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PubMed1989

Perinatal development of heart, kidney, and liver mitochondrial antioxidant defense.

Development of the mitochondrial antioxidant defense system was studied to assess its potential role in the newborn mammal's tolerance to oxidative challenge and to gain insight into the fetal adaptation to a relatively hyperoxic adult environment. Isolated heart, kidney, and liver mitochondria from fetal, newborn, and adult guinea pigs were used. In situ function of the antioxidant enzymes was estimated in mitochondrial suspensions after the addition to selenite or tert-butyl hydroperoxide by determining NAD(P)H oxidation rates spectrophotometrically at 340-375 nm. Kidney and liver mitochondria from newborn animals were less susceptible to selenite and tert-butyl hydroperoxide-induced NAD(P)H oxidation. The pattern of change, however, varied widely with tissue type. Kidney mitochondria displayed the largest change with a 3- to 4-fold increase in rate from the fetal to adult period. NAD(P)H oxidation rates in intact mitochondria did not correlate consistently with glutathione reductase and peroxidase activities in sonicated mitochondria suggesting in situ regulation by other endogenous factors. Immediately after birth, mitochondrial glutathione reductase and peroxidase activities dropped 38-50% and 50-70%, respectively, in all tissues studied. Total glutathione content of heart and liver mitochondria did not change with age. Adult kidney mitochondrial glutathione, however, declined to 24% of fetal values. Mitochondrial superoxide dismutase activity increased 150-300% from the fetal to the adult period in all tissues studied. Perinatal changes in the mitochondrial antioxidant system and their relationship to mitochondrial calcium metabolism are discussed in terms of the newborn's resistance to oxidative stress.

Animals↗
PubMed2000

Slug is an essential target of TGFbeta2 signaling in the developing chicken heart.

An epithelial-mesenchymal cell transformation (EMT) occurs during the development of endocardial cushions in the atrioventricular (AV) canal of the heart. This is a complex developmental process regulated by multiple extracellular signals and signal transduction pathways. It was recently shown that the transcription factor Slug is expressed in the AV canal and is required for initial steps of EMT. Treatment of AV canal explants with either antisense oligodeoxynucleotides toward Slug or anti-TGFbeta2 antibody inhibited initial steps of EMT. Others have identified roles for HGF and BMP during EMT in the heart. Both HGF and BMP are known to regulate Slug in other cell types. To determine whether TGFbeta2 or other signaling factors regulate Slug expression during EMT in the heart, we cultured AV canal explants in the presence of anti-TGFbeta2 antibody, anti-TGFbeta3 antibody, pertussis toxin, retinoic acid, noggin, or anti-HGF antibody. Only treatment with anti-TGFbeta2 antibody or retinoic acid inhibited Slug expression in AV canal explants. Consistent with these data, we found that retinoic acid disrupted initial steps of EMT, while antagonists of BMP and HGF signaling disrupted later steps of EMT. Transfection of AV canal explants with Slug rescued the inhibitory effect of anti-TGFbeta2 antibody but not retinoic acid on EMT. Slug is thus an essential target of TGFbeta2 signaling during EMT in the developing chicken heart.

Animals↗
PubMed1990

Significance of coronary circulation in hypertensive heart disease for development and prevention of heart failure.

Coronary hemodynamics (coronary blood flow, coronary reserve, myocardial oxygen consumption) were analyzed in both experimental and clinical essential hypertension. Significant reduced coronary reserve was found in hypertensive patients with left ventricular hypertrophy. Extracoronary reasons for these phenomena were ruled out. Considerable thickening of the coronary resistance vessels (medial hypertrophy) in hypertensive hypertrophy associated with a marked increase in the wall thickness/radius ratio was considered sufficient to explain the impairment of coronary flow. After long-term pharmacotherapy there was normalization of both medial hypertrophy and coronary reserve. This small-vessel abnormality correlates well with clinical findings in hypertensive heart disease (angina and electrocardiographic changes despite normal coronary arteriogram). Moreover, this structural adaptation of the small vessels may carry the inherent risk of an impaired oxygen supply to the hypertrophied myocardium. Thus, late cardiac failure of the hypertrophied heart in hypertension may be attributed, in part, to this microcirculation disorder. Conversely, reversal of left ventricular hypertrophy and of hypertrophy of vascular smooth muscle by specific pharmacotherapy can be considered a possible approach to the rational prevention of cardiac failure in hypertensive patients. For future investigations, controlled clinical trials are needed to confirm these findings with regard to prevention of heart failure, and pharmacotherapeutic studies are necessary to define the optimal drug regimen for reversal of vascular smooth muscle hypertrophy.

Adult↗
PubMed2005

Permanent pacing is a risk factor for the development of heart failure.

No previous study has examined the importance of right ventricular pacing as a risk factor for the development of heart failure (HF) in subjects without a history of HF. A cohort study of patients who underwent initial pacemaker implantation (n = 11,426) was conducted to test the hypothesis that patients with ventricular dyssynchrony created by permanent pacing would develop HF, as shown by new HF hospitalizations or HF-related deaths, at a higher rate than matched controls.

Adult↗
PubMed2001

Congenital heart block: development of late-onset cardiomyopathy, a previously underappreciated sequela.

OBJECTIVE: We report 16 infants with complete congenital heart block (CHB) who developed late-onset dilated cardiomyopathy despite early institution of cardiac pacing. BACKGROUND: Isolated CHB has an excellent prognosis following pacemaker implantation. Most early deaths result from delayed initiation of pacing therapy or hemodynamic abnormalities associated with congenital heart defects. METHODS: A multi-institutional study was performed to identify common clinical features and possible risk factors associated with late-onset dilated cardiomyopathy in patients born with congenital CHB. RESULTS: Congenital heart block was diagnosed in utero in 12 patients and at birth in four patients. Ten of 16 patients had serologic findings consistent with neonatal lupus syndrome (NLS). A pericardial effusion was evident on fetal ultrasound in six patients. In utero determination of left ventricular (LV) function was normal in all. Following birth, one infant exhibited a rash consistent with NLS and two had elevated hepatic transaminases and transient thrombocytopenia. In the early postnatal period, LV function was normal in 15 patients (shortening fraction [SF] = 34 +/- 7%) and was decreased in one (SF = 20%). A cardiac pacemaker was implanted during the first two weeks of life in 15 patients and at seven months in one patient. Left ventricular function significantly decreased during follow-up (14 days to 9.3 years, SF = 9% +/- 5%). Twelve of 16 patients developed congestive heart failure before age 24 months. Myocardial biopsy revealed hypertrophy in 11 patients, interstitial fibrosis in 11 patients, and myocyte degeneration in two patients. Clinical status during follow-up was guarded: four patients died from congestive heart failure; seven required cardiac transplantation; one was awaiting cardiac transplantation; and four exhibited recovery of SF (31 +/- 2%). CONCLUSIONS: Despite early institution of cardiac pacing, some infants with CHB develop LV cardiomyopathy. Patients with CHB require close follow-up not only of their cardiac rate and rhythm, but also ventricular function.

Cardiomyopathy, Dilated↗
PubMed2004

Compartmentation of glycolysis and glycogenolysis in the perfused rat heart.

Developing methods that can detect compartmentation of metabolic pathways in intact tissues may be important for understanding energy demand and supply. In this study, we investigated compartmentation of glycolysis and glycogenolysis in the isolated perfused rat heart using (13)C NMR isotopomer analysis. Rat hearts previously depleted of myocardial glycogen were perfused with 5.5 mm [U-(13)C]glucose plus 50 mU/mL insulin until newly synthesized glycogen recovered to new steady-state levels ( approximately 60% of pre-depleted values). After a short wash-out period, the perfusate glucose was then switched to [1-(13)C]glucose, and glycolysis and glycogenolysis were stimulated by addition of glucagon (1 microg/ml). A (13)C NMR multiplet analysis of the methyl resonance of lactate provided an estimate of pyruvate derived from glucose vs glycogen while a multiplet analysis of the C4 resonance of glutamate provided an estimate of acetyl-CoA derived from glycolytic pyruvate vs glycogenolytic pyruvate. These two indices were not equivalent and their difference was further magnified in the presence of insulin during the stimulation phase. These combined observations are consistent with functional compartmentation of glycolytic and glycogenolytic enzymes that allows pyruvate generated by these two processes to be distinguished at the level of lactate and acetyl-CoA.

Animals↗
PubMed1987

Protective effect of glucose on the anoxic myocardium of old and young mice.

To compare the function of old and young hearts contracting under identical conditions, isolated hearts of young and old C57BL/6J mice were perfused using a Langendorff preparation. During a 3-min period of anoxia some hearts showed a decrease in systolic pressure, while other hearts developed contracture. The incidence and magnitude of contracture was greater in the old hearts and they also showed a significantly larger decline in contractility. Increasing the glucose concentration improved the performance of both age groups but the performance of the old hearts was still inferior to that of the young. The glycogen content and utilization were virtually the same in the two age groups. When iodoacetate was added, all hearts developed contracture and the magnitude of the contracture was greater than in the absence of iodoacetate; during the period of reoxygenation, the young hearts recovered but, the old hearts developed a second contracture. A brief period of anoxia is more debilitating to old C57BL/6J hearts than to young ones.

Aging↗
PubMed1996

Differential displaying of mRNAs from the atrioventricular region of developing chicken hearts at stages 15 and 21.

In an effort to isolate novel genes that may be involved in the development of the cardiac cushions and then the formation of cardiac valves and septa, we utilized the differential mRNA display method in conjunction with the whole-mount in situ hybridization. The total RNAs used to differentially display were prepared from atrioventricular (AV) canal regions of stage 15 and stage 21 chicken hearts because critical events known to be important for the AV valve and septum formation occur during this period of the development. We have successfully obtained 14 potential candidate genes. Three examples, 15H16 (phospholamban), E13 (skeletal alpha-tropomyosin) and 21C (a novel gene), are discussed here. Levels of mRNA expression in developing hearts were determined by Northern blot analysis and their expression patterns were revealed and compared using whole-mount in situ hybridization. Both phospholamban and skeletal alpha-tropomyosin messages in the myocardium of the AV canal region showed significant decrease during this period of the development. The 21C differential display product detects a novel 9.5 Kb message whose expression is cardiac-specific at early stages of development. The expression level of the 21C gene appeared to be increased from stage 15 to stages 21 and 25 as determined by both Northern blot analysis and in situ hybridization. From these data, we demonstrate that the differential display method together with the whole-mount in situ hybridization could be an effective means for the isolation of novel and differentially expressed genes.

Animals↗
PubMed2002

[Prevention of ischemic heart disease. Testing of three different methods for prediction of the risk of developing ischemic heart disease].

INTRODUCTION: The purpose of this evaluation was to compare estimation of risk of IHD, according to PRECARD and guidelines from DSAM and DCS. MATERIAL AND METHOD: The evaluation was performed in a general practice setting with relatively few elderly patients. Fifty consecutive patients were evaluated, 29 men and 21 women. Thirty-four patients were evaluated according to the physician's assessment and 16 according to the wishes of the patients. RESULTS: Four persons with definite ischaemic heart disease were included. According to DSAM, a further eight persons were found to have a > 20% risk of developing IHD. According to DCS, ten persons and to PRECARD three persons had a > 20% risk. DISCUSSION: Evaluation with PRECARD gives a more precise estimation than do DSAM and DCS. PRECARD uses the same risk factors as DSAM and DCS, but the HDL level and height/weight are also included. In addition, PRECARD estimates the risk of AMI, stroke, and fatal events, as well as the most important risk factors. PRECARD is recommended for use in general practice.

Adult↗
PubMed1985

Changes in carnitine levels in the embryonic chick heart during development.

Carnitine levels in the embryonic chick heart were measured. The amount of total carnitine, free plus short chain acyl carnitine (acid-soluble fraction), and long chain acyl carnitine (acid-insoluble fraction) were examined at days 7, 11, 17, and 21 of incubation. These concentrations were found to correspond favorably with data from previous investigators with regard to variations in palmitoylcarnitine transferase enzyme activity, mitochondrial chain elongation activity, and palmitic acid oxidation.

Animals↗
PubMed1992

[Sources and developments in heart surgery].

This contribution deals with the development of the individual ramifications of cardiac surgery from their inception to the presence and especially highlights the personalities responsible for these breakthroughs. The trials and errors of these developments are described along with the multitude of presently unanswered questions including those related to thoracic organ transplantation, cardiac assistance, and replacement as well as the socio-economical aspects of modern cardiac surgery.

Cardiac Surgical Procedures↗
PubMed2006

Atrial and ventricular myosin heavy-chain expression in the developing chicken heart: strengths and limitations of non-radioactive in situ hybridization.

Myosin heavy-chain (MHC) isoforms are major structural components of the contractile apparatus of the heart muscle. Their spatio-temporal patterns of expression have been used as a tool to dissect cardiac development and differentiation. Although extensively investigated, controversy still exists concerning the expression patterns of atrial (AMHC), ventricular (VMHC), and cardiac myosin heavy-chain (CMHC) during development in the heart. In this study, we describe that probe length, probe concentration, and staining time in the non-radioactive in situ hybridization procedure seriously influence the observed pattern of MHC expression and the subsequent interpretation, explaining the divergent opinions in the field. Using a variety of external and internal controls for the in situ hybridization procedure, we demonstrate that both AMHC and VMHC are expressed throughout the entire heart tube during early development. During subsequent development, VMHC becomes restricted to the ventricles, whereas AMHC remains expressed in the atria, and, at substantially lower levels, is detected in the ventricles. These results are discussed in the context of methodological constraints of demonstrating patterns of gene expression. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials.

Animals↗
PubMed1992

Urokinase activity in the developing avian heart: a spatial and temporal analysis.

Early events in cardiac morphogenesis are characterized by cell migrations and extensive tissue remodeling. This study was undertaken to determine the levels of urokinase in specific regions of the avian heart during early stages of development. Urokinase has previously been shown to be involved in both cell migration and matrix turnover. Elevated urokinase activity and mRNA levels were associated with the onset of ventricular trabeculation and mesenchymal cell migration in the endocardial cushion tissues. Urokinase was localized by immunostaining to the endocardial and mesenchymal cells of the developing atrioventricular canal (AVC) and outflow tract (OFT) as well as with evaginating ventricular endocardium. No immunoreactivity was seen associated directly with the matrix, suggesting that the enzyme remained mostly cell associated, a finding which was confirmed in isolated endocardial cells. Results from this study suggest a role for urokinase in the tissue remodeling and cell migration that occurs during the early stages of cardiac morphogenesis.

Animals↗
PubMed1999

Long-term exercise and atherogenic activity of blood mononuclear cells in persons at risk of developing ischemic heart disease.

CONTEXT: Increasing evidence demonstrates that atherosclerosis is an immunologically mediated disease in which the secretion of atherogenic and atheroprotective cytokines, by infiltrating blood mononuclear cells, plays an important role. It is not known whether long-term exercise alters this atherogenic and atheroprotective activity directly. OBJECTIVE: To determine the effect of long-term exercise on the atherogenic activity of blood mononuclear cells in persons at risk of developing ischemic heart disease. DESIGN: Before-after trial using a 6-month individualized, supervised exercise program, with an enrollment period from December 1996 to October 1997. SETTING: Hospital-based community wellness center. PARTICIPANTS: Of 110 persons who responded to a public request for volunteers, 52 met the inclusion criteria (risk ratio for myocardial infarction > or =1.7 based on serum complement and/or C-reactive protein levels, and normal exercise treadmill test results). Forty-three of the 52 enrollees (25 women [mean age, 49.7 years] and 18 men [mean age, 48.1 years]) completed the study; 9 withdrew for personal reasons. Additional risk factors for ischemic heart disease included hypercholesterolemia (65.1 %), a family history of coronary heart disease (62.8%), inactivity (60.5%), hypertension (32.6%), obesity (25.6%), smoking (11.6%), and diabetes mellitus (4.7%). MAIN OUTCOME MEASURES: Blood levels were compared at baseline and after the exercise program had been completed for the following: spontaneous and phytohemagglutinin-induced production of interleukin 1 alpha, tumor necrosis factor alpha, and interferon gamma (atherogenic cytokines), and interleukin 4, interleukin 10, and transforming growth factor beta 1 (atheroprotective cytokines) by blood mononuclear cells; lymphocyte phenotypes and mitogenic responses to phytohemagglutinin; and serum C-reactive protein levels. RESULTS: Subjects exercised for a mean of 2.5 (range, 0.3-7.4) hours per week. Mononuclear cell production of atherogenic cytokines fell by 58.3 % (P<.001) following the exercise program, where as the production of atheroprotective cytokines rose by 35.9% (P<.001). Changes in transforming growth factor beta 1 and in phytohemagglutinin-induced atherogenic cytokine production after the exercise program were proportionate to the time subjects spent performing repetitive lower-body motion exercises (P<.02), indicating a dose-response relationship. After the exercise program, changes in cellular function were reflected systemically by a 35% decrease in serum levels of C-reactive protein (P=.12). CONCLUSIONS: Our data suggest that long-term exercise decreases the atherogenic activity of blood mononuclear cells in persons at risk of developing ischemic heart disease. This may be a mechanism whereby physical activity protects against ischemic heart disease.

Arteriosclerosis↗
PubMed1988

Protein kinase C (calcium/phospholipid-dependent protein kinase) in developing chick heart: selective localization to atrium versus ventricle and changes in activity levels during cardiogenesis.

Activity levels of calcium/phospholipid-dependent protein kinase were examined in preparations of atria and ventricles from embryonic chick hearts at various stages of development. Activity of protein kinase C was much higher in atria than ventricles. Protein kinase C activity underwent a progressive increase in atria during cardiogenesis, being highest just prior to hatching, followed by a profound decrease in activity after hatching. In contrast, activity of cyclic AMP-dependent protein kinase (protein kinase A), while also higher in atria than ventricles, remained relatively constant at the developmental stages examined, likewise decreasing following hatching. These progressive changes in atrial protein kinase C activity suggest a potential regulatory role for this enzyme in cardiogenesis.

Animals↗