Cardioscience最新文献

{"title":"Influence of the phospholipid content in docosahexaenoic acid on electrophysiology and contraction of rat heart muscle cells.","authors":"A Fournier,&nbsp;E Fantini,&nbsp;J P Sergiel,&nbsp;P Athias,&nbsp;A Grynberg","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The cardiovascular beneficial effects of fish oils are currently attributed to docosahexaenoic (C22:6 n-3) and eicosapentaenoic (C20:5 n-3) acids, although most investigations have focused on eicosapentaenoic acid. This study was devoted to the specific effect of docosahexaenoic acid, as compared to eicosapentaenoic acid, on the basal electrophysiological and mechanical characteristics of cultured rat myocardial cells. The myocyte cultures were prepared from newborn rat heart ventricles. The cells were grown for 24 hours in a conventional seric medium, and then incubated in a medium enriched with either docosahexaenoic acid or eicosapentaenoic acid for 96 hours. This treatment resulted in docosahexaenoic acid-rich cells (16% of the phospholipid fatty acids) and docosahexaenoic acid-poor cells (1.5%), both displaying the same phospholipid n-6/n-3 polyunsaturated fatty acid ratio. The transmembrane potentials were recorded with glass microelectrodes. Contractions were monitored photometrically. The action potential amplitude was slightly smaller in docosahexaenoic acid-rich cells (-4 mv), due to a lower plateau phase. There was no difference in action potential duration and spontaneous rate. The contraction measurements were not significantly different between the two groups of cells. We conclude that increasing the docosahexaenoic acid content in cardiomyocyte membrane phospholipids may have modulated the calcium ionic channels governing the plateau phase of the action potential, whereas the other physiological activities remained unaffected.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"6 1","pages":"71-8"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18611104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of lysophosphatidylcholine on bovine aortic endothelial cells in culture.","authors":"Z Su,&nbsp;Q Ling,&nbsp;Z G Guo","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>To elucidate the vascular actions of lysophosphatidylcholine, we examined its effects on the concentration of cytosolic free calcium ([Ca2+]i), plasma membrane fluidity and release of lactate dehydrogenase in vascular endothelial cells cultured from bovine aortas. The [Ca2+]i of the endothelial cells was measured by a dual-wavelength fluorospectrophotometer using a fluorescent, calcium-specific indicator, Fura-2. Membrane fluidity was monitored by measuring changes in the steady-state fluorescence anisotropies, using 1,6-diphenyl-1,3,5-hexatriene as a fluorescence probe. In the presence of 1 mmol/L extracellular calcium, lysophosphatidylcholine caused a biphasic elevation of [Ca2+]i in Fura-2-loaded vascular endothelial cells, consisting of a large transient component followed by a relatively low, but more sustained component. At concentrations of lysophosphatidylcholine equal to or greater than 10 mumol/L, [Ca2+]i increased in a dose-dependent manner in the presence or absence of external calcium. In the absence of extracellular calcium, only an initial transient increment in the [Ca2+]i of endothelial cells was generated, the sustained component being eliminated. The sustained component was greatly depressed or almost abolished by the addition of the calcium influx blocker, NiCl2. Plasma membrane fluidity was greatly increased by incubation with lysophosphatidylcholine (30 and 50 mumol/L) concomitant with significant increases in the release of lactate dehydrogenase from the cells. At 50 mumol/L, lysophosphatidylcholine increased lactate dehydrogenase release and membrane fluidity in a time-related way.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"6 1","pages":"31-7"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18611129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiac hypertrophy induced by alpha- and beta-adrenergic receptor stimulation.","authors":"H G Zimmer,&nbsp;C Kolbeck-Ruhmkorff,&nbsp;W Zierhut","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The aim of the study was to examine whether stimulation of alpha- and beta-adrenergic receptors in intact rats induces cardiac hypertrophy and to characterize the metabolic alterations that precede or accompany the process of hypertrophy. Cardiac beta-adrenergic receptors were stimulated with a single subcutaneous injection of 25 mg/kg isoproterenol. This led to an increase in the cardiac cAMP level which was followed by the sequential enhancement of adenine nucleotide biosynthesis and protein synthesis. The increase in adenine nucleotide and protein synthesis induced by isoproterenol was prevented by propranolol (50 mg/kg) within the first 5 hours. Norepinephrine, given as a continuous intravenous infusion of 0.2 mg/kg for 3 days, induced an increase in heart rate, mean aortic pressure and total peripheral resistance. Cardiac output was slightly reduced. The cardiac RNA/DNA ratio and the left ventricular weight/body weight ratio were significantly increased by about 40%. Simultaneous intravenous administration of the alpha-receptor blocker prazosin (0.1 mg/kg/h) and of the beta-receptor blocker metoprolol (1 mg/kg/h) reversed the functional changes and attenuated the increase in the RNA/DNA ratio induced by norepinephrine. The left ventricular weight/body weight ratio was within the range of the control values. Selective stimulation of alpha-adrenergic receptors by continuous intravenous infusion of norfenephrine (2 mg/kg/h) for 3 days increased heart rate and total peripheral resistance, while cardiac output was significantly lower. The RNA/DNA and left ventricular weight/body weight ratios were increased. Prazosin attenuated the increase in the RNA/DNA ratio induced by norfenephrine and prevented the development of cardiac hypertrophy. In the isolated perfused working rat heart, norepinephrine (3 x 10(-8) M) increased the expression of the proto-oncogenes c-fos and c-myc after 30 and 60 minutes, respectively. This increase occurred at about the same time as that induced by volume overload (increase of preload from 8 to 16 cm H2O) and pressure overload (increase of afterload from 80 to 100 cm H2O), but was more pronounced. In intact rats, norepinephrine elicited an increase in the mRNA and activity of glucose-6-phosphate dehydrogenase, the first and regulating enzyme of the oxidative pentose phosphate pathway, in a time-dependent manner. It is suggested that this may be part of a long-term homeostatic mechanism to keep the cardiac adenine nucleotide level in the normal range.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"6 1","pages":"47-57"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18611131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Properties of the myocardium affecting the coronary circulation.","authors":"G Losano,&nbsp;D Gattullo,&nbsp;P Pagliaro","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The mean coronary blood flow increases in response to an increase in myocardial oxygen consumption. Conversely, an increase in coronary perfusion is itself reported to induce an increase in myocardial oxygen consumption. Such an effect can be explained by stretching of the myocardial fibers surrounding the vessels, which become more distended with an increase in perfusion. The flow in the left descending and circumflex coronary arteries is reduced in systole because of the compression exerted by the contracting myocardium on the intramyocardial vessels. Due to the thinner wall of the right ventricle, this reduction is not obvious in the right coronary artery. The intramyocardial pump model provides a satisfactory explanation of the mechanism by which contraction reduces the flow. It also explains the attenuation of the diastolic-systolic oscillations of flow which occurs in the presence of a stenosis of a large epicardial artery. The varying elastance model shows the dependence of the extent of the reduction of the flow in systole on myocardial contractile force rather than on the pressure developed in the ventricle by the contraction. However, although the ventricular systolic pressure does not affect the flow in hearts with a relatively thick wall, it contributes to the systolic reduction of flow in hearts with a relatively thin wall. Owing to a mechanism involving the coronary capacitance, contraction is also responsible for the level of coronary flow in diastole.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"6 1","pages":"13-7"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18611126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ontogenesis of the structural elements of the heart.","authors":"G Filogamo,&nbsp;S M Peirone","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A review of the birth locus and the first developmental stages of cardiomyocytes and Purkinje cells in the chick embryo is presented in the light of recent experimental results. Experiments done in vitro have shown that the stage of 2 somites is an important morphogenetic phase, characterized by mutual identification, selective adhesion and spatial organization of the putative cardiac cells of the splanchnopleural sheet in the cardiogenic area. Many experimental data suggest that the neural crest cells moving through the corridor of the dorsal mesocardium, as well as the cholinergic system related to them, may play a role of myogenic inductors on the mesothelial putative cardiac cells. In addition, other experimental findings suggest that the Purkinje cells of the conduction system may have a crestal origin. This hypothesis is well grounded, although the origin of Purkinje cells remains to be clarified.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"6 1","pages":"19-23"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18611127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Troponin I and T protein expression in experimental cardiac hypertrophy.","authors":"D V Cumming,&nbsp;A M Seymour,&nbsp;L K Rix,&nbsp;R Kellett,&nbsp;G K Dhoot,&nbsp;M H Yacoub,&nbsp;P J Barton","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We have examined four models of experimental cardiac hypertrophy and heart failure for alterations in troponin isoform expression, particularly in the re-expression of the fetal isoforms. Cardiac protein extracts from experimental and sham-operated control rats were analyzed using one dimensional gel electrophoresis, followed by Western blotting and detection with antibodies specific for troponin I and T. No alteration in protein profile was observed for these proteins between control, hypertrophied and failing heart samples. The data demonstrate that reversion to the fetal pattern of troponin expression is not a feature of experimental cardiac hypertrophy and heart failure in the rat.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"6 1","pages":"65-70"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18611103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short term effects of intra-arterial propionyl-L-carnitine on isolated canine hind-limbs.","authors":"A Cevese,&nbsp;F Schena,&nbsp;R Poltronieri,&nbsp;G Cerutti","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Treatment with propionyl-L-carnitine has been shown to increase the walking capacity of patients with peripheral vascular disease, but the mechanisms responsible for the effect are unknown. To study the effects of propionyl-L-carnitine on musculocutaneous vascular beds and the related mechanisms, a preparation of constant-pressure blood-perfused dog hind-limb was used. Since the propionyl-L-carnitine solution had a pH less than 4 the contralateral limb simultaneously received acidified saline. The substances were injected into the perfused arteries in 2 minutes or in 20 minutes, and the cumulative dose of propionyl-L-carnitine was 20 mg/kg for each administration. The preparation was well suited for this study, because there were no major systemic effects of propionyl-L-carnitine, nor signs of cross-circulation between the isolated limbs. Propionyl-L-carnitine increased flow by 130% in 2 minute infusions and by 49% in 20 minute infusions. Acidified saline increased flow by 47% in 2 minute infusions and by 34% in 20 minute infusions. The difference between propionyl-L-carnitine and acidified saline was significant in 2 minute infusions. The 2 minute infusions of propionyl-L-carnitine increased venous PO2 by 34% and PCO2 by 22% while pH decreased by 0.07. The 20 minute infusions of propionyl-L-carnitine increased PO2 by 22% and PCO2 by 24% while pH decreased 0.10 units. Acidified saline increased only venous PO2 in 2 minute infusions (16%). Calculated oxygen consumption of the perfused limbs increased in 2 minute infusions of propionyl-L-carnitine, but not significantly. It was concluded that propionyl-L-carnitine has a direct vasodilator effect in musculocutaneous vascular beds at high doses and probably enhances tissue metabolism.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"6 1","pages":"59-64"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18611102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dependence of the cardiac contractile force on the coronary perfusion pressure: difference between the isovolumic hearts of rat and guinea pig.","authors":"V I Kapelko,&nbsp;A N Khatkevich","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We have compared the contractile responses of the isovolumic hearts of rat and guinea pig to a rise in the coronary perfusion pressure in the range 60-120 mmHg (Gregg's phenomenon). Left ventricular systolic pressure was lower in guinea pig hearts than in rat hearts at a low coronary perfusion pressure and increased markedly less at a higher perfusion pressure, despite a greater increase in coronary flow. The rise in left ventricular systolic pressure in the guinea pig hearts was entirely due to an increased left ventricular end-diastolic pressure, while left ventricular developed pressure did not increase. The wet weight of the hearts in situ was similar in both species, but after perfusion the guinea pig hearts gained significantly more fluid than the rat hearts (65% of the initial heart weight compared to 37%). The group of rat hearts perfused with a low external concentration of Ca2+ developed a similar left ventricular pressure to the guinea pig hearts and gained a similar amount of fluid (63%), but Gregg's phenomenon was the same as in rat hearts perfused with a normal concentration of Ca2+. The results suggest that the weak Gregg's phenomenon seen in guinea pig hearts can be attributed to factors other than myocardial edema and a lower left ventricular systolic pressure.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"6 1","pages":"25-30"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18611128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Magnetic resonance relaxation times in ventricular hypertrophy induced by myocardial infarction in the rat.","authors":"Y Cottin,&nbsp;V Maupoil,&nbsp;C Mezeray,&nbsp;F Brunotte,&nbsp;L Rochette","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The purpose of this study was to evaluate changes in the proton nuclear magnetic resonance relaxation times (T1 and T2) after chronic infarction in the rat. Ligation of the left coronary artery was followed by various degrees of reduction in myocardial blood flow. The ligation induced infarction in the left ventricle and compensatory hypertrophy in the right ventricle, as evaluated by the ratio of right ventricle to body weight. The interventricular septum and the right ventricle did not become ischemic in this model and served as control areas. In the infarcted left ventricle our results showed an increase in the T1 and T2 relaxation times after 15 and 30 days of ligation and a slight decrease after 60 days. A similar change in the T1 values was observed in the right ventricle. In contrast, a persistent increase in the T2 relaxation times was observed in the right ventricle and correlated with the ratio of right ventricle to body weight (r = 0.54, p < 0.01). The observation that the magnetic resonance relaxation times in vitro are modified in the hypertrophic right ventricle after myocardial infarction could be important in interpreting magnetic resonance imaging in vivo. There was no relation between the changes in the relaxation times and the degree of myocardial ischemia.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"6 1","pages":"39-45"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18611130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Discovery of the myofibrillar regulatory proteins: tropomyosin and the troponin complex.","authors":"A M Katz","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"6 1","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18611125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}