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At least 1,297 records · Page 72Linked to original sources
PubMed2003

Mechanism of enhanced cardiac function in mice with hypertrophy induced by overexpressed Akt.

Transgenic mice with cardiac-specific overexpression of active Akt (TG) not only exhibit hypertrophy but also show enhanced left ventricular (LV) function. In 3-4-month-old TG, heart/body weight was increased by 60% and LV ejection fraction was elevated (84 +/- 2%, p < 0.01) compared with nontransgenic littermates (wild type (WT)) (73 +/- 1%). An increase in isolated ventricular myocyte contractile function (% contraction) in TG compared with WT (6.1 +/- 0.2 versus 3.5 +/- 0.2%, p < 0.01) was associated with increased Fura-2 Ca2+ transients (396 +/- 50 versus 250 +/- 24 nmol/liter, p < 0.05). The rate of relaxation (+dL/dt) was also enhanced in TG (214 +/- 15 versus 98 +/- 18 microm/s, p < 0.01). L-type Ca2+ current (ICa) density was increased in TG compared with WT (-9.0 +/- 0.3 versus 7.2 +/- 0.3 pA/pF, p < 0.01). Sarcoplasmic reticulum Ca2+ ATPase 2a (SERCA2a) protein levels were increased (p < 0.05) by 6.6-fold in TG, which could be recapitulated in vitro by adenovirus-mediated overexpression of Akt in cultured adult ventricular myocytes. Conversely, inhibiting SERCA with either ryanodine or thapsigargin affected myocyte contraction and relaxation and Ca2+ channel kinetics more in TG than in WT. Thus, myocytes from mice with overexpressed Akt demonstrated enhanced contractility and relaxation, Fura-2 Ca2+ transients, and Ca2+ channel currents. Furthermore, increased protein expression of SERCA2a plays an important role in mediating enhanced LV function by Akt. Up-regulation of SERCA2a expression and enhanced LV myocyte contraction and relaxation in Akt-induced hypertrophy is opposite to the down-regulation of SERCA2a and reduced contractile function observed in many other forms of LV hypertrophy.

Adenoviridae↗
PubMed1995

Effects of hypertonic saline and dextran 70 on cardiac functions after burns.

The effects of hypertonic saline-dextran (HSD) on cardiac contractility and hemodynamics after burns were studied in anesthetized animals with full-thickness 50% total body surface area burns that were resuscitated with HSD or lactated Ringer solution (LR) alone. No significant difference in cardiac contractility during 6 h postburn was observed between the two groups, as assessed by the end-systolic pressure-volume relationship and the stroke work-end-diastolic volume relationship. An additional bolus of HSD at 6 h postburn caused no significant changes in the end-systolic pressure-volume relationship and stroke work-end-diastolic volume relationship in the burned and sham-burned animals, both of which were resuscitated with HSD. Ten minutes of hemodynamic changes following HSD infusion at 30 min postburn revealed a sudden increase in stroke volume with biphasic responses in left ventricular systolic pressure, which first decreased, then increased, and finally returned to the pre-HSD value. End-diastolic volume was maintained at approximately 110% of the pre-HSD value during this period. We concluded that HSD does not enhance cardiac contractility after severe burns but does produce direct effects on postburn circulation to reduce afterload and augment preload, resulting in a short-lived increase in cardiac output.

Animals↗
PubMed2001

Dynamin, encoded by shibire, is central to cardiac function.

Employing the Drosophila heart, a model system for genetic and molecular investigation of cardiac physiology, we demonstrate here an essential role for the protein dynamin, encoded by the Drosophila gene shibire(ts) (shi(ts)), in maintaining normal heart function. In flies bearing two temperature-sensitive alleles of shi, shi(ts1) and shi(ts2), heartbeat is both slower and less rhythmic than in wild-type animals. Serotonin and norepinephrine, normally cardioacceleratory in wild type, are without effect in flies bearing the shi mutation. Electrocardiogram (EKG) analysis reveals a bigeminal beat in mutant hearts, unlike the single electrical pulse in wild-type. The gene no action potential (temperature sensitive), with previously-described cardiac aberrations similar to those of shi, interacts with shi: shi/shi;nap/nap mutants have almost wild-type heart function. J. Exp. Zool. 289:81-89, 2001.

Animals↗
PubMed1997

Regulatory effects of phospholamban on cardiac function in intact mice.

Phospholamban (PLB) regulates Ca(2+)-adenosinetriphosphatase activity in cardiac sarcoplasmic reticulum and participates in the regulation of myocardial performance. Animal models with altered levels of PLB permit in vivo evaluation of the physiological role of PLB. This study examined left ventricular (LV) performance in intact PLB heterozygous and homozygous mice under basal and stimulated conditions. A Millar Mikro-Tip transducer was inserted into the right carotid artery and advanced into the LV for direct measurement of ventricular pressure and the first derivative of intraventricular pressure (dP/dt). Baseline blood pressures were increased in PLB heterozygotes and even more so in PLB homozygotes compared with wild types (WT), and there were no differences in heart rate or LV end-diastolic pressure. The increase in pressure was primarily caused by an increase in systolic pressure. Baseline values for positive and negative dP/dt were linearly correlated with PLB levels. In PLB heterozygotes, contractile response to isoproterenol (Iso) was blunted compared with WT, but maximum rates of contraction were similar between the two groups. Contractile performance in PLB homozygous mice, which under baseline conditions was similar to maximum levels seen in WT, showed a blunted response to Iso, and maximum rates of contraction were significantly greater than in either of the other groups, indicating an essential but perhaps not exclusive role for PLB in mediating the inotropic effects of beta-adrenergic agonists. The effects of Iso on negative dP/dt were also blunted in both PLB heterozygous and PLB homozygous animals. Our results demonstrate that myocardial function in highly dependent on PLB level and suggest that the cardiovascular effects of PLB perturbations are largely uncompensated for in the intact mouse.

Animals↗
PubMed2005

Tuberoinfundibular peptide of 39 residues: a new mediator of cardiac function via nitric oxide production in the rat heart.

Tuberoinfundibular peptide (TIP39) was initially identified as a neurotransmitter and agonist of the PTH2 receptor, which is expressed in the cardiovascular system. This study documents for the first time the cardiac expression and function of TIP39. Expression was analyzed via RT-PCR. Function was characterized on Langendorff-perfused rat hearts as left ventricular developed pressure (LVDP) and on isolated cells via a cell edge detection system. cGMP levels were detected with RIA. Tuberoinfundibular peptide (TIP39) mRNA was found to be constitutively expressed in coronary endothelium cells, isolated cardiomyocytes, ventricles, atria, and aorta. At first we investigated the vasodilatory properties of TIP39 (100 nM) in the presence of L-nitro-arginine (L-NA, 100 microM). Surprisingly, TIP39 had no vasodilatory effect but decreased LVDP by 35 +/- 7%. In the absence of L-NA, addition of TIP39 decreased LVDP by 8 +/- 2%. The PTH2 receptor antagonist Trp23-Tyr36-PTHrP (1-36, 100 nM) abolished this TIP39 effect in the presence of L-NA. The experiments with isolated cardiomyocytes provided similar results. TIP39 (10 nM) lowered the contraction amplitude by 6 +/- 3%. In the presence of L-NA (100 micromol/liter), TIP39 lowered the amplitude by 34 +/- 6%. cGMP concentration in cardiomyocytes was stimulated by TIP39 (10 nM) in the same range as by the nitric oxide (NO) donor SNAP (100 microM). In the presence of L-NA, this increase was abolished. These results suggest that an inhibition of endogenous NO production unmasks a profound negative inotropic effect of TIP39 that is mediated by an activation of the PTH2 receptor. The results obtained with isolated cardiomyocytes suggest that myocyte-derived NO, rather than vascular NO, is responsible for this effect. cGMP seems to be the downstream signal of produced NO.

Animals↗
PubMed1969

A comparison of the anti-arrhythmic actions of I.C.I. 50172 and (--)-propranolol and their effects on intracellular cardiac action potentials and other features of cardiac function.

1. I.C.I. 50172 had marked quinidine-like effects on intracellular cardiac action potentials at concentrations above 20 mg/l. (6.61 x 10(-5)M). The rate of rise and overshoot of the action potential, conduction velocity and contractions were decreased. (-)-Propranolol had similar effects at less than 1/30 this concentration.2. I.C.I. 50172 had 1/100 the activity of (-)-propranolol as a local anaesthetic. Since this is also the ratio of their in vitro beta-receptor blocking activities, I.C.I. 50172 provides no net increase in specificity of beta-receptor blockade.3. In contrast, the in vivo activity of I.C.I. 50172 in protecting anaesthetized guinea-pigs against ouabain-induced ventricular fibrillation was 40% that of (-)-propranolol.4. Structure-activity relations of beta-receptor blocking drugs are discussed.

Acetanilides↗
PubMed2003

Antioxidants attenuate myocyte apoptosis and improve cardiac function in CHF: association with changes in MAPK pathways.

Antioxidant vitamins reduce cardiac oxidative stress and cardiomyocyte apoptosis produced by exogenous norepinephrine (NE) and attenuate cardiac dysfunction in animals with pacing-induced congestive heart failure (CHF). This study was carried out to determine whether the mitogen-activated protein kinase (MAPK) signal transduction pathways are involved in oxidative stress-induced myocyte apoptosis. Rabbits with rapid pacing-induced CHF and sham operation were randomized to receive either a combination of antioxidant vitamins (beta-carotene, ascorbic acid, and alpha-tocopherol), alpha-tocopherol alone, or placebo for 8 wk. Compared with sham-operated animals, CHF animals exhibited increased oxidative stress as evidenced by decreased myocardial reduced-to-oxidized glutathione (GSH/GSSG) ratio (27 +/- 7 vs. 143 +/- 24, P < 0.05), myocyte apoptosis (77 +/- 18 vs. 17 +/- 4 apoptotic nuclei/10,000 cardiomyocytes, P < 0.05), increased total and phosphorylated c-Jun NH2-terminal protein kinase (p-JNK; 1.95 +/- 0.14 vs. 1.04 +/- 0.04 arbitrary units, P < 0.05) and phosphorylated p38 kinase (p-p38), and decreased phosphorylated extracellular signal-regulated kinase (p-ERK). Administration of antioxidant vitamins and alpha-tocopherol attenuated oxidative stress, myocyte apoptosis, and cardiac dysfunction, with reversal of the changes of total JNK, p-JNK, and p-ERK in CHF. Furthermore, because NE infusion produced changes of JNK, p-p38, and p-ERK similar to those in CHF, we conclude that NE may play an important role in the production of oxidative stress, MAPK activation, and myocyte apoptosis in CHF.

Animals↗
PubMed1992

Exercise assessment of cardiac function in children and young adults before and after bone marrow transplantation.

Cardiac toxicity is a potential complication of bone marrow transplantation because recipients frequently receive cardiotoxic chemotherapy and/or irradiation before transplantation. Most studies indicate that transient cardiac toxicity occurs within weeks of transplantation, but few studies have evaluated either cardiac status before or late after transplantation. Cardiac performance was assessed via cycle ergometry in 20 children and young adults before transplantation and 31 other children and young adults after transplantation. Mean survival time in the group post-transplantation was 3.9 years with a range of 11 months to 12.1 years. Left ventricular size and shortening fraction at rest were assessed via echocardiography. Data were compared to those of 70 healthy subjects from our laboratory. Patients before and after transplantation had normal oxygen consumptions and cardiac indices at rest. During exercise, however, patients treated for cancer both before and after bone marrow transplantation had reduced exercise times, reduced maximal oxygen consumptions, and reduced ventilatory anaerobic thresholds. Cardiac reserve, as judged by the response of the cardiac output during exercise, was reduced severely. There were no significant differences between the groups tested before and after transplantation. Patients who had been treated for aplastic anemia, who had received less intensive therapy before transplantation, performed significantly better than did patients treated for cancer. Despite these findings, only four patients had abnormalities by echocardiography. In conclusion, before transplantation patients with oncologic diagnoses had serious limitations in exercise performance, most likely as a result of the effects of the cardiotoxic therapy given as part of their conventional cancer therapy. Long-term survivors of bone marrow transplantation also had similar abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1997

Modulation of human cardiac function through 4 beta-adrenoceptor populations.

In human heart there is now evidence for the involvement of four beta-adrenoceptor populations, three identical to the recombinant beta 1-, beta 2- and beta 3-adrenoceptors, and a fourth as yet uncloned putative beta-adrenoceptor population, which we designate provisionally as the cardiac putative beta 4-adrenoceptor. This review described novel features of beta-adrenoceptors as modulators of cardiac systolic and diastolic function. We also discuss evidence for modulation by unoccupied beta 1- and beta 2-adrenoceptors. Human cardiac and recombinant beta 1- and beta 2-adrenoceptors are both mainly coupled to adenylyl cyclase through Gs protein, the latter more tightly than the former. Activation of both human beta 1- and beta 2-adrenoceptors not only increases cardiac force during systole but also hastens relaxation through cyclic AMP-dependent phosphorylation of phospholamban and troponin 1, thereby facilitating diastolic function. Furthermore, both beta 1 and beta 2-adrenoceptors can mediate experimental arrhythmias in human cardiac preparations elicited by noradrenaline and adrenaline. Human ventricular beta 3-adrenoceptors appear to be coupled to a pertussis toxin-sensitive protein (Gi?). beta 3-Adrenoceptor-selective agonists shorten the action potential and cause cardiodepression, suggesting direct coupling of a Gi protein to a K+ channel. In a variety of species, including man, cardiac putative beta 4-adrenoceptors mediate cardiostimulant effects of non-conventional partial agonists, i.e. high affinity beta 1- and beta 2-adrenoceptor blockers that cause agonist effects at concentrations considerably higher than those that block these receptors. Putative beta 4-adrenoceptors appear to be coupled positively to a cyclic AMP-dependent cascade and can undergo some desensitisation.

Atrial Function↗
PubMed1975

[Experience with the intracardiac floating catheter in the diagnostics of cardiac function (author's transl)].

A report is made on the experience gained in more than 600 cardiac catheterizations using the Swan-Ganz-Intracardiac floating catheter. This procedure is an addition to the diagnostic possibilities and provides answers to cardiological and pulmonological questioning which, so far, had not been an indication for cardiac catheterism. Its advantage is the safety of application and little inconvenience to the patient with a high information content for the physician. If the investigations are carried out under ergometer load, new aspects of functional diagnostics arise with respect to problems requiring intimate knowledge of the myocardial function.

Arrhythmias, Cardiac↗
PubMed2003

Inhibition of cardiac myocyte apoptosis improves cardiac function and abolishes mortality in the peripartum cardiomyopathy of Galpha(q) transgenic mice.

BACKGROUND: Although the occurrence of cardiac myocyte apoptosis during heart failure has been documented, its importance in pathogenesis is unknown. Transgenic mice with cardiac-restricted overexpression of Galpha(q) exhibit a lethal, peripartum cardiomyopathy accompanied by apoptosis. To test whether apoptosis is causally linked to heart failure, we assessed whether inhibiting this cell death would improve left ventricular function and survival in the Galpha(q) peripartum cardiomyopathy model. METHODS AND RESULTS: The potent polycaspase inhibitor IDN-1965 or vehicle was administered subcutaneously to Galpha(q) mice by osmotic minipump beginning on day 12 of pregnancy and continuing through euthanasia at day 14 postpartum. As expected, IDN-1965 markedly suppressed cardiac caspase-3-like activity (86.5%; P<0.01), accompanied by reduction in the frequency of cardiac myocyte apoptosis from 1.9+/-0.3% to 0.2+/-0.1% (P<0.01). Animals receiving IDN-1965 exhibited significant improvements in left ventricular end-diastolic dimension (vehicle, 4.7+/-0.1 mm; IDN-1965, 4.2+/-0.1 mm; P<0.01), fractional shortening (vehicle, 30.7+/-1.2%; IDN-1965, 38.9+/-1.0%; P<0.01), positive (vehicle, 3972+/-412; IDN-1965, 5870+/-295; P<0.01) and negative (vehicle, 2365+/-213; IDN-1965, 3413+/-201; P<0.01) dP/dt, and complete suppression of mortality (vehicle, 6 of 20 died; IDN-1965, 0 of 14 died; P<0.05). CONCLUSIONS: Reduction in cardiac myocyte apoptosis by caspase inhibition improved left ventricular function and survival in pregnant Galpha(q) mice. These data indicate that cardiac myocyte apoptosis plays a causal role in the pathogenesis of cardiomyopathy in this model. Caspase inhibition may provide a novel therapeutic target for heart failure.

Animals↗
PubMed1989

An evaluation of cardiac function in malnourished children by non-invasive methods.

Forty-six malnourished children between 3-48 mo with varying grades of malnutrition (PEM) were evaluated for left ventricular function by echocardiography. None of these children had any pre-existing cardiac disease, chronic illness or significant anemia. Children with Grades III and IV PEM had significantly smaller cardiac chamber size and ventricular wall thickness as compared to normally nourished children. Cardiac output as well as other indices of left ventricular function (percentage fractional shortening, mean rate of circumferential fibre shortening and ejection fraction) were also significantly decreased in severe PEM. The atrophic PEM heart does appear to show left ventricular dysfunction in moderately severe malnutrition.

Cardiac Volume↗