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PubMed1996

Molecular cloning, chromosomal mapping, and characterization of the human cardiac-specific homeobox gene hCsx.

BACKGROUND: Csx/Nkx2.5, a murine nonclustered homeobox gene expressed primarily in the heart, has significant sequence similarity to the Drosophila tinman gene. Tinman is essential for heart and gut formation in Drosophila. Targeted mutation in the mouse gene, Csx/Nkx2.5, arrests cardiac development during early embryonic stages, suggesting an evolutionary conservation in cardiogenesis. MATERIALS AND METHODS: We have isolated and characterized a human homolog, hCsx, from an adult cardiac cDNA library. Northern blotting and ribonuclease protection was used to define the pattern of expression during normal development and in disease states. Chromosomal localization of the gene was determined by somatic cell hybrid analysis and fluorescent in situ hybridization. RESULTS: The predicted amino acid sequence of hCsx has 87% overall homology to the murine gene with 100% identity in the homeodomain. The homeodomain sequence of hCsx is 95% identical to its Xenopus homolog, and 65% to tinman. hCsx mRNA was detected exclusively in the heart. hCsx transcript was detected at 12 weeks in human embryonic heart, the earliest time point examined, and was up-regulated 5-fold between 12 and 19 weeks. There was no significant alteration of hCsx message level in the myocardium of 14 patients with end stage heart failure compared to a normal control. The human gene mapped to the distal portion of chromosome 5, the 5q34-q35 region. This defines a new synteny region between human chromosome 5q and the t-locus of mouse chromosome 17, where the mouse Csx gene is located. CONCLUSIONS: hCsx, the human homolog of Drosophila tinman, is expressed in heart in a tissue restricted manner. Distal 5q trisomies produce several phenotypic abnormalities, including a high incidence of congenital heart disease. Isolation of the hCsx gene will allow further studies of mutations in this gene and their potential associations with some forms of congenital heart disease in humans.

Amino Acid Sequence↗
PubMedDate not supplied

Epinephrine-induced cardiac arrhythmias in rabbits exposed to trichloroethylene: potentiation by caffeine.

Approximately 200 000 industrial workers are exposed to trichloroethylene in the United States. Individuals intoxicated with trichloroethylene are known to develop cardiac arrhythmias. Caffeine is known to be a cardiac stimulant and is one of the drugs most widely used by the American population. Therefore, it was of interest to study the effect of caffeine on the arrhythmogenicity of trichloroethylene. Rabbits were treated with a vehicle control (1 mL/kg, ip) or caffeine (10 mg/kg, ip, 30 minutes prior to exposure) and exposed for one hour to 6000 ppm trichlorethylene under dynamic airflow conditions. Epinephrine was infused until arrhythmias occurred after 7.5, 15, 30, 45 and 60 minutes of exposure and also 15 and 30 minutes post-exposure. Serial blood samples were collected at these time points and analyzed for trichloroethylene and the two major metabolites, trichloroethanol and trichloroacetic acid. Rabbits treated with caffeine and exposed to trichloroethylene developed more arrhythmias in response to epinephrine than rabbits exposed to trichloroethylene alone, and the arrhythmias occurred sooner and in response to lower doses of epinephrine. Caffeine treatment had no effect on trichloroethylene blood concentration, but significantly decreased trichloroethanol blood levels after 45 and 60 minutes of exposure to trichloroethylene. Caffeine also reduced blood levels of trichloroacetic acid. The data indicate that caffeine can potentiate the arrhythmogenicity of trichloroethylene in rabbits.

Animals↗
PubMed1986

Changes associated with rat heart chromatin during cardiac hypertrophy.

Studies with N-Pyrenemaleimide, a probe which binds to H3 among histones and tryptophan residues of nonhistone proteins and subsequently emits fluorescence, showed that during developing cardiac hypertrophy, conformational changes due to DNA-histone interactions may be maximum at an early stage of hypertrophy (17% hypertrophy) while the changes due to non-histone protein(s) interactions may be maximum at a latter stage (28% hypertrophy). In vitro transcription analysis in isolated nuclei obtained from normal and hypertrophic hearts showed that nuclei obtained from 40% hypertrophic hearts had a maximum incorporation ability than nuclei obtained from 17% or 28% hypertrophic hearts. Analysis of histones and 0.35 M NaCl extractable nuclear proteins by single dimensional polyacrylamide gel electrophoresis did not reveal any changes in these proteins when obtained from normal and different stages of hypertrophic hearts. DNase I sensitivity studies with nuclei obtained from normal and hypertrophic hearts and with reconstituted nuclei, showed that changes in 0.35 M NaCl extractable proteins may contribute to the respective DNase I sensitivity of various hypertrophic nuclei. These studies also indicated that though nuclei obtained from 40% hypertrophic hearts showed maximum incorporation during in vitro transcription, the DNase I sensitivity is maximum only in nuclei obtained from 28% hypertrophic hearts and not from 40% hypertrophic hearts.

Animals↗
PubMed1979

Effects of hyaluronic acid on cardiac cushion tissue cells in collagen matrix cultures.

To initiate the experimental exploration of the role of extracellular macromolecules in influencing developmental events in the heart, a 3-dimensional substrate culture model of the developing cardiac cushion was devised. One cardiac jelly component, hyaluronic acid, was tested for its effects on morphology and migratory capacity of cushion tissue cells within the collagen matrix substrate. Hyaluronate treatment resulted in: (1) an increase in the number and extent of filopodia, reflected as an increase in cell surface area, and (2) an increase in migratory capacity, reflected as an increase in maximum depth to which cells migrate through the collagen lattice. These results suggest one major role for hyaluronate in the early cardiac cushion is the promotion of a high level of motility capability in the newly seeded cushion tissue cells, required for the key event of cell migration across the developing cushion.

Animals↗
PubMed1998

Gap junction-mediated cell-cell communication modulates mouse neural crest migration.

Previous studies showed that conotruncal heart malformations can arise with the increase or decrease in alpha1 connexin function in neural crest cells. To elucidate the possible basis for the quantitative requirement for alpha1 connexin gap junctions in cardiac development, a neural crest outgrowth culture system was used to examine migration of neural crest cells derived from CMV43 transgenic embryos overexpressing alpha1 connexins, and from alpha1 connexin knockout (KO) mice and FC transgenic mice expressing a dominant-negative alpha1 connexin fusion protein. These studies showed that the migration rate of cardiac neural crest was increased in the CMV43 embryos, but decreased in the FC transgenic and alpha1 connexin KO embryos. Migration changes occurred in step with connexin gene or transgene dosage in the homozygous vs. hemizygous alpha1 connexin KO and CMV43 embryos, respectively. Dye coupling analysis in neural crest cells in the outgrowth cultures and also in the living embryos showed an elevation of gap junction communication in the CMV43 transgenic mice, while a reduction was observed in the FC transgenic and alpha1 connexin KO mice. Further analysis using oleamide to downregulate gap junction communication in nontransgenic outgrowth cultures showed that this independent method of reducing gap junction communication in cardiac crest cells also resulted in a reduction in the rate of crest migration. To determine the possible relevance of these findings to neural crest migration in vivo, a lacZ transgene was used to visualize the distribution of cardiac neural crest cells in the outflow tract. These studies showed more lacZ-positive cells in the outflow septum in the CMV43 transgenic mice, while a reduction was observed in the alpha1 connexin KO mice. Surprisingly, this was accompanied by cell proliferation changes, not in the cardiac neural crest cells, but in the myocardium- an elevation in the CMV43 mice vs. a reduction in the alpha1 connexin KO mice. The latter observation suggests that cardiac neural crest cells may have a role in modulating growth and development of non-neural crest- derived tissues. Overall, these findings suggest that gap junction communication mediated by alpha1 connexins plays an important role in cardiac neural crest migration. Furthermore, they indicate that cardiac neural crest perturbation is the likely underlying cause for heart defects in mice with the gain or loss of alpha1 connexin function.

Animals↗
PubMed1988

A prospective study on the dose dependency of cardiotoxicity induced by mitomycin C.

Since 1975 mitomycin C (MMC) has been suggested to be cardiotoxic, especially when combined with or given following doxorubicin. Data on dose dependency or incidence concerning this side effect were not known. We have initiated a prospective study to obtain some more data on these subjects. Forty-four MMC-treated patients were studied, 37 of them could be evaluated. All patients were studied by repeated physical examinations, chest X-rays, electro- and echocardiography and radionuclide left ventricular ejection fraction (EF) determinations. The results were evaluated per cumulative dose level. One of the patients developed cardiac failure after 30 mg m-2 MMC and only 150 mg m-2 doxorubicin. The cardiac failure was predicted by a drop in EF determined during a cold pressor test. None of the other patients developed clinical cardiotoxicity, nor did the studied parameters change. The literature on this subject was also reviewed. Based on the combined data from the present study and the literature, we suggest that MMC-related cardiotoxicity is dose dependent, occurring at cumulative dose levels of 30 mg m-2 or more, mainly in patients also (previously or simultaneously) treated with doxorubicin. The incidence is likely to be less than 10% even for this risk group.

Adult↗
PubMed2005

The Drosophila melanogaster T-box genes midline and H15 are conserved regulators of heart development.

The Drosophila melanogaster genes midline and H15 encode predicted T-box transcription factors homologous to vertebrate Tbx20 genes. All identified vertebrate Tbx20 genes are expressed in the embryonic heart and we find that both midline and H15 are expressed in the cardioblasts of the dorsal vessel, the insect organ equivalent to the vertebrate heart. The midline mRNA is first detected in dorsal mesoderm at embryonic stage 12 in the two progenitors per hemisegment that will divide to give rise to all six cardioblasts. Expression of H15 mRNA in the dorsal mesoderm is detected first in four to six cells per hemisegment at stage 13. The expression of midline and H15 in the dorsal vessel is dependent on Wingless signaling and the transcription factors tinman and pannier. We find that the selection of two midline-expressing cells from a pool of competent progenitors is dependent on Notch signaling. Embryos deleted for both midline and H15 have defects in the alignment of the cardioblasts and associated pericardial cells. Embryos null for midline have weaker and less penetrant phenotypes while embryos deficient for H15 have morphologically normal hearts, suggesting that the two genes are partially redundant in heart development. Despite the dorsal vessel defects, embryos mutant for both midline and H15 have normal numbers of cardioblasts, suggesting that cardiac cell fate specification is not disrupted. However, ectopic expression of midline in the dorsal mesoderm can lead to dramatic increases in the expression of cardiac markers, suggesting that midline and H15 participate in cardiac fate specification and may normally act redundantly with other cardiogenic factors. Conservation of Tbx20 expression and function in cardiac development lends further support for a common ancestral origin of the insect dorsal vessel and the vertebrate heart.

Animals↗
PubMed2003

HATs off to Hop: recruitment of a class I histone deacetylase incriminates a novel transcriptional pathway that opposes cardiac hypertrophy.

Histone acetylation, regulated by two antagonistic enzymes - histone acetyltransferases (HATs) and histone deacetylases (HDACs) - results in transcriptional changes and also plays a critical role in cardiac development and disease. A new study shows that overexpression of the atypical transcriptional corepressor homeodomain-only protein (Hop) causes cardiac hypertrophy via recruitment of a class I HDAC. In contrast to the body of work on transcriptional mechanisms that drive cardiac hypertrophy, including class II HDACs, this report elucidates a novel growth-suppressing transcriptional pathway in cardiac muscle that opposes hypertrophic growth.

Acetyltransferases↗
PubMed1980

Upper intestinal endoscopy induces hypoxemia in patients with obstructive pulmonary disease.

We studied the effects of fiberoptic upper intestinal endoscopy on blood oxygenation and cardiac rhythm in 13 patients. Six patients had normal pulmonary function or mild obstruction to air flow. None of these developed arterial oxygen desaturation during endoscopy. Seven patients had moderate to severe airflow obstruction. Six of these desaturated to less than 90%; the mean +/- SEM arterial oxygen tension changed from a baseline of 75 +/- 2 mm Hg to 54 +/- 2 mm Hg during endoscopy (P less than 0.01). Electrocardiographic changes during endoscopy occurred in 5 patients, 4 of whom had moderate to severe airflow obstruction. In 3 of these patients, the ECG changes were concurrent with desaturation. Patients with moderate to severe airflow obstruction frequently become hypoxemic and may develop cardiac arrhythmias during upper gastrointestinal endoscopy.

Airway Obstruction↗
PubMed1997

Cardiac metastasis from carcinoma breast--a case report.

Secondary neoplasms of the heart are more common than primary tumours. Metastasis occurs most commonly from bronchogenic carcinoma followed by lymphoma and carcinoma breast. Most often cardiac metastasis go undetected as they are asymptomatic and occurs as a terminal event. A 51 year old lady who developed cardiac metastasis from carcinoma breast diagnosed during life is reported with brief review of the literature.

Bone Neoplasms↗
PubMed1977

Acute intravenous administration of potassium chloride to furosemide pretreated dogs.

Twelve male mongrel dogs were used for this study; six were untreated (control) and six were given intravenous furosemide (1 mg/kg) daily for seven consecutive days before each study. Each animal received intravenous KCl 0.8, 1.6 or 3.2 mMol/kg/hr for one hour, but only one dose for each study and at least seven days were allowed between studies. The animals were given thiopentone for tracheal intubation and mechanically ventilated, maintaining a PaCO2 of 4.0 to 4.5 kPa (30-35 torr) and anaesthetized with nitrous oxide-oxygen and halothane. Daily administration of furosemide reduced serum potassium from 4.48 to 4.09 mMol/1 with no significant change in serum sodium. A greater number of furosemide-pretreated animals (6 vs 3) developed cardiac dysrhythmias during non-lethal intravenous KCl at 0.8, 1.6 mMol/kg/hr. The furosemide-pretreated group tended to succumb at a lower serum potassium concentration (12.2 vs 13.8 mMol/I, P less than 0.05) and developed earlier onset (44 vs 54 min, P less than 0.05) of cardiac standstill or ventricular fibrillation following intravenous KCl at 3.2 mMol/kg/hr. Cardiac output, heart rate and mean arterial pressure were significantly elevated during serum concentrations of 6.9-9.1 mMol/1, while no statistically significant changes were observed for stroke volume and peripheral resistance. There were no significant differences of urinary potassium excretion between the untreated and treated groups when like doses of KCl were infused. These data suggest that acute infusion of KCl in furosemide-pretreated dogs may not be an effective means of treating hypokalaemia and could be hazardous.

Animals↗
PubMed1987

Cardiac tamponade complicating anaesthetic induction for repair of ascending aorta dissection.

A case is described of a 69-year-old woman with dissection of the ascending aorta who developed cardiac tamponade during induction of anaesthesia. The tamponade was diagnosed by a haemodynamic profile showing approximation of the central venous, pulmonary wedge and pulmonary arterial diastolic pressures, and was treated with rapid surgical intervention and drainage of the haemopericardium. Cardiac tamponade and dissecting aneurysms of the ascending aorta are conditions with contrasting anaesthetic considerations and the problems encountered are discussed.

Aged↗
PubMed1992

[Postoperative cardiac intensive care for patients with thoracic cancer: analysis of 430 cases].

430 patients with thoracic cancer were given intensive care after major thoracic surgery. Of those 188 (43.72%) developed cardiac complication during their stay in ICU and 2 (0.46%) died. The results indicated that postoperative cardiac complications were closely related to the patients age, preoperative concomitant cardiovascular diseases, duration of operation, hypoxemia, hypercapnia, and surgical complications. Postoperative cardiac intensive care could reduce the mortality rate.

Adult↗
PubMedDate not supplied

Diagnosis and management of neoplastic pericardial effusion with cardiac tamponade; review of two case studies at the San Juan Veteran Administration Medical Center.

Two case reports of patients with known non-small cell lung cancer that developed cardiac tamponade related to metastatic pericardial disease are described. Both of these patients underwent urgent subxiphoid echocardiographic guided pericardiocentesis. They both were treated with sclerotherapy using intrapericardial bleomycin. There were no complications from these procedures and no recurrence of cardiac tamponade. They both lived more than 6 months after this intervention. This article reviews the pathogenesis, clinical presentation, diagnosis, and current therapeutic interventions of patients with neoplastic pericardial effusion and cardiac tamponade.

Adenocarcinoma↗
PubMed1997

[Acute left ventricular systolic dysfunction after pericardial effusion drainage].

A patient with a thymoma and initially normal ventricular systolic function developed cardiac tamponade, which was relieved by pericardiocentesis. After four days, the tumor was removed and, one week after the relief of tamponade, she developed severe left ventricular systolic dysfunction, that recovered in three days with venous therapy.

Acute Disease↗
PubMed2003

Forensic consideration of death in the bathtub.

About 100-120 cases of 'sudden death in bathroom' are reported every year in our prefecture, which is 8-10% of the total number of what is considered unnatural deaths. For reasons that are still unclear, the victims die while bathing in the bathtub. This baffling form of death occurs mostly in the winter season and 80-% of these are elderly persons. However, despite a full autopsy, it is sometimes still very difficult to determine the cause of death or the direct cause of drowning in the bathtub. To prevent others from this mysterious form of death and to determine the risk factors for the elderly while bathing, we examined several parameters such as physiological changes and biochemical blood analysis in a total of 54 volunteers during both the winter and summer seasons in Japan. We found that some of the elderly developed cardiac arrhythmia such as ventricular tachycardia, ventricular extrasystole, supraventricular extrasystole, and bradycardia. Also, decreases of systolic blood pressure during bathing were observed during this experiment. We conclude that the development of extrasysytole or ventricular tachycardia can be a stress involved in bathing. These changes might contribute to cardiac arrest or to drowning in the bathtub. Moreover, a sudden decrease of blood pressure is considered to be a risk factor of cerebrovascular accident.

Adult↗
PubMed1999

The mammalian Tolloid-like 1 gene, Tll1, is necessary for normal septation and positioning of the heart.

Mammalian Tolloid-like 1 (mTLL-1) is an astacin-like metalloprotease, highly similar in domain structure to the morphogenetically important proteases bone morphogenetic protein-1 (BMP-1) and Drosophila Tolloid. To investigate possible roles for mTLL-1 in mammalian development, we have used gene targeting in ES cells to produce mice with a disrupted allele for the corresponding gene, Tll1. Homozygous mutants were embryonic lethal, with death at mid-gestation from cardiac failure and a unique constellation of developmental defects that were apparently confined solely to the heart. Constant features were incomplete formation of the muscular interventricular septum and an abnormal and novel positioning of the heart and aorta. Consistent with roles in cardiac development, Tll1 expression was specific to precardiac tissue and endocardium in 7.5 and 8.5 days p.c. embryos, respectively. Tll1 expression was also high in the developing interventricular septum, where expression of the BMP-1 gene, Bmp1, was not observed. Cardiac structures that were not affected in Tll1-/- embryos either showed no Tll1 expression (atrio-ventricular cushions) or showed overlapping expression of Tll1 and Bmp1 (aortico-pulmonary septum), suggesting that products of the Bmp1 gene may be capable of functionally substituting for mTLL-1 at sites in which they are co-expressed. Together, the various data show that mTLL-1 plays multiple roles in formation of the mammalian heart and is essential for formation of the interventricular septum.

Animals↗
PubMed2005

Morphogenesis of the right ventricle requires myocardial expression of Gata4.

Mutations in developmental regulatory genes have been found to be responsible for some cases of congenital heart defects. One such regulatory gene is Gata4, a zinc finger transcription factor. In order to circumvent the early embryonic lethality of Gata4-null embryos and to investigate the role of myocardial Gata4 expression in cardiac development, we used Cre/loxP technology to conditionally delete Gata4 in the myocardium of mice at an early and a late time point in cardiac morphogenesis. Early deletion of Gata4 by Nkx2-5Cre resulted in hearts with striking myocardial thinning, absence of mesenchymal cells within the endocardial cushions, and selective hypoplasia of the RV. RV hypoplasia was associated with downregulation of Hand2, a transcription factor previously shown to regulate formation of the RV. Cardiomyocyte proliferation was reduced, with a greater degree of reduction in the RV than in the LV. Late deletion of Gata4 by Cre recombinase driven by the alpha myosin heavy chain promoter did not selectively affect RV development or generation of endocardial cushion mesenchyme but did result in marked myocardial thinning with decreased cardiomyocyte proliferation, as well as double-outlet RV. Our results demonstrate a general role of myocardial Gata4 in regulating cardiomyocyte proliferation and a specific, stage-dependent role in regulating the morphogenesis of the RV and the atrioventricular canal.

Animals↗