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S Mulay, P R Conliffe, and D R Varma

Abstract

The main purpose of these studies was to determine whether diabetic pregnancy altered maternal and fetal atrial natriuretic peptide (ANP). Diabetes was induced in rats by intravenous injection of 40 mg streptozotocin/kg on day 2 of gestation. Immunoreactive ANP in plasma, amniotic fluid and hearts on day 20 of gestation was measured by radioimmunoassay; fetal cardiac natriuretic peptides (ANP, proANP and BNP) were separated by reverse-phase high pressure liquid chromatography. Diabetes caused an increase in fetal plasma insulin, placental weight, amniotic fluid volume, the ratio of the fetal heart to body weight, maternal and fetal plasma ANP, fetal cardiac ANP and fetal cardiac BNP. It is suggested that the maternal diabetes-induced increase in fetal ANP might be related to fetal myocardial hypertrophy and could contribute to hydramnios.

Journal of Endocrinology (1995) 146, 255–259

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G Lombardi, A Colao, P Marzullo, D Ferone, S Longobardi, V Esposito, and B Merola

At present, there is growing evidence implicating GH and/or IGF-I in the intricate cascade of events connected with the regulation of heart development and hypertrophy. Moreover, GH excess and/or deficiency have been shown to include in their advanced clinical manifestations almost always an impaired cardiac function, which may reduce life expectancy. This finding is related both to a primitive impairment of heart structure and function and to metabolic changes such as hyperlipidemia, increase of body fat and premature atherosclerosis. Patients with childhood or adulthood-onset GH deficiency have a reduced left ventricular mass and ejection fraction and the indexes of left ventricular systolic function remain markedly depressed during exercise. Conversely, in acromegaly the cardiac enlargement, which is disproportionate to the increase in size of other internal body organs, has been a rather uniform finding. The severity of the acromegalic cardiomyopathy was reported to be correlated better with the disease duration than with circulating GH and/or IGF-I levels. Myocardial hypertrophy with interstitial fibrosis, lymphomononuclear infiltration and areas of monocyte necrosis often results in concentric hypertrophy of both ventricles. The treatment of GH deficiency and excess improved cardiac function. Interestingly, based on the evidence that GH increases cardiac mass, recombinant GH was administered to patients with idiopathic dilated cardiomyopathy. It increased the myocardial mass and reduced the size of the left ventricular chamber, resulting in improvement of hemodynamics, myocardial energy metabolism and clinical status. These promising results open new perspectives for the use of GH in heart failure.

Journal of Endocrinology (1997) 155, S33–S37

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K De, G Ghosh, M Datta, A Konar, J Bandyopadhyay, D Bandyopadhyay, S Bhattacharya, and A Bandyopadhyay

Experiments were carried out to identify the altered genes in hyperthyroid rat heart and their influence on the functions of cardiac myocytes. Chronic treatment of rats with 3,5,3' triiodo-L-thyronine (T3) resulted in a prominent increase in the size of the left ventricle with increased wall thickness and reduced chamber volume leading to concentric cardiac hypertrophy. The heart weight to body weight ratio (HW/BW) in hyperthyroid rats was increased by about 58% over that of normal rats. Using cDNA microarray comprising 588 genes, we compared the differences in mRNA expression of hyperthyroid and normal rat heart. Based on a threshold of greater than 10% change, about 37 genes were found to be regulated by T3. Further analyses by Western blotting, Northern blotting and real-time quantitative RT-PCR of some of the genes confirmed the microarray results. The T3-altered genes encode various types of proteins related to metabolism, matrix and cytoskeletal structures, growth factors, transcription factors, Ca(2+)-channels etc. The physiological significance of one of these altered proteins in hyperthyroid heart, insulin-responsive glucose transporter (GLUT) type 4 (GLUT4), was studied in detail. The expression of GLUT4 was drastically reduced in the ventricular tissues of hyperthyroid heart. Insulin-induced glucose uptake in hyperthyroid cardiomyocytes was reduced significantly, indicating the impaired glucose transport in cardiac cells. Interestingly, a few genes such as GLUT4, cytochrome P450 isoforms, superoxide dismutase (SOD), collagens, matrix metalloproteinases (MMP), tissue inhibitors of matrix metalloproteinases etc. which had not been reported earlier were found to be altered in hyperthyroid heart. Our results show some new aspects of hyperthyroid heart which will be important in assessing the pathophysiology of hypertrophied cardiomyocytes.

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M. L. AUGEE and I. R. McDONALD

SUMMARY

When exposed to a low ambient temperature of 5 °C, adrenalectomized echidnas were able to increase their metabolic rate and to maintain their body temperature within the normal range for no more than 48 h — less than 12 h in five out of six animals. Thereafter, activity, metabolic rate, cardiac rate and body temperature declined and the animals became torpid.

When maintained with daily i.m. injections of 1–2 mg cortisol acetate/kg, adrenalectomized echidnas maintained activity and normal body temperature in the cold environment indefinitely. When cortisol injections were withheld and exposure to cold continued, normal body temperature was maintained for a further 10 days, after which it declined rapidly.

The onset of torpor was always preceded by a marked fall in plasma glucose concentration, as occurred in normal, but fasted, echidnas after prolonged exposure to cold. Both cortisol and corticosterone have glucocorticoid activity in echidnas, and torpor was prevented in adrenalectomized echidnas by preventing the fall in plasma glucose with either intermittent injections or constant rate infusions of glucose solutions.

The adrenal glands of normal echidnas exposed repeatedly to low environmental temperatures showed marked hypertrophy and increase in lipid content.

It is concluded that adrenocortical secretions are necessary for the metabolic response to cold stress in these prototherian mammals, and a major role of the corticosteroids is in maintenance of normal blood glucose concentrations, presumably by enhancing hepatic gluconeogenesis.

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CI Pantos, VA Malliopoulou, IS Mourouzis, EP Karamanoli, SM Tzeis, HC Carageorgiou, DD Varonos, and DV Cokkinos

The present study was undertaken to investigate heat stress protein (HSP)-70 mRNA induction and p38 MAP kinase (MAPK) activity in response to ischaemic stress in the hyperthyroid rat heart. L-Thyroxine (T(4)) (25 microg/100 g body weight) was administered to Wistar rats for 2 days (THYRacute) or 14 days (THYR), while animals treated similarly with normal saline served as controls (NORMacute and NORM). In addition, abdominal aortic banding was performed in another group of rats to produce constriction-induced hypertrophy (HYP), while sham-operated (SOP) animals served as controls. Isolated rat hearts were perfused in a Langendorff mode. Hearts from NORMacute (n=6), THYRacute animals (n=8), NORM (n=6), THYR (n=6), SOP (n=5) and HYP (n=7) animals were subjected to 20 min of zero-flow global ischaemia followed by 45 min of reperfusion. HSP70 mRNA expression and phosphorylated p38 MAPK protein expression were detected in response to ischaemia and protein kinase C-epsilon (PKCepsilon) protein expression was detected at baseline. Thyroid hormones were measured in plasma. Long-term T(4) administration and aortic constriction resulted in the development of cardiac hypertrophy. Thyroid hormones were increased in both THYR and THYRacute as compared with normal groups (P<0.05). HSP70 mRNA induction was increased 2.3-fold in THYR as compared with NORM hearts (P<0.05), whereas there was not any difference between THYRacute and NORMacute hearts (P>0.05). Phosphorylated p38 MAPK protein expression was 2.2-fold more in NORM than in THYR hearts (P<0.05), but it was not different between NORMacute and THYRacute hearts (P>0.05). HSP70 mRNA induction was 1.8-fold greater in HYP than in SOP hearts (P<0.05), whereas phosphorylated p38 MAPK protein expression was similar between the two groups (P>0.05). PKCepsilon protein expression at baseline was 1.7-fold more in NORM than in THYR hearts (P<0.05), and not different between NORMacute and THYRacute hearts (P>0.05) as well as HYP and SOP hearts (P>0.05). This study shows that HSP70 mRNA expression is increased, whereas p38 MAPK activation is attenuated in response to ischaemia in long-term T(4)-treated rat hearts as compared with normal and acute hyperthyroid hearts.

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KG Matthews, GP Devlin, JV Conaglen, SP Stuart, W Mervyn Aitken, and JJ Bass

We have studied changes in the IGF axis in an ovine model of myocardial infarction (MI), in order to determine the relationship between time-based changes in post-infarct myocardium and IGF levels. IGF localization was studied by immunocytochemistry, production by in situ hybridization, and specific binding by radioligand studies. In surviving tissue, IGF-I peptide localized to cardiomyocytes, with strongest immunostaining at 1 and 2 days post-infarct in the immediate border area adjoining the infarct, where IGF-I mRNA also increased, reaching a maximum at 2 days. Binding of radiolabelled IGF-I in surviving tissue was initially lower than that seen in cardiomyocytes in control myocardium, subsequently increasing to become significantly greater by 6 days post-infarct. In necrotic tissue, IGF-I peptide was still detectable in cardiomyocytes at 0.5 days post-infarct, but had cleared from this area by 1 day, becoming detectable again at 6 days post-infarct in macrophages and fibroblasts infiltrating the repair zone. IGF-I mRNA was not detected in necrotic tissue until 6 days, when probe hybridized to macrophages and fibroblasts. Within the necrotic zone, high levels of radiolabelled IGF-I binding to a combination of receptors and binding proteins were observed in cardiomyocytes in islands of viable tissue located close to the border. Weak immunostaining for IGF-II was observed in cardiomyocytes of the surviving tissue. IGF-II mRNA was not detected in either surviving or necrotic areas. Binding of radiolabelled IGF-II was predominantly to macrophages in both surviving and infarct areas, although as with IGF-I, high levels of binding of radiolabelled IGF-II to a combination of receptors and binding proteins were observed in islands of viable tissue close to the border within the necrotic area. We conclude that, following MI, surviving cardiomyocytes at the infarct border show marked changes in IGF-I localization, production, and specific binding, indicating that the IGF axis is directly involved in post-infarct events, possibly in the maintenance of cardiac function by the induction of hypertrophy and in cell survival by decreasing apoptotic cell death, which has been demonstrated in other cell types.

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Priyanka De, Sreerupa Ghose Roy, Dipak Kar, and Arun Bandyopadhyay

for a prolonged duration may cause considerable changes in myocardium such as tissue remodeling, ventricular hypertrophy, and myocyte dysfunction ultimately leading to heart failure ( Maron 2002 , Xu et al . 2007 ). Initially, cardiac hypertrophy

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Å Tivesten, E Bollano, H C Nyström, C Alexanderson, G Bergström, and A Holmäng

function and experimental atherosclerosis in females ( Hodgin & Maeda 2002 , Mendelsohn & Karas 2005 ). Oestrogens have also been suggested to modulate cardiac mass and attenuate the development of cardiac hypertrophy in females ( van Eickels et al. 2001

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S S Jonker and S Louey

wall stress. When the increase in systemic pressure induced by exogenous AII is mitigated by co-infusion with a nitric oxide donor, cardiac hypertrophy, cellular hypertrophy and accelerated terminal differentiation are all eliminated ( Sandgren et al

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Cathy A Guo and Shaodong Guo

promotes synthesis of macromolecules and cardiac hypertrophy. Hexosamine biosynthetic pathway promotes glycosylation of many cellular proteins and bioactivity of target proteins and biological responses, particularly under hyperglycemia or insulin