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At least 703 records · Page 39Linked to original sources
PubMed2000

The effects of diffusible creosote-derived compounds on development in Pacific herring (Clupea pallasi).

The effects of diffusible creosote-derived compounds from weathered creosote-treated pilings on embryonic development in the Pacific herring were investigated. Parameters used to evaluate toxicity included embryonic development, cardiac function, embryo/larval activity (movement of developing embryos), hatching success, and larval morphology at hatch. For acute exposures, embryos were incubated in seawater containing either creosote-treated wood (creosote) or untreated wood (wood control), or seawater alone (control). All embryos adhering directly to creosote-treated wood and 40-50% of embryos not adhering to the creosote-treated wood failed to develop beyond the first few days of incubation. For surviving embryos, a 93% reduction in heart rate, and moderate to marked arrhythmia was observed. Surviving embryos also exhibited both an increase in frequency and an alteration in pattern of embryo/larval movement, with most embryos exhibiting tremors as compared with the vigorous movements of the control embryos. Cardiac function and embryo/larval movements of embryos exposed to untreated wood were not significantly different from controls. The hatching rate of embryos exposed to creosote was 90% lower than control embryos and 72.4% lower than embryos exposed to untreated wood, and the LC(50) for hatching success was 0.05 mg/l. Partial hatching (incomplete hatch) was observed in 15-20% of embryos exposed to creosote. All of the hatched larvae exposed as embryos to creosote exhibited morphological deformities, including scoliosis, pericardial edema and/or ascites. Similar effects were observed in embryos collected from creosoted pilings in San Francisco Bay, with a 72% decrease in hatching success compared with embryos collected from the Bay and severely deformed larvae. To investigate the combined effects of creosote and salinity on hatching success, larval morphology, and cardiac function, embryos were exposed to a sublethal concentration of creosote (0.003 mg/l) at three salinities; sub-optimal (8 parts per thousand (ppt)), optimal (16 ppt), and high salinity (28 ppt). The presence of creosote decreased hatching success at all three salinities, but the effect was greatest at 8 ppt (34% reduction) and the least in 28 ppt (14% reduction). The increased incidence of morphological abnormalities was also smallest at the high salinity (10% compared with 24 and 33% in 8 and 16 ppt). While exposure to creosote resulted in reduced heart rates at all three salinities, no additive effect of creosote and salinity was observed.

Animals↗
PubMed1991

[Transplantation of the heart-lung complex (the first clinical experience)].

The article deals with experience in the first transplantation of a heart-lung complex in the USSR. The recipient was a 34-year-old male with dilation cardiomyopathy. It was decided to perform the transplantation because the terminal stage of cardiac failure and secondary pulmonary hypertension developed (cardiac index 1.3 l/m, pressure in pulmonary artery 80/50 mm Hg, resistance of pulmonary vessels 10.4 units after Wood). The heart and lung were transplanted from a 19-year-old male who died from a craniocerebral injury. Cyclosporine, metipred , imuran, dopamine in small doses, cardiotonics, and antibiotics were given in the postoperative period; the patient was kept on artificial respiration for 48 hours. For up to 10 days the patient's condition was relatively stable and his consciousness was clear. Bilateral pneumonia developed, however, from which he died on the 12th postoperative day. The article discusses organizational problems and some questions of immunosuppressive therapy, immunological monitoring, and the management of patients after transplantation of a heart-lung complex.

Adult↗
PubMed1996

Advantage of Inoue balloon catheter in mitral balloon valvotomy: experience with 220 consecutive patients.

Percutaneous mitral balloon valvotomy (PMV) using the Inoue balloon catheter was attempted in 220 consecutive patients with severe symptomatic mitral stenosis. Their age range was 10-63 mean 30 +/- 10 years; 161 patients were females and 59 were males; 29 patients were in atrial fibrillation. Eleven patients were pregnant; 14 patients underwent previous surgical commissurotomy. The procedure was technically successfully performed in 215 (97.7%) patients. The mean fluoroscopy time was 15.5 +/- 6.4 min and mean procedure time was 109 +/- 79 min. Optimal results (group I) was achieved in 207 patients who have mitral score of 7 +/- 1. PMV resulted in decrease in left atrial pressure from 23 +/- 5 to 14 +/- 4 mm Hg (P < 0.001), the mean mitral valve gradient (MVG) decreased from 15 +/- 4 to 6 +/- 3 mm Hg (P < 0.001). The mitral valve area (MVA) by catheter increased from 0.7 +/- 0.2 to 1.7 +/- 0.5 cm2 (P < 0.001) and MVA as determined by echocardiography (2DE) increased from 0.8 +/- 0.1 to 1.9 +/- 0.3 cm2 (P < 0.001). The results were suboptimal in eight patients who have a mitral score of 10 +/- 1 (group II) MVA by catheter increased from 0.7 +/- 0.2 to 1 +/- 0.1 cm2 and Doppler MVA increased from 0.8 +/- 0.1 to 1.3 +/- 0.1 cm2. There were no deaths or thromboembolism. Two patients developed cardiac tamponade; mild mitral regurgitation (MR) developed in 24 patients (11%) and increased by one grade in another 22 patients (10%). Severe MR was encountered in three patients (1.4%). A small ASD (QP/QS < or = 1.3) was detected by oximetry in 5% of patients and by color-flow mapping in 26% of patients. One hundred fifty-eight patients from group I were followed up, for a mean of 32 +/- 12 months; MVA remained at 1.7 +/- 0.4 cm2. Seven patients developed mitral restenosis in group I, and 5 out of 8 patients developed restenosis in group II. We conclude that the hemodynamic results are good and comparable with those reported with double balloon technique. However, the Inoue balloon has several advantages over the double balloon technique: (1) low incidence of mitral regurgitation and ASDs; (2) shorter procedure and fluoroscopy time; and (3) low complication rates and the valve anatomy affects the immediate and late outcome of mitral balloon valvotomy.

Adolescent↗
PubMed1998

Noninvasive, in utero imaging of mouse embryonic heart development with 40-MHz echocardiography.

BACKGROUND: The increasing number of transgenic and targeted mutant mice with embryonic cardiac defects has resulted in the need for noninvasive techniques to examine cardiac structure and function in early mouse embryos. We report the first use of a novel 40-MHz ultrasound imaging system in the study of mouse cardiac development in utero. METHODS AND RESULTS: Transabdominal scans of mouse embryos staged between 8.5 and 13.5 days of gestation (E8.5 to E13.5) were obtained in anesthetized mice. Atrial and ventricular contractions could be discerned from E9.5, and changes in cardiac morphology were observed from E9.5 to E13.5. Hyperechoic streaming patterns delineated flow through the umbilical, vitelline, and other major blood vessels. Diastolic and systolic ventricular areas were determined by planimetry of the epicardial borders, and fractional area change was measured as an index of contractile function. Significant increases in ventricular size were documented at each stage between E10.5 and E13.5, and the ability to perform serial imaging studies over 3 days of embryonic development is described. Finally, the detection of vascular cell adhesion molecule 1 (VCAM-1) homozygous null mutant embryos demonstrates the first example of noninvasive, in utero analysis of cardiac structure and function in a targeted mouse mutant. CONCLUSIONS: We used 40-MHz echocardiography to identify key elements of the early mouse embryonic cardiovascular system and for noninvasive dimensional analysis of developing cardiac ventricles. The ability to perform serial measurements and to detect mutant embryos with cardiac defects highlights the usefulness of the technique for investigating normal and abnormal cardiovascular development.

Animals↗
PubMed1996

Involvement of the neuregulins and their receptors in cardiac and neural development.

The neuregulin gene encodes a series of polypeptide growth factors that can influence the growth state of target vertebrate cells in culture. Recently, three studies have explored the in vivo function of the neuregulin signaling system in mice by disrupting the genes encoding the neuregulin ligand(1) and two of its receptors, ErbB2(2) and ErbB4(3). Each of the genes is essential for development, and aberrations in cardiac and neural development are particularly prominent in mutant embryos. The observed defects, together with the localization of expression of the neuregulin signaling components within these tissues, highlight a paracrine mechanism for neuregulin-mediated intercellular communication.

Animals↗
PubMed1990

Routine exercise testing to detect coronary artery disease in patients with atherosclerotic vascular disease.

The ability of patients with peripheral vascular disease to perform exercise studies on a conventional treadmill is often hampered by claudication, amputation, ischemic ulceration or rest pain. This study was undertaken to investigate the use of the arm ergometer in these patients. Eighty-three patients admitted with peripheral vascular or carotid artery disease were subjected to electrocardiographic-monitored exercise testing, using both the arm ergometer and conventional treadmill, where possible. Coronary arteriography was performed consecutively on 32 of these patients to establish a control group from which the sensitivity, specificity and predictive accuracy of both methods of exercise testing could be calculated. Nineteen of the 70 arm ergometry tests and 22 of the 48 treadmill tests were positive. Nineteen of the patients with a positive test using either of the methods were asymptomatic for cardiac disease. All five patients who developed cardiac events during surgery had positive exercise tests, preoperatively. The sensitivity of arm ergometry in detecting coronary artery disease was 45.5% and the specificity 100%, while the figures for treadmill testing were 82.4% and 83.3%, respectively. The combined sensitivity for the two tests was 81.8% and the specificity 87.5%. Using a combination of these two tests thus provided a highly specific and adequately sensitive means of detecting the presence of coronary artery disease in patients presenting for peripheral vascular surgery.

Adult↗
PubMed1999

Genetic determination of cardiac mass in normotensive rats: results from an F344xWKY cross.

Genetic determinants affect adult cardiac mass and the predisposition to develop cardiac hypertrophy. The aim of this study was to identify quantitative trait loci (QTL) that control heart and left ventricular (LV) weight by use of normotensive inbred rat strains that differ in their adult cardiac mass phenotype. We studied 126 male F2 rats derived from a cross of normotensive Wistar-Kyoto and Fischer 344 rats. At 12 weeks of age, total heart weight and LV weight were measured. Genomic DNA from these animals was screened by use of polymorphic microsatellite markers across the whole genome (excluding the sex chromosomes). In this cross, the genetic contribution to total heart weight variation was 56%, and the genetic contribution for LV weight was 55%. Using the Mapmaker/QTL computer package, we identified a significant QTL on chromosome 3 with a log10 likelihood (LOD) score of 4.8, which accounted for 16.5% of the total variance of LV weight. This QTL was centered close to the marker D3Rat29. The QTL was also found to be significantly linked with total heart weight (LOD=4.4). These data provide the first demonstration of a QTL on chromosome 3 that plays a role in determining the difference in LV mass between normotensive Fischer 344 and Wistar- Kyoto inbred rat strains. The prostaglandin synthase 1 gene is located within the QTL.

Animals↗
PubMedDate not supplied

Cardiac arrest due to a vagal reflex potentiated by thoracic epidural analgesia.

Reflex bradycardia and cardiac arrest may be the result of a vagal reflex, which can occur during a variety of surgical procedures. We report a patient who developed cardiac arrest as a result of a vagal reflex that was potentiated by thoracic epidural analgesia during general anaesthesia. A 53-year-old man was scheduled for subtotal gastrectomy because of an early gastric adenocarcinoma. After an epidural catheter had been inserted, general anaesthesia was induced. During surgery, an abdominal self-retaining retractor was set up but bradycardia and cardiac arrest developed. The patient returned to a normal sinus rhythm after successful resuscitation. We conclude that bradycardia as a result of a vagal reflex is mediated by potent abdominal wall traction and is potentiated by epidural analgesia. Early diagnosis and proper treatment can allow a full recovery, even in high-risk patients.

Abdomen↗
PubMed2002

Distinct enhancers regulate skeletal and cardiac muscle-specific expression programs of the cardiac alpha-actin gene in Xenopus embryos.

During vertebrate embryonic development, cardiac and skeletal muscle originates from distinct precursor populations. Despite the profound structural and functional differences in the striated muscle tissue they eventually form, such progenitors share many features such as components of contractile apparatus. In vertebrate embryos, the alpha-cardiac actin gene encodes a major component of the myofibril in both skeletal and cardiac muscle. Here, we show that expression of Xenopus cardiac alpha-actin in the myotomes and developing heart tube of the tadpole requires distinct enhancers within its proximal promoter. Using transgenic embryos, we find that mutations in the promoter-proximal CArG box and 5 bp downstream of it specifically eliminate expression of a GFP transgene within the developing heart, while high levels of expression in somitic muscle are maintained. This sequence is insufficient on its own to limit expression solely to the myocardium, such restriction requiring multiple elements within the proximal promoter. Two additional enhancers are active in skeletal muscle of the embryo, either one of which has to interact with the proximal CArG box for correct expression to be established. Transgenic reporters containing multimerised copies of CArG box 1 faithfully detect most sites of SRF expression in the developing embryo as do equivalent reporters containing the SRF binding site from the c-fos promoter. Significantly, while these motifs possess a different A/T core within the CC(A/T)(6)GG consensus and show no similarity in flanking sequence, each can interact with a myotome-specific distal enhancer of cardiac alpha-actin promoter, to confer appropriate cardiac alpha-actin-specific regulation of transgene expression. Together, these results suggest that the role of CArG box 1 in the cardiac alpha-actin gene promoter is to act solely as a high-affinity SRF binding site.

Actins↗
PubMed1991

Proliferating cell nuclear antigen in developing and adult rat cardiac muscle cells.

During early development, rat cardiac muscle cells actively proliferate. Shortly after birth, division of cardiac muscle cells ceases, whereas DNA synthesis continues for approximately 2 weeks at a progressively diminishing rate. Little DNA synthesis or cell division occurs in adult cardiocytes. Thus, developing cardiac muscle cells are an ideal system in which to examine the expression of cell cycle-regulated genes during development. We chose to examine proliferating cell nuclear antigen (PCNA), a gene expressed at the G1/S phase boundary of the cell cycle. Northern blots of RNA from cardiac muscle cells from 18-day-old rat fetuses and from day 0, 5, and 14 neonatal as well as adult rat hearts revealed that the PCNA mRNA was found in cardiac muscle cells from all ages. However, because it was possible that this was a result of fibroblast PCNA gene expression, we used reverse transcription followed by polymerase chain reaction to see if it was possible to detect the message for PCNA in cardiac muscle cells from all ages. Because of the great sensitivity of this technique, RNA was recovered from 25 isolated adult cardiac muscle cells. Polymerase chain reaction amplification products for PCNA produced from the RNA isolated from these cells conclusively demonstrated that mRNA for this gene, which normally is associated with proliferating cells, is expressed in adult cardiac muscle cells that no longer divide. Furthermore, Western blot analysis demonstrated that the PCNA protein was found only in embryonic and neonatal cells and not in adult rat cardiac muscle cells. Therefore, it might be inferred from these data that PCNA might be regulated at the posttranscriptional level in adult cardiac muscle cells.

Animals↗
PubMed2004

Cardiac arrhythmias in neonates receiving lidocaine as anticonvulsive treatment.

UNLABELLED: Lidocaine has been used in neonates as an effective drug in controlling neonatal seizures not responding to traditional anticonvulsant therapy. Little is known about the effect of lidocaine on heart rate or occurrence of cardiac arrhythmias in neonates. The purpose of the present study was to assess the incidence of cardiac arrhythmias associated with lidocaine use for neonatal seizures. A retrospective review was performed in 207 neonates who received lidocaine for treatment of neonatal seizures. All were given a loading dose of 2 mg/kg in 10 min followed by a continuous infusion of 6 mg/kg per h, tailed off over the next 48 h. A total of ten (4,8%) infants developed cardiac arrhythmias during lidocaine infusion. In five infants a bradycardia developed, associated with a prolonged QRS complex in one. In one infant a tachycardia was seen following the bolus administration. In the other four an irregular heart rate was noted. In eight infants the arrhythmias disappeared immediately following discontinuation of lidocaine. In two infants, with severe encephalopathy, who died, the association was not so clear. CONCLUSION: The present study demonstrates that continuous cardiac monitoring of neonates who receive lidocaine for neonatal seizures is indicated, as there is a risk to develop cardiac arrhythmias. Lidocaine should be discontinued immediately when a cardiac arrhythmia occurs. Lidocaine should not be given to patients with a congenital heart disease and to infants who have already been treated with diphantoine.

Anticonvulsants↗
PubMed2001

Enhanced angiotensin II activity in heart failure: reevaluation of the counterregulatory hypothesis of receptor subtypes.

There are strong data favoring the pathogenic role of angiotensin II type 1 receptor (AT(1)) activation with subsequent promotion of myocyte growth and cardiac fibrosis in the development of cardiac hypertrophy and heart failure. An emerging hypothesis suggests that the activity of the angiotensin II type 2 receptor (AT(2)) may counterregulate AT(1) receptor effects during cardiac development and during the evolution of cardiac hypertrophy and heart failure. In this review, we examine the potential role of AT(2) activity in the context of this hypothesis. In contrast to the counterregulatory hypothesis, studies in mice with an overabundance of, or a deficiency in, the AT(2) receptor do not suggest that AT(2) signaling is essential for cardiac development. Moreover, the proposed antigrowth effects of AT(2) receptor signaling in pathological cardiac hypertrophy could not be shown in two mice models both deficient in AT(2) receptors. The role of AT(2) receptor signaling in cardiac fibrosis is, however, still debatable because of conflicting data in the same two studies. In angiotensin II-evoked apoptosis in cardiomyocytes, the proposed proapoptotic role of AT(2) activity could not be confirmed. Furthermore, in the progression from the bench to bedside, the results of two large clinical trials in heart failure, namely ELITE II and Val-HeFT, can be explained without ascribing a major protective role to the unopposed activity of the AT(2) receptor in the failing myocardium. In this review, we conclude that the collective evidence does not strongly support a net beneficial effect of AT(2) stimulation in the diseased myocardium.

Angiotensin II↗
PubMed1992

Discharge dependencies of amygdala central nucleus neurons to the cardiac and respiratory cycle following local cocaine administration.

We examined dependencies of amygdala central nucleus neuronal discharge to the cardiac and respiratory cycles in freely behaving cats following local microinjection of cocaine (100 micrograms/0.2 microliter). Cross-correlation histograms showed cycle-by-cycle dependencies between neuronal discharge and the cardiac and respiratory cycles in 10 of 30 cells and 7 of 30 cells, respectively, during baseline periods. After cocaine delivery, the discharge rate of half of the central nucleus of the amygdala cells (16/30, 53%) were partly or completely inhibited in a reversible manner. Excluding cardiac- and respiratory-dependent neurons which ceased firing after cocaine, more than half (5/8) of the remaining cardiac and two-thirds (4/6) of respiratory-dependent neurons altered discharge dependencies following cocaine administration. Of the cells that did not exhibit cardiac and respiratory dependencies pre-cocaine, 2 of 20 developed cardiac correlations and 3 of 23 developed respiratory correlations following cocaine administration. We speculate that a portion of the cardiac and respiratory responses induced by cocaine may be mediated through the central nucleus of the amygdala.

Amygdala↗
PubMed1987

Cardiac size during prenatal development.

In this study, the cardiac circumference as measured in a four-chamber view was analyzed to determine its relationship to three linear, sonar measurements--biparietal diameter, femoral length, and abdominal circumference--and two sonographically derived fetal parameters--gestational age and estimated fetal weight. The results showed that the cardiac circumference correlates significantly with these direct and derived variables. It is recommended that the magnitude of the cardiac circumference as a function of any or all of these variables be used as an index of organ size when assessing fetuses at risk for anomalous cardiac development.

Abdomen↗
PubMed1982

Cardiac perforation with tamponade during cardiac catheterization.

Among 6,675 adult patients undergoing cardiac catheterization in our institution, three patients developed cardiac perforation and tamponade (incidence 0.04%). Two perforations involved the left atrium, and one the right atrium. Tamponade developed in the three patients. Hemodynamic confirmation of tamponade was available in two patients. Pericardiocentesis was performed in all three patients. Two patients required emergency surgery. All patients recovered.

Cardiac Catheterization↗
PubMed2002

Induction of cardiogenesis by Hensen's node and fibroblast growth factors.

The earliest events underlying cardiac induction and morphogenesis remain largely unknown. In the present study, we show that Hensen's node, the organizer of the avian embryo, induces cardiogenesis. Specifically, following heterotopic transplantation, Hensen's node induces ectopic host tissue that expresses two early cardiac markers ( cNkx-2.5 and cNkx-2.8), as well as a ventricular marker ( VMHC1), but not an atrial marker ( AMHC1). Moreover, we examine the potential roles of candidate growth factors known to be secreted by Hensen's node. Our results show that fibroblast growth factors (FGF-2 and FGF-4) when ectopically expressed can initiate cardiac development, inducing host tissue to express the two cardiac transcription factors cNkx-2.5 and cNkx-2.8, as well as the cardiac-restricted structural gene VMHC1, but not AMHC1. In contrast to FGFs, TGFbeta family members fail to induce ectopic tissue and expression of cardiac marker genes. We also examined the effects of growth factors on the morphogenesis of the host embryo's heart. Both exogenous FGFs and TGFbeta family members perturb normal morphogenesis of the early cardiac tube and alter patterns of ventricular and atria gene expression in characteristic ways. Namely, exogenous FGFs expand areas expressing the ventricular marker VMHC1 at the expense of areas expressing the atrial marker AMHC1. Conversely, exogenous TGFbeta1 inhibits expression of VMHC1, expanding AMHC1 expression. We show here that Hensen's node and FGFs induce ectopic expression of cardiac lineage markers, and that FGF and TGFbeta family members can modulate early development of the heart. Collectively, these data suggest that the organizer plays a crucial role in cardiac induction and morphogenesis, mediated in part by endogenous members of the FGF and TGFbeta families.

Animals↗
PubMed2001

Those who faced turbulence and launched the era of flow dynamic concepts for cardiac investigation.

This paper puts emphasis on pioneers who developed cardiac flow dynamics concepts during the second half of the 20th century at a period where pressure measurements were the rule. Thinking flow instead of pressure dynamics corresponded to in-depth conceptual changes: whereas blood pressure generally has a single positive sign and a similar pattern at all points of a cardiac chamber or a vessel, flow fluctuates around the zero line and its pattern changes within a given cardiac chamber or vessel level. These specific changes and fluctuations were the exciting tools needed to renew our pathophysiological insights, just in time with the take off of Doppler ultrasound making noninvasive investigation of fluid dynamics easily available. Each decade was marked by a specific historical contribution to evolving concepts. Instead of a merely phenomenological approach to flow dynamics, pioneers assigned a value of paradigms to basic flow patterns. They generated a system of heuristical hypotheses which turned out to underlay a modernistic understanding of flow dynamics in normal and diseased hearts. So far, flow investigation had definitely gained acceptance completing pressure data at the middle of the 1980s, widely opening a breakthrough for future pathophysiological insights.

Cardiology↗
PubMed1985

Endocardial fibroelastosis and infantile polycystic disease.

A child with infantile polycystic disease who developed cardiac failure from endocardial fibroelastosis is described. Endocardial fibroelastosis has been reported in adult type polycystic disease in childhood. Endocardial fibroelastosis should be suspected in a child with polycystic disease who develops unexplained cardiac failure.

Endocardial Fibroelastosis↗