UMLS:C0018801 - FACTA Search

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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biogenic amines are formed in foods as a result of amino acid decarboxylation catalyzed by bacterial enzymes. When consumed in sufficient quantities, these compounds will cause headache, hypertension, fever, and heart failure. Technologies such as vacuum packaging and carbon dioxide-modified atmosphere packaging (CO2-MAP), when combined with low-temperature storage (-1.5 degrees C), allow fresh pork to have a storage life long enough for export to overseas markets. During low-temperature storage of pork in these packaging systems, the lactic acid bacteria (LAB), which possess the enzymes for biogenic amine formation, dominate the microflora. The objectives of this study were to determine the quantities of biogenic amines in packaged fresh pork, to monitor LAB growth, and to determine the storage life by sensory evaluation. Vacuum-packaged and CO2-MAP pork were stored at -1.5+/-0.5 degrees C for 9 and 13 weeks, respectively. Phenylethylamine, putrescine, cadaverine, histamine, tyramine, spermidine, and spermine concentrations were determined weekly by high-performance liquid chromatography and capillary gel electrophoresis. LAB and carnobacteria were enumerated weekly. Samples were evaluated for odor and appearance. The CO2-MAP was successful in delaying bacterial growth and the development of unacceptable off-odors compared with the vacuum packaging. The storage lives of the vacuum-packaged and CO2-MAP pork were 5 and 13 weeks, respectively. High-performance liquid chromatography was the superior method for biogenic amine quantification. Tyramine and phenylethylamine in pork of both packaging treatments approached levels considered to be potentially toxic. Given Canada's increasing role in the export of fresh meat to foreign markets, it is recommended that the formation of biogenic amines in vacuum-packaged and CO2-MAP pork be further investigated.
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PMID:Biogenic amines in vacuum-packaged and carbon dioxide-controlled atmosphere-packaged fresh pork stored at -1.50 degrees C. 1127 71

The acute contractile function of the heart is controlled by the effects of released nonepinephrine (NE) on cardiac adrenergic receptors. NE can also act in a more chronic fashion to induce cardiomyocyte growth, characterized by cell enlargement (hypertrophy), increased protein synthesis, alterations in gene expression and addition of sarcomeres. These responses enhance cardiomyocyte contractile function and thus allow the heart to compensate for increased stress. The hypertrophic effects of NE are mediated through Gq-coupled alpha(1)-adrenergic receptors and are mimicked by the actions of other neurohormones (endothelin, prostaglandin F(2alpha) angiotensin II) that also act on Gq-coupled receptors. Activation of phospholipase C by Gq is necessary for these responses, and protein kinase C and MAP kinases have also been implicated. Gq stimulated cardiac hypertrophy is also evident in transgenic mouse models. In contrast, stimulation of G(s)-coupled beta-adrenergic receptors or G(i)-coupled receptors do not directly effect cardiomyocyte hypertrophy. Apoptosis is also induced by G-protein-coupled receptor stimulation in cardiomyocytes. Sustained or excessive activation of either Gq- or Gs-signaling pathways results in apoptotic loss of cardiomyocytes both in vitro and in vivo. Apoptosis is associated with decreased ventricular function in the failing heart. Cardiomyocytes provide an ideal model system for understanding the basis for G-protein mediated hypertrophy and apoptosis, and the mechanisms responsible for the transition from compensatory to deleterious levels of signaling. This information may prove critical for designing interventions that prevent the pathophysiological consequences of heart failure.
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PMID:G-proteins in growth and apoptosis: lessons from the heart. 1131 10

A variety of seemingly unrelated clinical conditions manifest the same effects on the heart. These effects include: (1) reversible myocardial dysfunction, (2) beta-adrenergic desensitization, and (3) activation of inflammatory mediators. We provide evidence supporting a role for cytokines, mitogen activated protein kinases (MAP kinases), and nitric oxide (NO) as common mediators of reversible myocardial dysfunction and beta-adrenergic desensitization. Data from animal models and human studies support a pathogenic role for these inflammatory mediators in ischemic as well as non-ischemic myocardial dysfunction. It is suggested that compensatory cellular programs are activated to provide short-term protection from brief periods of ischemia and infection. Continuous activation of these compensatory pathways leads to cardiomyopathy and chronic (congestive) heart failure. Elucidating the signaling pathways involved has the potential to provide the opportunity to exploit the cardioprotective advantages of these agents without bearing the burden of excessive stimulation.
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PMID:Inflammatory mediators and reversible myocardial dysfunction. 1259 3

Activation of MAPK pathways by angiotensin II (Ang II) is important for cardiac fibroblast (CFB) proliferation and migration. Activity of MAP-kinases is closely controlled by a group of dual-specific MAP kinase phosphatases (MKPs). Lipopolysaccharides (LPS) and cytokines are elevated in patients with heart failure and may contribute to disease progression. In this study, we investigate the effect of LPS on Ang II-induced CFB function. Pretreatment of CFBs with LPS (1 microg/mL; 30 min) almost completely inhibited Ang II-induced DNA-synthesis and inhibited Ang II directed chemotaxis by more than 80%. Compared to controls, LPS pretreatment significantly reduced phosphorylation levels of ERK1/2- and p38 MAPK and induced MKP-1 levels. Silencing MKP-1 with antisense oligodesoxynucleotides reversed the antimitogenic effect of LPS on Ang II-induced CFB DNA-synthesis and migration. Induction of MKP-1 by LPS was inhibited by the protein kinase C (PKC)-inhibitor calphostin C, but not by the ERK1/2-pathway inhibitor PD98059, suggesting that PKC but not ERK1/2 is required for LPS-mediated MKP-1 induction in CFBs. Our data demonstrate that LPS have direct cellular effects in CFBs through an inhibition of Ang II-induced MAPK activity via PKC-mediated induction of MKP-1. This might be relevant with regard to the decreased MAPK activity and increased levels in MKPs reported during chronic heart failure in humans.
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PMID:LPS regulate ERK1/2-dependent signaling in cardiac fibroblasts via PKC-mediated MKP-1 induction. 1264 69

1. The isolated circulatory response to intravenous application of the phosphodiesterase (PDE) inhibitors piroximone and enoximone was studied. 2. In a randomized sequence of 30 male patients undergoing elective aortocoronary bypass grafting either piroximone (0.5 mg kg(-1); n = 10) or enoximone (0.5 mg kg(-1); n = 10) were given during steady state of cardiopulmonary bypass (CPB). A group in which NaCl was given as a placebo served as a control (n = 10). 3. MAP was reduced by piroximone (maximum -23 mm Hg) and enoximone (maximum -18 mm Hg), whereas it increased in the control (+20 mm Hg). Volume of the extracorporeal circuit indicating venous pooling decreased more pronouncedly in the enoximone patients (-440 ml) than in the piroximone group (-300 ml). 4. Laser Doppler flows (LDFs) increased in both PDE-III inhibitor groups with the higher and longer increase in the enoximone-treated patients (LDF-forehead maximum +44%, LDF-forearm maximum +33%). Piroximone-induced increase in both LDFs was less pronounced with respect to both time and degree (LDF-forehead maximum +30%, LDF-forearm +12%). 5. Oxygen consumption (VO2) was significantly higher in the PDE-III inhibitor-treated than in the control patients. 6. Piroximone and enoximone showed significant vasodilatory properties at the arterial and venous side (= 'venous pooling'), from which patients with heart failure would profit. 7. Vasodilation could be observed for a longer period and was more pronounced in the enoximone-treated than in the piroximone patients. Alterations in capillary skin blood flow measured by laser Doppler technique gave evidence for an improvement in nutritive microcirculation, which was slightly more pronounced in the enoximone patients.
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PMID:Circulatory effects of the PDE-inhibitors piroximone and enoximone. 1295 8

The purpose of this study was to determine the effect of nitric oxide (NO) in the rostral ventrolateral medulla (RVLM) on the central integration of the cardiac sympathetic afferent reflex (CSAR) in normal rats and in rats with coronary ligation-induced chronic heart failure (CHF). Under alpha-chloralose and urethane anesthesia, mean arterial pressure, heart rate and renal sympathetic nerve activity (RSNA) were recorded at baseline and during elicitation of the CSAR evoked by electrical stimulation of the cardiac afferent sympathetic nerves in sino-aortic denervated and cervical vagotomized rats. A cannula was inserted into the left RVLM for microinjection of NO synthase inhibitor, S-methyl-L-thiocitruline (MeTC) or NO donor, S-nitroso-N-acetyl-penicillamine (SNAP). The CSAR was tested by electrical stimulation (5, 10, 20 and 30 Hz at 10 V for 1 ms) of the afferent cardiac sympathetic nerves. It was observed that (1) the responses of RSNA to stimulation were enhanced in rats with CHF; (2) MeTC (80 nmol) potentiated the responses of RSNA to stimulation in sham rats but not in rats with CHF; (3) SNAP (50 nmol) depressed the enhanced RSNA response to stimulation in CHF rats but had no effect in sham rats; and (4) MeTC increased the baseline RSNA and MAP only in sham rats, but SNAP inhibited the baseline RSNA and MAP in both sham and CHF rats. These results indicate that reductance of NO in the RVLM is involved in the augmentation of CSAR in CHF rats.
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PMID:Reduced nitric oxide in the rostral ventrolateral medulla enhances cardiac sympathetic afferent reflex in rats with chronic heart failure. 1498 29

This study was designed to determine if the thyroid hormone analog 3,5 diiodothyropropionic acid (DITPA), now in clinical trials for heart failure, alters endothelial function after myocardial infarction (MI). Three weeks after MI, adult Sprague-Dawley rats were randomly assigned to DITPA (375 microg/100 g subcutaneous) or no treatment of 3 weeks. In MI rats, left ventricular (LV) end-diastolic pressure and LV dP/dt decreased (P < 0.05). DITPA did not change MAP (87 +/- 10 versus 90 +/- 7 mm Hg) or LV end-diastolic pressure (23 +/- 3 versus 19 +/- 9 mm Hg) but did lower (P < 0.05) LV dP/dt (4,633 +/- 797 versus 3,650 +/- 1,236 mm Hg/s). In aortic segments from MI rats, DITPA enhanced the acetylcholine dependent vasorelaxation (59 +/- 11% at 10(-4) M, P < 0.05) and isoproterenol induced vasorelaxation (57 +/- 13% at 10(-4) M, P < 0.05). The increases in vasorelaxation were blocked with l-NAME and restored with L-arginine. Treatment with DITPA increased (P < 0.05) eNOS protein content in aortic tissue from sham rats (3.8 +/- 2.8 to 44.5 +/- 7.1 integrated intensity units (II)/microg) and in MI rats (5.3 +/- 3.4 to 28.3 +/- 8.9 II/microg). In endothelial cells, 24 hours' treatment with DITPA (10 microM) increased (P < 0.01) eNOS protein expression from 22.1 +/- 4.8 to 52.7 +/- 16.8 II/microg protein and DITPA (20 microM) increased eNOS to 49.1+/- 15.2 II/microg protein. The thyroid analog DITPA enhances endothelial nitric oxide and beta-adrenergic-mediated vasorelaxation by increasing nitric oxide in the vasculature.
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PMID:Thyroid hormone analog, DITPA, improves endothelial nitric oxide and beta-adrenergic mediated vasorelaxation after myocardial infarction. 1545 53

Cardiomyocyte-specific overexpression of the wild-type alpha(1B)-adrenergic receptor (alpha(1B)-AR) produces a slowly progressing cardiomyopathy associated with clinical signs of heart failure and premature death around middle age (Lemire et al. 2001). In the heart, alpha(1)-AR activate the extracellular signal-regulated kinase (ERK) MAPK cascade. The aim of this project was to determine if cardiac-specific overexpression of the wild-type alpha(1B)-AR results in sustained activation of the ERK pathway. At 3 and 9 months, ERK activity was increased in alpha(1B)-AR overexpressing hearts relative to non-transgenic animals. Similarly, phosphorylation of MEK and p90(rsk) were also elevated. MAP kinase phosphatases (MKPs), which inactivate MAP kinases, are transcriptionally regulated. MKP2 mRNA levels were reduced at 3 months in alpha(1B)-AR overexpressing hearts. Interestingly, there was a general trend for reduced expression of MKP-1, -2, and -3 with increased age. In addition, expression of the modulatory calcineurin-interacting protein (MCIP) 1, an indicator of calcineurin activity, was elevated 3-fold in alpha(1B)-AR overexpressing hearts at both 3 and 9 months. These results indicate that the overexpression of the wild-type alpha(1B)-AR leads to chronic changes in the activation of signalling pathways previously shown to be associated with the hypertrophic response.
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PMID:Cardiac-specific transgenic overexpression of alpha1B-adrenergic receptors induce chronic activation of ERK MAPK signalling. 1567 39

Pulmonary hypertension is a rare disease of the pulmonary vasculature defined as a mean pulmonary artery pressure >25 mmHg at rest or 30 mmHg with exercise. Recent therapies such as epoprostenol, bosentan and sildenafil are directed at the arterial vascular bed, causing vasodilatation and reducing pulmonary vascular resistance. However idiopathic pulmonary artery hypertension (IPAH) occurs predominantly in women, with three times the incidence compared to men and this suggests that sex hormones may be involved in the pathogenesis. 17beta -oestradiol is a pulmonary vasodilator, proposed to act via an endothelium-dependant pathway, involving nitric oxide (NO) and has also been shown to alter responses to hypoxia. Progesterone is also a pulmonary vasodilator but differs from 17beta-oestradiol in having endothelial-dependant and independent processes implicated. Interestingly testosterone has been shown to be a vasodilator in both the coronary and pulmonary circulation with a mechanism of action involving calcium channel blockade of the vascular smooth muscle and without endothelial involvement. In clinical trials testosterone confers symptomatic benefits in patients with coronary heart disease and heart failure, acting as a vasodilator. These observations lend support to the notion that testosterone could be a potential treatment for patients with PAH as vasodilator therapy remains the mainstay of treatment. Other potential beneficial effects of testosterone in the pulmonary circulation include immuno-modulation, altering expression of cytokines and an anti-thrombotic action. In this review the influence of sex hormones on the pulmonary vasculature will be discussed, with specific focus on pulmonary hypertension and the potential treatment of this condition.
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PMID:The influence of sex hormones on pulmonary vascular reactivity: possible vasodilator therapies for the treatment of pulmonary hypertension. 1647 72

Omega-3 polyunsaturated fatty acids such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) have beneficial effects on the heart and vasculature. We tested the hypothesis that 6 weeks of dietary supplementation with DHA (2.0 g/day) and EPA (3.0 g/day) enhances exercise-induced increases in brachial artery diameter and blood flow during rhythmic exercise. In seven healthy subjects, blood pressure, heart rate and brachial artery diameter, blood flow, and conductance were assessed before and during the last 30 s of 90 s of rhythmic handgrip exercise (30% of maximal handgrip tension). Blood pressure (MAP), heart rate (HR), and brachial artery vascular conductance were also determined. This paradigm was also performed in six other healthy subjects who received 6 weeks of placebo (safflower oil). Placebo treatment had no effect on any variable. DHA and EPA supplementation enhanced contraction-induced increases in brachial artery diameter (0.28+/-0.04 vs. 0.14+/-0.03 mm), blood flow (367+/-65 vs. 293+/-55 ml min-1) and conductance (3.86+/-0.71 vs. 2.89+/-0.61 ml min-1 mmHg-1) (P<0.05). MAP and HR were unchanged. Results indicate that treatment with DHA and EPA enhances brachial artery blood flow and conductance during exercise. These findings may have implications for individuals with cardiovascular disease and exercise intolerance (e.g., heart failure).
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PMID:Supplementation with omega-3 polyunsaturated fatty acids augments brachial artery dilation and blood flow during forearm contraction. 1677 Apr 72

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