Unilateral pulmonary edema related to pulmonary artery compression resulting from acute dissecting aortic aneurysm.
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Acute Disease↗
Biomedical subjects
U Ikeda
Publications and source records attributed to U Ikeda.
Expression of intercellular adhesion molecule-1 on rat vascular smooth muscle cells by pro-inflammatory cytokines.
Infiltration of mononuclear cells is an early pathological finding in human and experimental atherosclerosis. However, the cellular and molecular basis for cell infiltration is incompletely understood. While the intercellular adhesion molecule-1 (ICAM-1) is expressed on endothelial cells and promotes the adhesion of mononuclear cells, there is little information on the expression of ICAM-1 on vascular smooth muscle cells (SMC). In this study, we investigated the expression of ICAM-1 on cultured rat SMC and its regulation by pro-inflammatory cytokines, interleukin 1 alpha (IL-1 alpha), interleukin 6 (IL-6) and monocyte chemoattractant protein 1 (MCP-1). In immunohistochemical staining, ICAM-1 molecules were constitutively expressed on the surface of SMC. In flow cytometric and ELISA analyses, ICAM-1 molecule expression on SMC was significantly upregulated by IL-1 alpha and MCP-1, but not by IL-6, in a dose-dependent manner. The effects of IL-1 alpha and MCP-1 were observed as early as 4 h. In Northern blot analysis, ICAM-1 mRNA was slightly detectable in unstimulated SMC, but its expression was clearly observed following exposure to IL-1 alpha or MCP-1. These results suggest that ICAM-1 on SMC, as well as on endothelial cells, could participate in the focal accumulation of mononuclear cells in human atherosclerotic lesions.
Animals↗
Positive chronotropic and inotropic responses to lysophosphatidylcholine are mediated by norepinephrine released from myocardial sympathetic nerve terminals.
1. The effects of beta-adrenoceptor blockade and reserpinization on the positive chronotropic and inotropic responses to lysophosphatidylcholine (LPC) were examined in isolated atrial and ventricular preparations from rat hearts. 2. The positive responses to 10(-4) M LPC were about 40-55% of those to 10(-5) M norepinephrine (NE) in each preparation. 3. The responses to LPC in the presence of propranolol or in the reserpinized preparations were significantly smaller than the corresponding values obtained in control preparations, and were about 10-25% of those to NE. 4. It was concluded that positive chronotropic and inotropic responses to LPC are at least partially mediated by release of NE from myocardial sympathetic nerve terminals.
Animals↗
Tuberculous pericarditis presumably diagnosed by polymerase chain reaction analysis.
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Aged↗
Alterations in cytosolic calcium-binding proteins that increase felodipine fluorescence in spontaneously hypertensive rats.
OBJECTIVE: To clarify the role of calcium-binding proteins (CaBP) in hypertension. DESIGN: CaBP from several organs of spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) rats were purified and their characteristics compared between the two strains. The CaBP were purified by applying the soluble cytosolic fractions from mesenteric vessels, heart, kidney and brain of 4- and 10-week-old SHR and WKY rats to a phenyl-Sepharose column. Felodipine binding to the purified CaBP was then measured. RESULTS: The fluorescence intensity of felodipine increased in a calcium-dependent manner when it bound to CaBP. The pK 0.5 Ca2+ values derived from the calcium ion-felodipine fluorescence curves for each CaBP preparation from organs of the two strains were similar, indicating that the calcium sensitivities of the CaBP to the felodipine binding process are similar in SHR and WKY rats. In 10-week-old SHR the mean levels of felodipine-bound CaBP in heart, brain and kidney were significantly altered compared with those in WKY rats. No such alterations were observed in heart, kidney and brain from 4-week-old SHR and WKY rats. Conversely, the mean levels of felodipine-bound CaBP in mesenteric vessels from 4- and 10-week-old SHR were reduced significantly compared with those of age-matched WKY rats. CONCLUSIONS: These results suggest that the levels of cytosolic felodipine-bound CaBP from heart, kidney and brain are altered in response to elevated blood pressure, and that reduced levels of felodipine-bound CaBP in the mesenteric vessels of SHR might be a primary characteristic of this rat strain.
Animals↗
Increased expression of interleukin 6 mRNA in cardiac myxomas.
In three patients with cardiac myxoma increased expression of interleukin 6 (IL-6) mRNA was found in the myxoma tissue by polymerase chain reaction (PCR) and in situ hybridisation. These cases suggest that IL-6 is overproduced in the myxoma tissue and secreted into the systemic circulatory system. This might contribute to the systemic inflammatory or autoimmune manifestations seen in cardiac myxoma. This study also showed the usefulness of PCR and in situ hybridisation for the evaluation of mRNA expression in small samples of tissue.
Aged↗
Regulation of Na-K-ATPase gene expression by aldosterone in vascular smooth muscle cells.
Na-K-adenosinetriphosphatase (ATPase) activity profoundly influences vascular cell excitability, contractility, and volume regulation. The recent finding of mineralocorticoid hormone receptors in vascular tissue suggests the possibility that Na-K-ATPase gene expression in vascular tissue is regulated by the mineralocorticoid aldosterone. In this study, we investigated Na-K-ATPase gene expression by aldosterone in cultured rat vascular smooth muscle cells (VSMC). Na-K-ATPase alpha 1- and beta 1-isoform mRNAs, but not alpha 2- and alpha 3-isoform mRNAs, were expressed in cultured rat VSMC. Aldosterone caused a 2.3-fold increase in the alpha 1 mRNA and a 4.7-fold increase in the beta 1 mRNA accumulation with peak elevations at 24 and 6 h, respectively. Aldosterone induced the alpha 1 mRNA expression at physiological concentrations (half-maximum effective concentration = 2-3 nM), consistent with the binding of aldosterone to mineralocorticoid hormone receptors. The augmented alpha 1 mRNA expression by aldosterone was associated with a twofold increase in the alpha 1-subunit protein accumulation. Pretreatment of VSMC with cycloheximide caused a 10-fold increase in the alpha 1 mRNA expression, and the aldosterone-mediated alpha 1 mRNA accumulation was not observed in the presence of cycloheximide. Transfection experiments with the luciferase reporter gene revealed that aldosterone response sequences are located within the 5'-flanking regions of the alpha 1-isoform gene. These data demonstrate that the mineralocorticoid aldosterone directly stimulates Na-K-ATPase gene expression and protein accumulation in VSMC.
Aldosterone↗
Thyroid hormone stimulates Na(+)-K(+)-ATPase gene expression in cultured rat mesangial cells.
Thyroid hormone 3,3',5-triiodothyronine (T3) is an important regulator of Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) activity in a variety of mammalian target tissues. In the present study, we examined the expression of Na(+)-K(+)-ATPase alpha- and beta-subunit mRNAs by T3 in cultured rat mesangial cells. Northern blot analysis of total RNA isolated from cultured rat mesangial cells revealed the expression of mRNAs encoding Na(+)-K(+)-ATPase alpha 1- and beta 1-subunits; mRNAs encoding alpha 2- and alpha 3-subunits were undetectable. Exposure of mesangial cells to T3 (10(-8) M) caused a threefold increase in the alpha 1-mRNA expression, which was first detected at 6 h and sustained for at least 48 h. The beta 1-mRNA expression was gradually increased by T3, with a maximum fourfold elevation at 48 h. The 50% effective concentration (EC50) for the alpha 1- and beta 1-mRNA induction by T3 was approximately 10(-10) M. The half-life of alpha 1-mRNA analyzed by actinomycin D chase was approximately 3 h and was not affected by T3. The augmented alpha 1-mRNA expression by T3 was associated with a 2.4-fold increase in the alpha 1-subunit protein accumulation and a 1.6-fold increase in Na(+)-K(+)-ATPase activity. These data suggest that thyroid hormone stimulates Na(+)-K(+)-ATPase gene expression, protein accumulation, and enzyme activity in rat mesangial cells.
Animals↗
Regulation of Na,K-adenosine triphosphatase gene expression by sodium ions in cultured neonatal rat cardiocytes.
Na,K-ATPase (Na,K-pump) plays an important role in the regulation of intracellular ion composition. The purpose of this study is to determine whether Na+ regulates the levels of mRNA coding for Na,K-ATPase alpha and beta subunits in cultured neonatal rat cardiocytes. We measured intracellular Na+ levels ([Na+]i) in cardiocytes using a Na(+)-sensitive fluorescence dye (SBFI). 1 mM ouabain caused a significant increase in [Na+]i in cardiocytes; from 12.8 +/- 0.3 to 28.8 +/- 1.8 mM. Exposure of cardiocytes to 1 mM ouabain resulted in a three- to fourfold increase in alpha 1, alpha 2, and alpha 3 mRNA accumulation, and an approximate two-fold increase in beta 1 mRNA accumulation. A maximum elevation was reached at 60 min in both cases. The ouabain-induced alpha 1 mRNA accumulation was still observed in the Ca(2+)-free culture medium. Exposure of cardiocytes to 10 microM monensin in the absence of extracellular Ca2+ also resulted in a threefold increase in alpha 1 mRNA accumulation. The increased alpha 1 mRNA expression by 1 mM ouabain was associated with a fourfold increase in alpha 1 subunit protein accumulation. Transfection experiments with chimeric plasmids containing 5'-flanking sequences of alpha 1, alpha 2, and alpha 3 isoform genes and a luciferase reporter gene revealed that 1 mM ouabain caused a twofold increase in luciferase activity in each alpha system. These results suggest that Na+ directly regulates Na,K-ATPase gene expression in cardiocytes. The transfection study further supports the premise that Na(+)-responsive elements are located within the 5'-flanking sequences of each alpha isoform gene.
Animals↗
Becker muscular dystrophy with early manifestation of left heart failure.
We encountered a case of dystrophin-verified Becker muscular dystrophy which exhibited left heart failure as an initial symptom but no subjective muscle weakness. Severe cardiac involvement has been thought to rarely occur in the early stage of this disease, however accurate diagnosis was limited until the dystrophin diagnosis became available. This case suggests that some cases of dilated cardiomyopathy might be Becker muscular dystrophy, and that dystrophin tests should be added to the conventional investigation of patients with dilated cardiomyopathy.
Adolescent↗
Pasteurella ureae endocarditis.
Pasteurella ureae is found in the normal human respiratory flora. We encountered a case of endocarditis caused by Pasteurella ureae. The patient was a 59-year-old man with a history of Staphylococcus aureus endocarditis. After treatment with antibiotics, blood cultures became negative, and the patient recovered completely. The incidence of endocarditis due to this organism is very rare; this case is the second clinically diagnosed case report.
Anti-Bacterial Agents↗
[Two adult cases with corrected transposition of the great arteries treated with permanent endocardial pacemaker implantation].
[Case 1] A 32 year-old male had (I, D, D) type corrected transposition of the great arteries (cTGA) associated with ventricular septal defect and pulmonary stenosis. [Case 2] A 69 year-old male had (S, L, L) type cTGA associated with tricuspid regurgitation. Both cases showed advanced atrioventricular (AV) block due to HV block. Both patients had endocardial DDD pacemakers implanted, with no complication. (I, D, D) type cTGA is rarely accompanied with AV block, while the incidence of AV block is high in (S, L, L) type cTGA. We speculate that this results from the difference in the position of the AV node between these two types.
Adult↗
[Na, K-ATPase gene expression in hypertrophic and failing hearts].
Na, K-ATPase (Na, K-pump) maintains intracellular ion composition by transporting Na+ and K+ across the cell membrane, and plays an important role in many fundamental cellular and physiological processes such as the control of contractility, excitability, and cell volume regulation. The Na, K-ATPase protein comprises two subunits, a large catalytic alpha subunit and a smaller glycosylated beta subunit. At least three alpha subunit isoforms, alpha 1, alpha 2 and alpha 3, and two beta subunit isoforms, beta 1 and beta 2, have been characterized in rats and humans. The expression of Na, K-ATPase alpha and beta subunits in cardiocytes is directly regulated at a transcriptional level by hormones and ions, such as thyroid hormone and Na+. In the hypertrophic and failing hearts, the expression of cardiac Na, K-ATPase gene is altered, and which might play an important role in the pathogenesis of those disorders.
Animals↗
[Role of hypertension in atherosclerosis].
Hypertension is frequently associated with clinical cardiovascular complications due to atherosclerosis. However, several previous studies have showed that incidence of cardiovascular complication due to atherosclerosis hypertensives do not decrease even when the blood pressure was well controlled. The effects of hypertension on atherogenesis appears to be mainly due to two factors: (1) The mechanical stress which induces the change of cell functions of arterial wall cells such as endothelial cells, smooth muscle cells and extracellular matrix, (2) Vasoactive substances, such as angiotensin and endothelin, which may plays a role for smooth muscle cell proliferation. The tropic changes in smooth muscle cells induced by above two factors in hypertension might reflect common alternations in cellular reactivity as observed in atherosclerosis. If so, hypertension and atherosclerosis could be regarded as two effects with one underlying cause.
Animals↗
Interleukin 6 gene transcripts are expressed in atherosclerotic lesions of genetically hyperlipidemic rabbits.
We have investigated the involvement of interleukin 6 (IL-6), a growth-regulatory molecule for vascular smooth muscle cells (SMC), in the development of atherosclerotic lesions of Watanabe heritable hyperlipidemic (WHHL) rabbits. In in situ hybridization analysis, quite low levels of IL-6 mRNA were expressed in 'quiescent' SMC cultured from WHHL rabbits; however, high levels of IL-6 mRNA were induced in SMC exposed to 10% fetal bovine serum (FBS), suggesting that growth-stimulated SMC themselves can synthesize IL-6. In in vivo WHHL aortae, transcripts for the IL-6 gene were clearly observed in the fibrous plaques. These findings support the premise that IL-6 is an important autocrine and/or paracrine regulator of SMC proliferation and of pathogenesis of atherosclerosis in this animal model.
Animals↗
Serum interleukin 6 levels become elevated in acute myocardial infarction.
We have examined serum interleukin 6 (IL-6) levels in 12 patients with acute myocardial infarction (AMI). IL-6 levels became elevated in all patients, following the rise of serum creatine kinase (CK) activity. Peak IL-6 levels showed a good correlation with peak serum C-reactive protein (CRP) levels, while there was no direct relationship between peak IL-6 levels and peak CK activity. IL-6 mRNA was not detected in unstimulated "quiescent" rat cardiocytes cultured in serum-free medium, but its expression was induced by exposure of the cells to serum or ionomycin. These results show that IL-6 is synthesized in the myocardium and serum IL-6 levels become elevated in AMI, suggesting that IL-6 could affect the progression and/or healing processes of AMI.
Aged↗
Enhanced spontaneous calcium efflux and decrease of calcium-dependent calcium release from the isolated perfused heart of spontaneously hypertensive rats.
OBJECTIVE: The aim of this study was to clarify the further details of calcium handling in hypertension. DESIGN: By preserving the physiological environment of cell membrane, whole hearts were used for comparison of calcium flux between spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. METHODS: Hearts from SHR and WKY rats were perfused with Krebs-Henseleit solution under constant flow and the effluent collected. RESULTS: After labelling of the heart with 45Ca2+ (100 mumol/l), 45Ca2+ binding was found to be saturated, and washing with calcium-free perfusion solution showed two exponential curves for calcium dissociation, indicating a fast (alpha-) and slow (beta-) phase. The half-lives of the beta-phase for both 4- and 8-week-old SHR were significantly shorter than those for age-matched WKY. Also in this phase, infusion of non-radioactive Ca2+ caused a transient dose-dependent release of 45Ca2+. A significant reduction in the amount of 45Ca2+ release induced by 2 mmol/l Ca2+ was observed in both 4- and 8-week-old SHR compared with age-matched WKY rats. Infusion of lanthanum, caffeine, ionomycin (calcium ionophore) and treatment of the hearts with ethyleneglycol-bis-(beta-aminoethylether)-N,N,N,',N'-tetraac etic acid did not alter 45Ca2+ release by non-radioactive Ca2+. From these observations, 45Ca2+ is presumably released from the intracellular calcium pool, and not from extracellular binding sites or sarcoplasmic reticulum. CONCLUSIONS: These findings suggest that an abnormal calcium-handling defect (enhanced calcium efflux and reduction of membrane-bound Ca2+) exists under physiological conditions before and after the onset of hypertension, and that this may be a primary characteristic of SHR.
Aging↗
Conduction disturbance and pacemaker therapy in patients with corrected transposition of the great arteries.
We observed 4 adult patients with corrected transposition of the great arteries (CTGA) who developed complete atrioventricular block: of 4 patients, 2 received endocardial pacemakers (DDD mode), 1 an epicardial pacemaker (VVI mode), and 1 patient did not have a permanent pacemaker implantation. Endocardial lead fixation in the systemic venous atrium and ventricle is adequate to provide permanent electrode stability in patients with CTGA.
Adult↗