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At least 325 records · Page 18Linked to original sources
PubMed2004

Dynamic changes of gene expression profiles during postnatal development of the heart in mice.

OBJECTIVE: To study postnatal cardiac differentiation in the mouse. HYPOTHESIS: There might be mechanisms or factors in cardiac differentiation that could be identified by systematic gene expression analysis during postnatal cardiac development. METHODS: Expression of 6144 genes was examined in mouse heart, from the newborn period (day 0), through day 7 and day 14 day, to adulthood, using the cDNA microarray approach. Northern blotting and immunohistochemical techniques were used to confirm the microarray results. RESULTS: Various cardiac development related genes involving the cell cycle (cyclin B1, proliferating cell nuclear antigen (PCNA), and Ki67), growth factors (IGF-II, pleiotrophin (PTN), and midkine (MK)), and transcriptional regulation, cytoskeleton, and detoxification enzymes were identified by microarray analysis. Some of these genes were also confirmed by Northern blotting and immunohistochemistry of their RNA and protein content. In vivo treatment with PTN (20 ng/g) increased bromodeoxyuridine incorporation (by 2.24-fold) and PCNA expression (by 1.71-fold) during day 7 to day 14, indicating that PTN induces cell proliferation in mouse heart. CONCLUSIONS: Global gene expression analysis in the whole heart may be useful in understanding the orchestrated process of postnatal development or terminal differentiation in the cardiac environment. These data are likely to be helpful in studying developmental anomalies of the heart in neonates.

Animals↗
PubMedDate not supplied

University of Wisconsin solution versus Stanford cardioplegic solution and the development of cardiac allograft vasculopathy.

BACKGROUND: University of Wisconsin (intracellular) solution has been shown to offer some distinct benefits of myocardial preservation over Stanford (extracellular) solution, including a more rapid functional recovery, improved adenosine triphosphate preservation, and a tendency for less postoperative inotropic agents. However intracellular solutions with high potassium content have been reported to cause a functional if not structural endothelial injury in laboratory experiments. METHODS: Because of this information we retrospectively viewed our follow-up angiographic data for the development of the cardiac allograft vasculopathy in a consecutive series of 195 heart transplant recipients. These patients were treated in identical fashion, with the same immunosuppression regimen, except for the type of cardioplegia used--Stanford solution (group I n = 95) and University of Wisconsin solution (group II n = 100). RESULTS: With a mean follow-up of 24 months after transplantation, a significant difference was seen in the development of cardiac allograft vasculopathy in group II (22%) versus group I (14%, p < 0.03). Although significant differences were observed with univariate analysis with respect to donor age and ischemic time favoring group I and with multivariate statistical analysis with respect to overall rejections favoring group II, the only significant variable for the difference in the development of allograft vasculopathy was University of Wisconsin cardioplegic solution (p < 0.003). A subgroup of 30 patients previously randomized for a functional study comparing the two cardioplegic agents showed a tendency for statistical significance with a freedom from allograft vasculopathy of 93% in group I, as compared with 83% in group II, after 13 months follow-up (p = 0.09). The overall probability of being free of vasculopathy at 24 months was 86% for group I and 70% for group II. CONCLUSIONS: The data support the conclusion that University of Wisconsin intracellular solution is associated with an increased incidence of vasculopathy versus Stanford solution and warrants investigation for modification of this preservation agent in heart transplantation.

Adenosine↗
PubMed1975

Role of adrenergic mechanisms in the development of cardiac hypertrophy.

This experiment was designed to study the role of cardiac beta-adrenergic mechanisms in the development of hypertrophy in rats. The suprarenal abdominal aorta was banded, resulting in an increase in cardiac wt-body wt ratio. A group of rats received a sham operation. Half of the banded rats were treated with practolol, 2.0 mg/kg intraperitoneally every 12 hr for the 6 days after banding. The effectiveness of cardiac beta-adrenergic blockade was confirmed by absence of an increase in heart rate following intravenous isoproterenol at various times between practolol injections. Practolol did not affect the gradient in the banded groups. Six animals in each banded group were sacrificed daily for 6 days. The right and left ventricles were dissected separately and weighed. RV-body weight ratios increased similarly in both banded groups. LV-body weight ratio (g/kg) was 2.17 +/- 0.043 in sham rats, and it attained maximal levels of 3.03 +/- 0.10 within 6 days in banded untreated rats and 2.96 +/- 0.14 in banded rats receiving practolol. Therefore, beta-adrenergic mechanisms were not involved in the development of hypertrophy due to increased afterload. Also, these findings are not consistent with the Meerson hypothesis, since hypertrophy occurred despite the reduction in myocardial O2 consumption due to practolol.

Animals↗
PubMed2001

Identification of the t-type calcium channel (Ca(v)3.1d) in developing mouse heart.

During cardiac development, there is a reciprocal relationship between cardiac morphogenesis and force production (contractility). In the early embryonic myocardium, the sarcoplasmic reticulum is poorly developed, and plasma membrane calcium (Ca(2+)) channels are critical for maintaining both contractility and excitability. In the present study, we identified the Ca(V)3.1d mRNA expressed in embryonic day 14 (E14) mouse heart. Ca(V)3.1d is a splice variant of the alpha1G, T-type Ca(2+) channel. Immunohistochemical localization showed expression of alpha1G Ca(2+) channels in E14 myocardium, and staining of isolated ventricular myocytes revealed membrane localization of the alpha1G channels. Dihydropyridine-resistant inward Ba(2+) or Ca(2+) currents were present in all fetal ventricular myocytes tested. Regardless of charge carrier, inward current inactivated with sustained depolarization and mirrored steady-state inactivation voltage dependence of the alpha1G channel expressed in human embryonic kidney-293 cells. Ni(2+) blockade discriminates among T-type Ca(2+) channel isoforms and is a relatively selective blocker of T-type channels over other cardiac plasma membrane Ca(2+) handling proteins. We demonstrate that 100 micromol/L Ni(2+) partially blocked alpha1G currents under physiological external Ca(2+). We conclude that alpha1G T-type Ca(2+) channels are functional in midgestational fetal myocardium.

Animals↗
PubMedDate not supplied

Technical developments in cardiac MRI: 2000 update.

In recent years, the technological developments in MRI have made it possible to perform routine cardiovascular imaging with MR. The availability of a vectorcardiogram, real time interactive scanning, SENSE and optimized protocols (balanced FFE) have made it possible to evaluate wall motion, perfusion and viability at rest and under stress. All vessels can be visualized, including the coronary arteries. In the near future, MRI will be capable of distinguishing between calcified and lipid plaque, and will even allow interventional applications.

Cardiovascular Diseases↗
PubMed2003

Role of the autonomic nervous system in the development of cardiac arrhythmias in cats with acute myocardial ischemia receiving thyroliberin.

The role of the autonomic nervous system in the development of ischemic cardiac arrhythmias was studied in acute experiments on cats receiving thyrotropin-releasing hormone. Bilateral vagotomy attenuated, while bilateral transection of cardiac branches of the stellate ganglia completely abolished the antiarrhythmic effect of thyrotropin-releasing hormone.

Animals↗
PubMed2003

Cardiac chamber formation: development, genes, and evolution.

Concepts of cardiac development have greatly influenced the description of the formation of the four-chambered vertebrate heart. Traditionally, the embryonic tubular heart is considered to be a composite of serially arranged segments representing adult cardiac compartments. Conversion of such a serial arrangement into the parallel arrangement of the mammalian heart is difficult to understand. Logical integration of the development of the cardiac conduction system into the serial concept has remained puzzling as well. Therefore, the current description needed reconsideration, and we decided to evaluate the essentialities of cardiac design, its evolutionary and embryonic development, and the molecular pathways recruited to make the four-chambered mammalian heart. The three principal notions taken into consideration are as follows. 1) Both the ancestor chordate heart and the embryonic tubular heart of higher vertebrates consist of poorly developed and poorly coupled "pacemaker-like" cardiac muscle cells with the highest pacemaker activity at the venous pole, causing unidirectional peristaltic contraction waves. 2) From this heart tube, ventricular chambers differentiate ventrally and atrial chambers dorsally. The developing chambers display high proliferative activity and consist of structurally well-developed and well-coupled muscle cells with low pacemaker activity, which permits fast conduction of the impulse and efficacious contraction. The forming chambers remain flanked by slowly proliferating pacemaker-like myocardium that is temporally prevented from differentiating into chamber myocardium. 3) The trabecular myocardium proliferates slowly, consists of structurally poorly developed, but well-coupled, cells and contributes to the ventricular conduction system. The atrial and ventricular chambers of the formed heart are activated and interconnected by derivatives of embryonic myocardium. The topographical arrangement of the distinct cardiac muscle cells in the forming heart explains the embryonic electrocardiogram (ECG), does not require the invention of nodes, and allows a logical transition from a peristaltic tubular heart to a synchronously contracting four-chambered heart. This view on the development of cardiac design unfolds fascinating possibilities for future research.

Animals↗
PubMed2000

Effects of anisotropy on the development of cardiac arrhythmias associated with focal activity.

The anisotropy that normally exists in the myocardium may be either enhanced in peri-infarction zones by loss of lateral cell connections or reduced by redistribution of gap junctions. To test how the degree of anisotropy affects the development of ectopic focal activity, we carried out computer simulations in which a model of an ectopic focus is incorporated as the central element of a two-dimensional sheet of ventricular cells. At low values of intercellular coupling conductance (Gc), the focus region is spontaneously active, but the limited intercellular current flow inhibits propagation. At high Gc, automaticity is suppressed by the loading effects of the surrounding cells. At intermediate Gc, the ectopic activity may propagate into the sheet. In the case of isotropic coupling, the minimum size of the focus region for propagation to occur (in terms of number of collaborating cells within the focus) is as small as approximately ten cells, and this number decreases with increasing anisotropy. Thus, the presence of anisotropy facilitates the development of ectopic focal activity. We conclude that the remodeling that occurs in peri-infarction zones may create a substrate that either facilitates (enhanced anisotropy) or inhibits (reduced anisotropy) the development of cardiac arrhythmias associated with ectopic focal activity.

Action Potentials↗
PubMed1989

A simple method for producing graded aortic insufficiencies in rats and subsequent development of cardiac hypertrophy.

Selective perforation of the right cusp of the aortic valve alone (1V) or in combination with that of the left valve cusp (2V) by a plastic rod inserted from the right common carotid artery was performed to cause aortic insufficiency (AI) in rats. The development of cardiac hypertrophies subsequent to these interventions to cause graded cardiac volume overloads was followed up every week till the end of week 4 after the operations by radiographic measurement of the cardiothoracic ratio (CTR). Rats were killed 2 and 4 weeks after the operations, and the density of beta-adrenoceptors in hypertrophied cardiac muscle membranes was determined by radioligand binding assay and compared with sham-operated (sham) rats. Production of AI resulted in an enlargement of the cardiac shadow in 1VAI and 2VAI rats, with significant graded increases in the CTR at the end of week 3. The occurrence of graded cardiac hypertrophies was well revealed in graded increases of the heart weight/body weight ratio among the sham, 1VAI, and 2VAI rats at the end of both week 2 and week 4. There was a tendency to stepwise increases due to graded AI in the density of binding sites for 3H-dihydroalprenolol, with a significant increase in 2VAI rats at the end of week 2. At the end of week 4, plasma norepinephrine levels of 2VAI rats was raised significantly as compared with the sham rats. Selective perforation of either one or two cusps of the aortic valve can be performed with ease using touch alone and provides us with a simple method for producing graded cardiac hypertrophies in rats due to pure volume overload.

Animals↗
PubMed1995

Renal dopamine receptors are involved in the development of cardiac hypertrophy.

The present study examined the effect of fenoldopam, a known dopamine-1 receptor (DA1) agonist in order to understand its involvement in the cardiac hypertrophic process. Male Sprague-Dawley rats underwent abdominal aortic constriction (AB) with placement of a suprarenal ligature while sham operated animals served as controls. The AB groups showed an increase in their heart wt, left ventricular (LV) wt, heart wt/body wt and LV wt/body ratio. Furthermore, the length of these hearts, as measured from the auriculoventricular border to the apex, LV wall and interventricular (IV) septal thickness were increased from control levels. Treatment with SCH 23390, a DA1 antagonist, on the other hand, was able to partially regress the cardiac hypertrophic changes. All these parameters were also increased in control animals treated with fenoldopam (F). Such changes were more striking in the F+AB group which showed a significant acceleration of the cardiac hypertrophic process on superimposing the two treatments. Plasma dopamine and renin activity were increased in all the groups as compared to control. These results indicate that dopamine receptors are implicated in the development of cardiac hypertrophy.

Animals↗
PubMedDate not supplied

Changes of myocardial adenine nucleotide and protein synthesis during development of cardiac hypertrophy.

1. Studies on three models of cardiac hypertrophy (aortic constriction, application of isoproterenol, daily administrations of 3,3'5-triiodo-L-thyronine, respectively) reveal that the enhancement of de novo synthesis of adenine nucleotides occurs very early during the development of cardiac hypertorphy and always precedes the increase of protein synthesis. Therefore, it seems likely that the accelerated synthesis of adenine nucleotides is an important factor among those metabolic processes involved in the stimulation of protein synthesis in the hypertrophying heart. 2. As far as the mechanism for the observed enhancement of adenine nucleotide synthesis is concerned, it has been demonstrated that the available pool of 5-phosphoribosyl-l-pyrophosphate, an essential precursor substance of de novo synthesis, is increased in the hypertrophying heart due to isoproterenol and 3,3'5-triiodo-L-thyronine, respectively.

Adenine Nucleotides↗
PubMed1993

Differential regulation of natriuretic peptide receptor messenger RNAs during the development of cardiac hypertrophy in the rat.

The heart expresses the three natriuretic peptide receptors (NPR), namely NPR-A, NPR-B, and NPR-C. We have examined the temporal relationship between the expression of mRNA transcripts for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) and their receptors in the heart during the development of cardiac hypertrophy in the aortovenocaval fistula rat. Messenger RNAs were measured by cDNA amplification. Progressive cardiac hypertrophy was accompanied by increased ANP mRNA prevalence throughout the heart and increased BNP mRNA in the left atrium. The most striking observation was the gradual disappearance of NPR-C transcripts (the putative "clearance" receptor) in all chambers; this was in marked contrast to the increase in mRNA levels for NPR-A and NPR-B (the guanylyl cyclase-linked receptors). Our observations have important therapeutic implications if the transcript changes are mirrored at the receptor protein level because (a) the apparent down-regulation of NPR-C may enhance the local action of natriuretic peptides on the heart, and (b) the loss of NPR-C, particularly if it is widespread, may reduce the rate of elimination of the natriuretic peptides, restricting the therapeutic potential of specific NPR-C ligands designed to reduce peptide clearance.

Animals↗
PubMed1987

Development of cardiac sympathetic and adrenal-medullary responses in borderline hypertensive rats.

Borderline hypertensive (BHR) rats are the first generation offspring of a cross of spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive rats. In adulthood, BHRs have systolic blood pressures in the 140-160 mm Hg range. If subjected to chronic stress paradigms, however, BHRs develop sustained and permanent elevations in systolic blood pressure (180-200 mm Hg). In the present study, we examined the functional development of cardiac and adrenal medullary responses to reflex activation of the sympathetic nervous system in preweanling BHR and WKY rats. Pups of the two groups were injected with insulin or saline at 4, 8, 12, or 16 days of age and sacrificed 3 h later. Insulin produces an acute lowering of blood glucose which is attended by a centrally mediated increase in sympathetic activity. The induction of ornithine decarboxylase (ODC) activity in heart and the depletion of epinephrine from the adrenal medulla were biochemical indicators of functional sympathetic neurotransmission. WKY and BHR pups had similar levels of cardiac ODC activity under basal conditions and following administration of insulin. In contrast, BHRs had higher amounts of adrenal norepinephrine and epinephrine from 4 to 16 days of age and greater depletion of adrenal epinephrine following insulin administration at 8, 12 and 16 days of age. These findings indicate that BHRs have a greater capacity for catecholamine biosynthesis, storage and release in the adrenal medulla during the preweanling period compared to age-matched normotensive WKY controls. This alteration in the adrenal medulla during the preweanling period may contribute to the susceptibility of adult BHR rats to stress-induced hypertension.

Adrenal Medulla↗
PubMed1998

Physiological cardiac reserve: development of a non-invasive method and first estimates in man.

OBJECTIVE: To investigate whether physiological cardiac reserve can be measured in man without invasive procedures and whether it is a major determinant of exercise capacity. DESIGN: Development of method of measurement and an observational study. SETTING: A regional cardiothoracic centre. SUBJECTS: 70 subjects with a wide range of cardiac function, from heart failure patients to athletes. METHODS: Subjects underwent treadmill, symptom limited cardiopulmonary exercise tests to measure aerobic exercise capacity (represented by VO2max) and cardiac reserve. Cardiac output was measured non-invasively using the CO2 rebreathing technique. RESULTS: Cardiac power output (CPOmax) at peak exercise was found to be significantly related to aerobic capacity: CPOmax (W) = 0.35 + 1.5 VO2max (1/min), r = 0.87, p < 0.001. It also correlated well with exercise duration (r = 0.62, p < 0.001), suggesting that cardiac reserve is a major determinant of exercise capacity. In the study, cardiac reserve ranged from 0.27 to 5.65 W, indicating a 20-fold difference between the most impaired cardiac function and that of the fittest subject. CONCLUSIONS: A non-invasive method of estimating physiological cardiac reserve was developed. The reserve was found to be a major determinant of exercise capacity in a population of normal subjects and patients with heart disease. This method may thus be used to provide a clearer definition of the extent of cardiac impairment in patients with heart failure.

Adolescent↗
PubMed1999

The history and development of cardiac transplantation.

The history of heart surgery, spanning only 100 years to date, has seen some of the most daring and persistent men and women in all of medical history. Many aspects of heart surgery, including such innovations as the heart-lung machine, aortic aneurysm surgery, and the correction of congenital heart defects, have provided future surgeons with an important lesson: diligent research can solve complex problems. The history and development of cardiac transplantation is particularly full of challenges that have been overcome, with the research phase alone spanning more than 90 years. During that time, essential contributions came from all over the world, including the United States, Russia, England, and South Africa. As is typical of medical advancement, individual contributions did not stand alone but added to the experience of those who had come before. Even so, the work of a few particular groups deserves special recognition. Most notable is the Stanford team, led by Dr. Norman Shumway, who continued to transplant human hearts when other institutions had abandoned hopes for the operation. Largely because of the commitment of that team, cardiac transplantation has become a standard option in the treatment of end-stage heart disease. Currently, only the availability of donor hearts limits the number of cardiac transplantations performed worldwide.

Animals↗
PubMed2004

Recent developments in cardiac output determination by bioimpedance: comparison with invasive cardiac output and potential cardiovascular applications.

PURPOSE OF REVIEW: To describe recent developments in bioimpedance technique and its application in cardiovascular diseases. Cardiac output determination has been used selectively during recent years because of the need for invasive right heart catheterization. Hence, experience with its application in patients with cardiovascular diseases and especially heart failure is limited. Bioimpedance is a novel noninvasive technique determining changes in instantaneous (during one heartbeat) conductance of a small electrical current transferred through the body. By using different algorithms correcting for various body composition constants, it calculates the change in instantaneous arterial blood volume (that is, stroke volume) and cardiac output. Traditionally, bioimpedance cardiac output is determined using either thoracic or whole body techniques according to the location of the electrodes transmitting and receiving the small electrical current. RECENT FINDINGS: Significant progress was achieved in recent years in cardiac output determination by bioimpedance. Newer algorithms using thoracic and whole body bioimpedance have demonstrated better correlation with invasive cardiac output determination. In a few preliminary studies bioimpedance-determined cardiac output was found useful in the diagnosis, risk stratification, and treatment titration of some cardiovascular conditions. Further, larger prospective studies are required to determine the true independent value of cardiac output measurement by bioimpedance for the evaluation of cardiovascular diseases and especially heart failure. SUMMARY: Recently, significant improvement was achieved in cardiac output measurement by bioimpedance with both newer thoracic and whole body techniques. Preliminary studies imply that this measure may be of value in managing some cardiovascular disorders.

Algorithms↗
PubMedDate not supplied

Role of myocardial lipids in development of cardiac necrosis.

Significant alterations in fatty acyl composition of cardiac phospholipids and neutral lipids are induced by dietary cod liver oil in the rat. Increased dietary availability of docosahexaenoic acid (22:6 omega3) leads to extensive replacement of linoleic acid (18:2omega6) and arachidonic acid (20:4omega6) in phospholipids. Dietary cod liver oil (10%) reduces isoproterenol stress tolerance and results in increased development of cardiac necrosis and mortality following isoproterenol treatment. It is suggested that diminished catecholamine stress tolerance may be related to altered synthesis of prostaglandins or related products.

Animals↗
PubMedDate not supplied

[To the history of organisation and development of cardiac anesthesiology in the A. N. Bakulev Research Center of Cardiovascular Surgery of the Russian Academy of Medical Sciences: the start of activities (1956-1965)].

The authors present data on the development and introduction of anesthetic techniques during cardiac surgery at the Institute of Thoracic Surgery, USSR Academy of Medical Sciences, in 1956-1960 and after its reorganization to the Institute of Cardiovascular Surgery, USSR Academy of Medical Sciences, in 1961-1965. It is shown that in the years of introduction of closed operations on the heart, the methods of one- and many component inhalational anesthesia were mastered, its techniques were developed, anesthesia apparatuses and an anesthesia schedule were designed, cardiac anesthesiological studies were conducted, training of physicians from the country's regions was initiated, and the first guidelines for general anesthesia were published. In these years, the firm foundation was laid for the development of cardiac anesthesia. Later on the Institute developed and introduces all basic types of inhalational anesthesia during operations on the open heart under both extracorporeal circulation and hypothermia. The gained experience allowed the laboratory staff to defend several dissertations, to issue two monographs, and to analyze errors and risks of general anesthesia in patients with cardiovascular diseases at surgery.

Academies and Institutes↗