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PubMed2000

The ShcA phosphotyrosine docking protein sensitizes cardiovascular signaling in the mouse embryo.

The ShcA gene products have served as a model for the analysis of phosphotyrosine-recognition domains, and for the functions of docking proteins during tyrosine kinase signaling. Here we show that ShcA is primarily expressed in the cardiovascular system during early mouse embryogenesis and regulates both heart development and establishment of mature blood vessels. Targeted mutation suggests that the ShcA adaptor is a pivotal target of tyrosine kinases that selectively potentiates activation of the MAP kinase pathway in the remodeling vasculature. Biochemical analysis of mutant cells shows that ShcA sensitizes cells to growth factor-induced MAP kinase activation, and also organizes cytoskeletal rearrangement in response to the extracellular matrix. ShcA may therefore orchestrate complex interactions within the vascular compartment by rendering cells permissive to respond to soluble and adhesive external cues.

Adaptor Proteins, Signal Transducing↗
PubMed1975

Sequential atrioventricular pacing as a stress test. Evaluation of left ventricular function in second-degree AV heart block developing during atrial pacing.

Advanced or second-degree atrioventricular (AV) heart block pre-existing or developing during atrial pacing (AP) at low heart rates of smaller than 130 per minute, limits the value of AP to stress the left ventricle. When Wenkebach type AV block is present, the heart rate can be increased by administration of atropine before atrial pacing or by right ventricular pacing. Atropine, however, occasionally may cause serious supraventricular or ventricular arrhythmias, and high rate right ventricular pacing is not tolerated by many patients with left ventricular dysfunction because of the absence of the atrial contribution. Twenty-eight out of 101 patients with angina pectoris (27.7 percent) developed second degree AV heart block during atrial pacing studies performed for evaluation of left ventricular function. In 8 of the 28 patients, sequential AV pacing (SP) was performed successfully, with the heart rate being increased to 150-167 per minute. In 4 of the 8 patients, left ventricular dysnfunction was demonstrated during and immediately after SP. Typical angina pectoris developed in two of the four patients during SP, one of whom proved to have normal coronary arteriogram. Sequential AV pacing is an alternative method to increase the heart rate for the purpose of stressing the left ventricle when advanced degree or second-degree AV heart block pre-exists or develops during right atrial pacing. In some patients the method of SP might be preferable to administration of atropine or to ventricular pacing.

Adult↗
PubMed1995

Cytochrome-c oxidase in developing rat heart. Enzymic properties and amino-terminal sequences suggest identity of the fetal heart and the adult liver isoform.

Perinatal development of cytochrome-c oxidase (complex IV) and ubiquinol-cytochrome-c reductase (complex III) was investigated in rat heart and liver by analysing catalytic properties, protein amounts, and subunit isoforms during the transition from the fetal to the adult state. The total amounts of complexes from milligram quantities of tissue, and the portions of isoforms of complex IV, were quantified densitometrically after isolation of the native complexes by blue native polyacrylamide gel electrophoresis and separation of the protein subunits by Tricine/SDS/PAGE [Schägger, H. & von Jagow, G. (1991) Anal. Biochem. 199, 223-231]. A parallel increase of protein amounts and catalytic activities during perinatal development was observed in heart and liver for complex III, but only in liver for complex IV. In heart, both a doubling of the turnover number of complex IV and a lowered Km for cytochrome c were observed. The altered enzymic properties correlated with the increase of heart type subunits VIa and VIII. The fetal enzymes from heart and liver seem to be identical to the adult liver isoform, as deduced from their enzymic properties and identical aminoterminal sequences of subunits VIa and VIII.

Amino Acid Sequence↗
PubMed1991

Changes in force and calcium sensitivity in the developing avian heart.

The aim of this study was to characterize the development of the contractile properties of intact and chemically skinned muscle from chicken heart and to compare these characteristics with those of developing mammalian heart reported by others. Small trabeculae were dissected from left ventricles of Arbor Acre chickens between embryonic day 7 and young adulthood (7 weeks post-hatching). At all ages, increasing extracellular calcium (0.45-3.6 mM) progressively increased twitch force of electrically stimulated trabeculae. Twitch force at 1.8 mM extracellular calcium, normalized to cross-sectional area, increased to a maximum at 1 day post-hatching, remained constant through 3 weeks post-hatching, but then decreased at 7 weeks post-hatching. The maximal calcium-activated force of trabeculae chemically skinned with Triton X-100 detergent increased to a maximum 2 days before the time of hatching and was not significantly changed up to 7 weeks post-hatching. Over the ages studied, average twitch force in 1.8 mM calcium was between 26 and 66% of maximal calcium-activated force after skinning, suggesting that the contractile apparatus is not fully activated during the twitch in normal Ringer. In skinned trabeculae, the calcium sensitivity of the contractile apparatus was higher in the embryo than in the young adult. These age-dependent changes in calcium sensitivity are correlated with isoform switching in troponin T. A decrease in pH from 7.0 to 6.5 decreased the calcium sensitivity of the contractile apparatus to a greater degree in skinned trabeculae from young adult hearts than in those from embryonic hearts. This change in susceptibility to acidosis is temporally associated with isoform switching in troponin I.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed2003

Women smokers' perceptions of smoking-related health risks.

OBJECTIVE: Unrealistic perceptions of personal susceptibility to the health hazards of smoking may be an important determinant of cigarette smoking and a barrier to smoking cessation. This study was undertaken to assess perceptions of smoking-related health risks among women smokers. METHODS: A secondary analysis was conducted using cross-sectional data collected from 1184 (response rate 61%) perimenopausal women patients from one university-affiliated health system. RESULTS: The majority of respondents were white and college-educated and had an annual household income of over $60,000. Twelve percent of respondents were current smokers, 37% were former smokers, and 51% were never smokers. Sixty percent of current smokers rated their lifetime risk for developing heart disease or lung cancer as average or below average, and 75% of current smokers rated their lifetime risk for developing osteoporosis as average or below average. Multivariable logistic regression analysis revealed that any smoking history (past or current) was associated with perception of above average risk for developing lung cancer, but only heavier smoking (> or =10 cigarettes per day) was associated with perception of above average risk for developing heart disease. No level of smoking was associated with perception of above average risk for developing osteoporosis. CONCLUSIONS: The majority of women smokers surveyed perceived their lifetime risk for developing heart disease, lung cancer, and osteoporosis as average or below average. It appears that women smokers are more aware of their increased risk for developing lung cancer than their increased risk for developing heart disease or osteoporosis.

Attitude to Health↗
PubMed2005

Opposing effect of p38 MAP kinase and JNK inhibitors on the development of heart failure in the cardiomyopathic hamster.

OBJECTIVE: p38 MAP kinase (p38 MAPK) and c-Jun NH2-terminal kinase (JNK) have been implicated in the pathophysiology of heart failure. We investigated the effects of chronic treatment with p38 MAPK and JNK inhibitors on the development of heart failure in dilated cardiomyopathy (DCM) hamster heart. METHODS AND RESULTS: BIO14.6 hamster hearts showed markedly increased p38 MAPK and JNK activities at 6 weeks of age when there was no significant increase in the area of fibrosis, heart weight/body weight, left ventricular (LV) chamber dilation and LV dysfunction. p38 MAPK and JNK activities were attenuated at 26 weeks of age and abolished at 40 weeks of age in BIO14.6 hamster hearts. BIO14.6 hamsters and the control BIOF1B hamsters were chronically treated (i.p.) with the p38 MAPK inhibitors, SB203580 (1 mg/kg/day) and FR167653 (3 mg/kg/day), or the JNK inhibitor, SP600125 (1 mg/kg/day) or vehicle for 20 weeks starting from 6 weeks of age. Treatment of BIO14.6 hamster hearts with SB203580 and FR167653 reduced the number of TUNEL-positive myocytes, the area of fibrosis and heart weight/body weight associated with a significant decrease of LV dimension and an increase in LV ejection fraction and LV contractility compared to the vehicle-treated counterpart. In contrast, treatment with SP600125 increased the number of TUNEL-positive myocytes and the area of interstitial fibrosis associated with aggravation of LV chamber dilation and LV dysfunction. CONCLUSIONS: These results suggest that chronic treatment with p38 MAPK and JNK inhibitors produces opposing effects on the development of heart failure in the DCM hamster heart.

Animals↗
PubMed1998

Do males 30-50 years of age with chronic epilepsy and on long-term anticonvulsant medication have lower-than-expected risk of developing coronary heart disease?

PURPOSE: It has been claimed that long-term use of antiepileptic drugs (AEDs) brings about changes in the lipid profile which might resist development of cardiovascular disease. The aim of this study was to test the following hypothesis: Do males with chronic epilepsy and on long-term treatment with AEDs have a lower than expected risk of developing coronary heart disease? METHODS: The coronary risk profile in 40 male patients with chronic epilepsy, aged 30-50 years, was explored, using an American individual coronary risk factor test program (the Cooper test). We made a survey of the patients' risk factors: total cholesterol, high density lipoprotein (HDL) cholesterol, triglycerides, glucose, blood pressure, body fat percentage, physical fitness, hereditary factors, smoking habits, and degree of stress. Each factor was given a score, and the sum of scores constituted the total coronary risk profile. Eighty men in the same age group, casually selected from an industrial medical service, served as controls. RESULTS: There was no statistically significant difference in the total coronary risk profile between the epilepsy patients and the controls. Nor were there any significant differences among the individual risk factors except for physical fitness level, which was significantly lower among the epilepsy group than among the controls. In the epilepsy group, however, there was a trend toward higher levels of total cholesterol, higher levels of HDL-cholesterol, lower levels of total cholesterol/HDL-cholesterol ratio, increased body fat percentage, greater heredity and somewhat greater coronary risk score as compared with the healthy controls, but the differences did not reach statistical significance. The protective effect against coronary heart disease exercised by the enzyme-inducing AEDs seems to be counteracted by other factors, like reduced physical fitness and increased body fat percentage. CONCLUSIONS: Our hypothesis was not confirmed, because we found that the 40 patients with chronic epilepsy tested had about the same risk of developing coronary heart disease as did the control group.

Adipose Tissue↗
PubMed1999

Mechanisms of development of heart failure in the hypertensive patient.

Hypertension is a major risk factor for the development of heart failure. Mechanisms which maintain normal function in the short term in the pressure overloaded heart have longer term deleterious effects. These include left ventricular (LV) hypertrophy and chronic activation of the adrenergic and renin-angiotensin systems. beta-Blocking agents are capable of blocking the adrenergic system and, to some extent, the renin-angiotensin system. They are therefore attractive in treating hypertension, both for preventing the development of abnormalities and for reversing established LV dysfunction and hypertrophy. Trials in heart failure have shown that these agents prevent progressive myocardial dysfunction, prevent and reverse remodelling and improve intrinsic systolic function. Non-selective beta-blocking agents appear to offer greater anti-adrenergic effects than selective ones. However, more research is needed, including direct comparisons of different agents.

Adrenergic beta-Antagonists↗
PubMed2002

MMP inhibition modulates TNF-alpha transgenic mouse phenotype early in the development of heart failure.

Myocardial extracellular matrix remodeling regulated by matrix metalloproteinases (MMPs) is implicated in the progression of heart failure. We hypothesized that MMP inhibition may modulate extracellular matrix remodeling and prevent the progression of heart failure. The effects of the MMP inhibitor BB-94 (also known as batimastat) on MMP expression, collagen expression, collagen deposition, collagen denaturation, and left ventricular structure and function in transgenic mice with cardiac-restricted overexpression of tumor necrosis factor-alpha (TNF-alpha) (TNF1.6) were assessed. The results showed that BB-94 reduced the expression of collagens, increased insoluble collagen and the ratio of undenatured to total soluble collagen, and prevented myocardial hypertrophy and diastolic dysfunction in young TNF1.6 mice. Furthermore, the treatment significantly improved cumulative survival of TNF1.6 mice. However, MMP inhibition did not have salutary effects on ventricular size and function in old mice with established heart failure. The results suggest that MMP activation may play a critical role in changes of myocardial function through the remodeling of extracellular matrix, and MMP inhibition may serve as a potential therapeutic strategy for heart failure, albeit within a narrow window during the development of heart failure.

Animals↗
PubMed2001

Relation between expression of TNF alpha, iNOS, VEGF mRNA and development of heart failure after experimental myocardial infarction in rats.

An injury to the heart due to myocardial infarction (MI) may progress to heart failure. Among factors, whose interactions promote remodeling of ischemic myocardium, the increased expression of tumor necrosis factor alpha (TNFalpha), inducible nitric oxide synthase (iNOS) and Vascular Endothelial Growth Factor (VEGF) was found. However, little is known about the temporal and spatial relation between expression of iNOS, cytokine TNFalpha, and growth factor VEGF during pathological process of development of heart failure after the myocardial infarction. Male Sprague-Dawley rats were used for experimental myocardial infarction. The procedure was performed by anterolateral thoracotomy and snearing LAD with the metal clip. The hemodynamic measurements were done with the Langendorff preparation converted into a working heart system. The hemodynamic parameters were recorded at day 6, 11, 28, 40 and the myocardium for gene expression was collected at day 1, 4, 11, 28, 40. Control group was sham operated rats. The VEGF, TNFalpha, iNOS, and GAPDH genes were detected by RT-PCR assay from samples taken at border zone of myocardial infarction. Expression of isoform VEGF120 was found at day 1 and 4 after MI, whereas isoforms VEGF164 and VEGF188 along with expression of TNFalpha and iNOS was found at day 1, 4, 11, 28, 40. No expression of examined genes was detected in the myocardium of control rats. The expression of studied factors was parallel with development of heart failure after myocardial infarction assessed by hemodynamic measurements. These findings confirm the postulated involvement of TNFalpha, iNOS and growth factor VEGF in the remodeling of the myocardium and development of heart failure after experimental myocardial infarction.

Animals↗
PubMed1989

Development of heart rate variation over the first 6 months of life in normal infants.

Development of heart rate variation in three frequency ranges was examined during sleep-walking states in normal infants over the first 6 mo of life. Extent of all three types of heart rate variation decreased from 1 wk to 1 mo of age. Extent of respiratory sinus arrhythmia increased from 1 mo to 6 mo during all sleep-waking states, with the increase most pronounced during quiet sleep. Variation in two bands of lower frequencies showed increases in extent from 1 to 3 mo, then a slowing or reversal of the increase between 3 and 4 mo of age. During rapid eye movement sleep, the two types of lower frequency heart rate variation decreased in extent from 3 through 6 mo of age. These results suggest that alterations in autonomic control of heart rate occur at several time periods over the first 6 mo of life and that these alterations may have an effect only on particular types of heart rate variation and only during particular sleep-waking states. The diminution of all three types of heart rate variation at 1 mo may indicate a reduction in vagal tone at this age.

Aging↗
PubMed1996

Doppler echocardiography of normal and abnormal embryonic mouse heart.

To evaluate normal embryonic mouse heart development using Doppler echocardiography and to quantify changes in normal embryonic mouse cardiac function with increasing gestational age from the time of cardiac septation, a new method was applied using Doppler echocardiography. Trisomic embryos were screened to evaluate a model of abnormal cardiac anatomy. The development of the embryonic heart in mice has been well studied anatomically, but there are limited physiologic studies. A new method has been developed to assess the mouse fetal heart in a similar fashion to the current use of echocardiography in the chick embryo and the human fetus. This method was applied to normal mouse embryos known to survive and to abnormal trisomy embryos that die during gestation and have cardiac failure. To analyze early normal embryonic heart hemodynamics, Doppler echocardiograms were performed on n = 129 C57B1/6J mouse embryos from d 10 through 19 of gestation and 20 embryos with trisomy 16 (gestational d 11-14). The maximal blood velocities recorded at the inflow and outflow of the embryonic heart were analyzed for heart rate, peak early and peak late inflow and outflow velocities, and measurements were made of systolic ejection, filling, and other time intervals normalized for heart rate. A high velocity holosystolic or diastolic velocity with altered time intervals was identified as atrioventricular or semilunar valvular regurgitation, respectively. Inflow and outflow velocities increased with increasing gestational age. The time period of isovolemic contraction time was present before and undetectable after gestational d 17, whereas the total filling time increased. Ejection time and isovolemic relaxation time had no significant change. No valvular regurgitation was detected in normal embryos. These echocardiographic patterns are similar to those observed for human embryos. Abnormal Doppler findings were present (inflow or outflow valvular regurgitation) in 55% of trisomy 16 embryos. Echocardiographic data can now be obtained beginning at d 11 in the mouse embryo for analyses relating to abnormal heart development. A noninvasive technique may be invaluable to monitor the physiologic condition of embryos within a litter and to detect and monitor those embryos where heart defects may be expected. Qualitative markers of embryonic congestive heart failure such as valvular regurgitation may be present and detectable with structural valvular abnormalities or failing cardiac physiology. The mouse embryo is an appropriate animal model to analyze normal and abnormal mammalian heart development and function.

Animals↗
PubMed1995

Angiotensin II type-1 receptor antagonist as well as angiotensin converying enzyme inhibitor attenuates the development of heart failure in aortocaval fistula rats.

OBJECTIVES: We investigated the effect of chronic administration of an angiotensin II type-1 receptor antagonist in the development of heart failure due to volume overload in rats. METHODS: Aortocaval fistula (AVF), a model of volume overloaded heart failure, was induced in rats by our newly developed technique using a simple and rapid 18-gauge needle multipuncture. After 3 weeks of oral administration of an angiotensin II receptor antagonist TCV-116, 1 mg/kg per day, we evaluated the hemodynamics, heart weight, and degree of left ventricular dilatation. We also compared the effect of TCV-116 with that of an angiotensin-converting enzyme inhibitor delapril, 1 g/L in drinking water. RESULTS: AVF heart failure produced by our technique exhibited significant increases in the left ventricular end-diastolic pressure (LVEDP) (12 = 1 vs 4 +/- 1 mmHg, p < 0.05), right atrial pressure (RAP) (5.0 +/- 0.6 vs 1.0 +/- 0.4 mmHg, p < 0.05), right ventricular systolic pressure (RVSP) (58 +/- 6 vs 33 +/- 1 mmHg, p < 0.05), left ventricular weight (LVW) (3.00 +/- 0.13 vs 2.09 +/- 0.04 g/kg BW, p < 0.05), right ventricular weight (RVW) (0.93 +/- 0.05 vs 0.59 +/- 0.01 g/kg BW, p < 0.05), and left ventricular end-diastolic volume index (LVEDVI) (2.55 +/- 0.14 vs 0.80 +/- 0.12 ml/kg BW, p < 0.05) as compared with these values in sham-operated rats. There were no differences in shunt ratio between untreated and TCV-116- and delapril-treated AVF groups. TCV-116 improved these hemodynamics, as did delapril (TCV-116 vs delapril: LVEDP 8 +/- 1 vs 8 +/- 1, RAP: 3.8 +/- 0.6 vs 2.3 +/- 1.4, RASP: 50 +/- 2 vs 46 +/- 3, LVW: 2.53 +/- 0.11 vs 2.52 +/- 0.15, RVW: 0.80 +/- 0.04 vs 0.77 +/- 0.06, LVEDVI: 1.67 +/- 0.15 vs 1.70 +/- 0.17). CONCLUSION: These results suggest that AVF rats with volume overload produced by a new multipuncture method exhibit both right- and left-side heart failure. Angiotensin II type-1 receptor antagonist as well as angiotensin converting enzyme inhibitor attenuate the development of this type of heart failure in rats.

Analysis of Variance↗
PubMed1998

Development of heart failure following isoproterenol administration in the rat: role of the renin-angiotensin system.

OBJECTIVE: High dosages of catecholamines induce cardiomyocyte necrosis and interstitial fibrosis in rats. We investigated whether this initial damage is followed by the development of heart failure and assessed the particular role of the renin-angiotensin system using ramipril. METHODS AND RESULTS: Following the administration of 0 mg or 150 mg isoproterenol/kg 6 groups of Wistar rats were followed for 2 or 16 weeks: Sham, isoproterenol, isoproterenol + ramipril. Isoproterenol induced significant increases of echocardiographically measured left ventricular end-diastolic posterior wall thickness and dimension, whereas ramipril treatment significantly attenuated these changes. Left ventricular end-diastolic pressure was markedly increased in isoproterenol-treated rats and normalized following ramipril. Isoproterenol rats were further characterized by hormonal activations including transient elevations of plasma renin activity, aldosterone and cardiac angiotensin converting enzyme activity. Histomorphological characterization of isoproterenol-treated hearts demonstrated cardiomyocyte necrosis and reparative fibrosis. Ramipril treatment only slightly reduced the amount of necrosis as well as the expression of extracellular matrix proteins. CONCLUSIONS: In rats, a toxic dosage of isoproterenol caused characteristic myocardial damage that subsequently resulted in mild heart failure. Ramipril administration following isoproterenol was highly effective to attenuate hemodynamic and hormonal alterations as well as the development of left ventricular hypertrophy, but had only little influence on the expression of extracellular matrix proteins. Since angiotensin converting enzyme inhibition had no impact on the initial myocardial injury, the development of heart failure in this model seems to require functional integrity of the renin-angiotensin system.

Adrenergic beta-Agonists↗
PubMed1995

[Development of heart rate in newborn infants during quiet sleep].

The small number of investigations of the development of heart rhythm during the first half year of life provide only rough ideas regarding the maturation of heart rate control. In the present study, in 10 newborns, ECG and respiratory effort were recorded in 13 sessions from birth up to the sixth month. The total power (TP), power in the low (LF) and high frequency range (HF), and the ratio LF/HF were used from the heart rate power spectra. All parameters reveal no linear developmental patterns: TP, LF, and HF increase during the first days to a maximum, then decrease subsequently and remain low until the second month. TP and HF increase between the second and sixth month. LF/HF increases up to the second month followed by a decrease down to the sixth month. The developmental courses of TP, HF and LF/HF correlate with the course of breathing rate (BR), whereby high BR is associated with low HF and TP. The results hint at a maturated cardiorespiratory system.

Child Development↗
PubMed2006

Physiopathology of the embryonic heart (with special emphasis on hypoxia and reoxygenation).

The adaptative response of the developing heart to adverse intrauterine environment such as reduced O2 delivery can result in alteration of gene expression with short- and long-term consequences including adult cardiovascular diseases. The tolerance of the developing heart of acute or chronic oxygen deprivation, its capacity to recover during reperfusion and the mechanisms involved in reoxygenation injury are still under debate. Indeed, the pattern of response of the immature myocardium to hypoxia-reoxygenation differs from that of the adult. This review deals with the structural and metabolic characteristics of the embryonic heart and the functional consequences of hypoxia and reoxygenation. The relative contribution of calcium and sodium overload, pH disturbances and oxidant stress to the hypoxia-induced cardiac dysfunction is examined, as well as various cellular signaling pathways (e.g. MAP kinases) involved in cell survival or death. In the context of the recent advances in developmental cardiology and fetal cardiac surgery, a better understanding of the physiopathology of the stressed developing heart is required.

Animals↗
PubMed2003

Expression of cardiac neural crest and heart genes isolated by modified differential display.

The invasion of the cardiac neural crest (CNC) into the outflow tract (OFT) and subsequent outflow tract septation are critical events during vertebrate heart development. We have performed four modified differential display screens in the chick embryo to identify genes that may be involved in CNC, OFT, secondary heart field, and heart development. The screens included differential display of RNA isolated from three different axial segments containing premigratory cranial neural crest cells; of RNA from distal outflow tract, proximal outflow tract, and atrioventricular tissue of embryonic chick hearts; and of RNA isolated from left and right cranial tissues, including the early heart fields. These screens have resulted in the identification of the five cDNA clones presented here, which are expressed in the cardiac neural crest, outflow tract and developing heart in patterns that are unique in heart development.

Animals↗