distribution studies demonstrated that CX40 is widely expressed in 11 days post-coitum (dpc) embryonic heart, where it is detected in both the atria and ventricle primordia. As development proceeds, the CX40 distribution pattern in the atria is maintained, whereas a more dynamic pattern is observed in the ventricles. From 14 dpc onwards, as the adult ventricular conduction system differentiates, CX40 decreases in the trabecular network and it is preferentially distributed in the ventricular conduction system. CX40 is thus the marker of the early differentiating conduction system. It is hypothesized that the conduction system is present in unorganized "embryonic" form at 11 dpc and transdifferentiates by 14 dpc into the adult conduction system.

Animals↗
PubMedDate not supplied

Diving heart rate development in postnatal harbour seals, Phoca vitulina.

Harbour seals, Phoca vitulina, dive from birth, providing a means of mapping the development of the diving response, and so our objective was to investigate the postpartum development of diving bradycardia. The study was conducted May-July 2000 and 2001 in the St. Lawrence River Estuary (48 degrees 41'N, 68 degrees 01'W). Both depth and heart rate (HR) were remotely recorded during 86,931 dives (ages 2-42 d, n = 15) and only depth for an additional 20,300 dives (combined data covered newborn to 60 d, n = 20). The mean dive depth and mean dive durations were conservative during nursing (2.1 +/- 0.1 m and 0.57 +/- 0.01 min, range = 0-30.9 m and 0-5.9 min, respectively). The HR of neonatal pups during submersion was bimodal, but as days passed, the milder of the two diving HRs disappeared from their diving HR record. By 15 d of age, most of the dive time was spent at the lower diving bradycardia rate. Additionally, this study shows that pups are born with the ability to maintain the lower, more fully developed dive bradycardia during focused diving but do not do so during shorter routine dives.

Age Factors↗
PubMed1987

Diagnosis and management of traumatic ventricular septal defect.

Four cases of ventricular septal defect secondary to stab wounds of the heart are presented. One of three patients arriving at the Emergency Department in shock and who were resuscitated required an emergency thoracotomy. These patients had immediate repair of their external cardiac wounds in the Operating Room. Cases 1 and 3 developed heart failure and loud systolic murmur postoperatively. Case 4 was treated with chest tube for a left hemothorax and developed heart failure after discharge. In Cases 1, 2, and 3, 2-D echocardiography detected and located a VSD. In Case 3 Doppler measurement showed elevated RV pressure (45 mm Hg) and decreased peak tricuspid to mitral flow ratio (0.36, normal = 0.6). All patients underwent cardiac catheterization. In Case 4 there was associated mitral regurgitation. Cases 1 and 3 had pulmonary to systemic flow ratios greater than 3:1. Cases 1, 3, and 4 underwent operative repair. In Case 1 the VSD was closed with a dacron patch, and in Cases 3 and 4 it was sutured with Teflon pledgets. In Case 4 a puncture wound of the mitral valve annulus was simultaneously repaired. All patients are alive but in Case 1 postoperative 2-D echocardiography demonstrated partial dehiscence of the patch which has not required reoperation and in Case 3 post-repair 2-D echocardiography and Doppler flow studies have shown an intact VSD repair. This series of post-traumatic VSD demonstrates its varying clinical presentation and the diagnostic and followup benefits offered by 2-D echocardiography, especially when combined with Doppler flow measures.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Effects of trichloroethylene and its metabolite trichloroacetic acid on the expression of vimentin in the rat H9c2 cell line.

Trichloroethylene (TCE) and its metabolite trichloroacetic acid (TCAA) are environmental contaminants with specific toxicity for the embryonic heart. In an effort to identify the cellular pathways disrupted by TCE and TCAA during heart development, we investigated their effects on expression of vimentin, a marker of cardiac differentiation. Previous studies had shown that the level of vimentin transcript was inhibited in rat embryonic heart after maternal exposure to TCE via drinking water. In the same study, maternal exposure to TCAA produced the opposite effect, inducing an increased level of vimentin mRNA. In this study, we selected an in vitro system, the rat cardiac myoblast cell line H9c2, to further characterize the molecular mechanisms used by TCE and TCAA to disrupt normal heart development. In particular, we investigated the effects of both toxicants on vimentin, at both the RNA and protein levels, using dose-response and time course curves. Our experimental findings indicate that vimentin expression is affected by TCE and TCAA in H9c2 cells similarly as in vivo. The work is significant because it provides a suitable in vitro model for studies looking at toxicant effects on myocardiac cells, and it suggests that vimentin is a good marker of TCE exposure in the embryonic heart.

Animals↗
PubMed1999

Development of heart rate rhythmicity in Muscovy duck embryos.

The heart rate (HR) of Muscovy duck embryos (Cairina moschata f. domestica) was continuously recorded from as early as the 21st day of incubation (D21) until hatching (D34/35). The aim of the study was to investigate the influence of phonoperiods consisting of different acoustic stimuli on the course of HR and the development of HR periodicities during this period. Incubation was carried out at a constant temperature and in constant darkness. Until D25 HR was dominated by decelerative fluctuations only, indicating a main input from the parasympathetic system on the heart. Later sympathetic influences increased progressively. HR periodicity was investigated by means of chi 2-periodogram and fast Fourier transformation. Between D26 and D30 statistically significant and stable HR periodicities developed gradually. They had periods in the range from 5 to 38 h. Ultra-, circa- and infradian rhythms (< 20, 24 +/- 4 and > 28 h, respectively) occurred in parallel in some cases in the same embryo. The for the HR course important periods were dissimilar between individual embryos and had different intensities. There was no indication that acoustic stimulation (phonoperiods) had any effect on the development of HR periodicities.

Acoustic Stimulation↗
PubMed1989

[Heart transplant: development and maturity of the program at the University of South Florida and the General Hospital of Tampa].

Cardiac transplantation has evolved from an experimental procedure to an accepted mode of therapy that prolongs life in patients with severe heart failure. The University of South Florida-Tampa General Hospital began performing cardiac transplantation for the treatment of end-stage cardiac disease in June 1985. Since then, 50 heart transplantations have been performed and 37 patients are alive and well. The one-year actuarial survival is 78% and the two-year actuarial survival is 72%. Multiple complications have been encountered, most notably rejection and infection. The recent approval of the USF/TGH program as a Medicare funded cardiac transplantation center is expected to greatly expand the number of potential recipients and will provide the residents of Florida, the Southeastern United States and the Caribbean with an additional health care resource.

Aftercare↗