Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Nine paatients with clinically unimportant heart disease or benign essential hypertension were given frusemide intravenously during right-heart catheterization. 2. Pressures in both atria decreased rapidly and in parallel. The magnitude of the pressure decrease was clearly related to decrease in plasma volume loss. 3. Plasma renin activity increased significantly after 5 min (P less than 0-01), but did not correlate with plasma volume loss. 4. Venous tone in the forearm was unchanged. 5. It is concluded that the pressure reduction was secondary to plasma volume depletion through diuresis and that increased plasma renin activity was mainly caused by intrarenal changes.
Clin Sci Mol Med 1975 Dec
PMID:The early effects of intravenous frusemide on central haemodynamics, venous tone and plasma renin activity. 120 85

In this report we describe the development and application of single-stranded RNA probes for strand-specific detection of enterovirus RNA in infected heart tissue by in situ hybridization. For synthesis of RNA probes a full-length reverse-transcribed, recombinant CVB3 cDNA was inserted into the transcription vector pSPT18. Run-off transcripts of plus-strand and minus-strand orientation were produced using either T7 or SP6 RNA polymerase. Binding specificity and sensitivity of the radioactively labelled RNA probes were determined by slot-blot hybridization. Due to the high degree of genetic identity among enteroviruses, the in vitro transcribed CVB3 RNA probes hybridized with various enterovirus serotypes, including group A and B coxsackieviruses and echoviruses, which are commonly implicated in human viral heart disease. Strand-specific in situ hybridization led to detection of viral plus-strand or minus-strand RNA in infected cell cultures and in myocardial tissue sections of infected mice. In consecutive sections either viral genomic plus-strand RNA or complementary minus-strand RNA were localized in the same infected myocardial cells. In situ hybridization with enterovirus-specific and highly sensitive single-stranded RNA probes is of particular interest for the diagnosis of myocardial infections and for studies concerning viral RNA replication.
Mol Cell Probes 1991 Feb
PMID:Strand-specific detection of enteroviral RNA in myocardial tissue by in situ hybridization. 185 Jan 15

The extracellular matrix of the myocardium contains an elaborate structural matrix composed mainly of fibrillar types I and III collagen. This matrix is responsible for the support and alignment of myocytes and capillaries. Because of its alignment, location, configuration and tensile strength, relative to cardiac myocytes, the collagen matrix represents a major determinant of myocardial stiffness. Cardiac fibroblasts, not myocytes, contain the mRNA for these fibrillar collagens. In the hypertrophic remodeling of the myocardium that accompanies arterial hypertension, a progressive structural and biochemical remodeling of the matrix follows enhanced collagen gene expression. The resultant significant accumulation of collagen in the interstitium and around intramyocardial coronary arteries, or interstitial and perivascular fibrosis, represents a pathologic remodeling of the myocardium that compromises this normally efficient pump. This report reviews the structural nature, biosynthesis and degradation of collagen in the normal and hypertrophied myocardium. It suggests that interstitial heart disease, or the disproportionate growth of the extracellular matrix relative to myocyte hypertrophy, is an entity that merits greater understanding, particularly the factors regulating types I and III collagen gene expression and their degradation.
Mol Cell Biochem 1990 Jul 17
PMID:Collagen and the myocardium: fibrillar structure, biosynthesis and degradation in relation to hypertrophy and its regression. 214 89

To examine the role of endogenous proteases in limiting the bronchodilating effects of vasoactive intestinal peptide (VIP) in human airway, we studied precontracted bronchial rings from five nonsmokers undergoing heart-lung transplantation for pulmonary hypertension, either primary or secondary to congenital heart disease. The protease inhibitors aprotinin, leupeptin, phosphoramidon, and soybean trypsin inhibitors significantly potentiated the bronchodilator response to VIP. Even in the presence of the four protease inhibitors, VIP-induced bronchodilation reversed spontaneously in some tissues. These studies show that degradation by endogenous airway proteases is an important determinant of the bronchodilating potency of VIP in isolated human airway.
Am J Respir Cell Mol Biol 1990 May
PMID:Protease inhibitors potentiate smooth muscle relaxation induced by vasoactive intestinal peptide in isolated human bronchi. 218 92

We have previously identified the adenine nucleotide translocator (ANT), an intrinsic protein of the inner mitochondrial membrane, as an auto-antigen in dilated cardiomyopathy (DCM). Further immunochemical characterization by crossed immunoelectrophoresis, indirect solid phase radioimmunoassay and immunoadsorption studies on the isolated translocator protein and mitochondria from heart, kidney and liver showed the existence of organ-specific antigenic determinants although partial crossreactivity between the three proteins was observed. Sera from 18 patients with histologically proven dilated cardiomyopathy were studied for their capacity to bind to the translocator protein. Seventeen of 18 patients showed significant binding, while in the sera of patients with coronary heart disease, suspected alcoholic heart disease or healthy blood donors, no anti-ANT antibodies were observed. Further studies showed organ-specific and functionally active autoantibodies, which decreased the ADP/ATP exchange rate from heart mitochondria. A close correlation was found between the antibody-titer and the hemodynamic function. These results give new evidence for autoimmunological events in dilated cardiomyopathy.
J Mol Cell Cardiol 1985 Jun
PMID:Immunological analysis of auto-antibodies against the adenine nucleotide translocator in dilated cardiomyopathy. 299 41

In previous studies ribose has been recognized as a substrate that has beneficial effects on myocardial metabolism. It leads to an elevation of the available 5-phosphoribosyl-1-pyrophosphate pool and stimulates adenine nucleotide de novo synthesis in the rat heart under control and various pathophysiological conditions (Zimmer and Gerlach, 1978; Zimmer and Ibel, 1983, 1984). When the clinical application of ribose in patients with heart disease is envisaged, it is understood that conventional cardiac therapy must be continued. It is therefore necessary to demonstrate in animal experiments that ribose retains its stimulating metabolic effect when administered in conjunction with therapeutically used drugs. In this study we have selected representatives of two pharmacological principles, the calcium antagonist verapamil and the beta 1-specific adrenoceptor blocker metoprolol. Measurements of functional parameters in closed-chest rats revealed that i.v. administration of ribose alone for 24 h (200 mg/kg/h) had no hemodynamic or vasoactive influence, whereas verapamil and metoprolol (i.v. infusion of 2 mg/kg/h each for 24 h) induced negative chronotropic and negative inotropic effects. Cardiac output was reduced by metoprolol, but not by verapamil. Ribose did not affect these drug-induced hemodynamic alterations, and verapamil as well as metoprolol did not interfere with the characteristic metabolic effect of ribose, the stimulation of cardiac adenine nucleotide de novo synthesis. Administration of ribose in combination with these pharmacological agents is therefore compatible.
J Mol Cell Cardiol 1987 Jul
PMID:Combination of ribose with calcium antagonist and beta-blocker treatment in closed-chest rats. 311 64

The purpose of the present study was to compare protein profiling of atria and ventricles in children operated for congenital heart disease. Tissue samples were obtained during surgery from patients with normoxemic (ventricular and atrial septal defects) and hypoxemic (tetralogy of Fallot) diseases. Protein fractions were isolated by stepwise extraction from both right ventricular and atrial musculature. The concentration of total atrial protein in the normoxemic patients exceeded the ventricular value (110 +/- 2.1 vs 99.9 +/- 4.0 mg.g-1 wet weight, respectively); in the hypoxemic group this atrio-ventricular difference disappeared. The concentration of contractile proteins in all cardiac samples was significantly higher in the ventricles as compared with atria, while the concentration of collagenous proteins was significantly higher in the atria (due to a higher amount of the insoluble collagenous fraction). The concentration of sarcoplasmic proteins (containing predominantly enzyme systems for aerobic and anaerobic substrate utilization), however did not differ between ventricles and atria. Furthermore, ventricular contractile fractions obtained from both normoxemic and hypoxemic patients were contaminated with the myosin light chain of atrial origin. Soluble collagenous fractions (containing newly synthesized collagenous proteins, predominantly collagen I and III), derived from all ventricular samples, were contaminated by low molecular weight fragments (mol. weight 29-35 kDa). The proportion of the soluble collagenous fraction was significantly higher in atrial but not in ventricular myocardium of hypoxemic children as compared with the normoxemic group. It seems, therefore, that lower oxygen saturation affects the synthesis of collagen preferentially in atrial tissue.
Mol Cell Biochem
PMID:Differences between atrial and ventricular protein profiling in children with congenital heart disease. 749 53

This paper presents a review of the significant body of literature liking dietary iron overload, not only to heart disease, but also to cancer, diabetes, osteoporosis, arthritis, and possibly other disorders. Following an analysis of our understanding of the mechanistic role iron plays in oxidative damage, an interpretation of the fact that plasma concentrations of several antioxidants are decreased in the presence of disease is offered. Evaluation of (1) age-related dietary trends over time and (2) factors involved in iron absorption leads to the hypothesis that the combination of citric acid and ascorbic acid (a synergistic pair of strong enhancers) is instrumental in causing a deleterious increase in iron load in aging populations. Iron overload may be the most important common etiologic factor in the development of the diseases mentioned; therefore, the synergistic combination of citric and ascorbic acids may play a major role in our worsening disease statistics. Evidence to support this hypothesis and possible experiments to test it are included. This combination needs further study, particularly because the iron overload produced may be correctable.
Biochem Mol Med 1995 Feb
PMID:Proposed role for a combination of citric acid and ascorbic acid in the production of dietary iron overload: a fundamental cause of disease. 755 10

Deletions within 22q11 have been associated with a wide variety of birth defects embraced by the acronym CATCH22 and including the DiGeorge syndrome, Shprintzen syndrome (velocardiofacial syndrome) and congenital heart disease. It is not known how many genes contribute to this phenotype. Previous studies have shown that a balanced translocation disrupts sequences within the shortest region of deletion overlap for DiGeorge syndrome. A P1 clone was isolated which spans this breakpoint and used to isolate a cDNA encoding a transmembrane protein expressed in a wide variety of tissues. This gene (called IDD) is not disrupted by the translocation, but maps within 10 kb of the breakpoint. Mutation analysis of five affected cases with no previously identified chromosome 22 deletion was negative, but a potential protein polymorphism was discovered. No deletions or rearrangements were detected in these patients following analysis with markers closely flanking the breakpoint, data which emphasize that large (i.e. over 1 Mb) interstitial deletions are the rule in DiGeorge syndrome. The proximity of IDD to the balanced translocation breakpoint and its position within the shortest region of deletion overlap indicate that this gene may have a role, along with other genes, in the CATCH22 haploinsufficiency syndromes.
Hum Mol Genet 1995 Jun
PMID:Isolation of a gene encoding an integral membrane protein from the vicinity of a balanced translocation breakpoint associated with DiGeorge syndrome. 765 55

Ca influx in cultured neonatal myocardium can be augmented by metabolic inhibition or free radical exposure. This increase cannot be prevented by blockade of L-type Ca channels or inhibition of Na-Ca exchange. It is speculated that a specific Ca leak may be involved in this process. In the present study patch clamp techniques were used to examine this hypothesis. Currents were measured in a recording configuration of cell attached or excised inside-out membrane patches in adult rat ventricular myocytes as affected by metabolic inhibition or free radical exposure. The metabolic inhibition was achieved by use of 1 mM iodoacetic acid and 10 mM 2-deoxyglucose with omission of glucose in the perfusate. Free radicals were generated by application of 100 microM hydrogen peroxide in the perfusate. Specific Ca leak channels were identified. The channels were not significantly permeable to monovalent cations. The activity of these channels was increased markedly over a period of minutes by metabolic inhibition or free radical exposure. In the presence of 100 microM hydrogen peroxide the open probability (NPo) of the channels increased from 0.0083 +/- 0.003 (mean +/- S.D.) in control to 0.09 +/- 0.024 (P < 0.01). During metabolic inhibition it was augmented from 0.0075 +/- 0.0035 to 0.062 +/- 0.018 (P < 0.01). The increase of the Ca leak channel activity under both conditions could be completely blocked by addition of polycationic protamine to the patch pipette solution. The results support the hypothesis that Ca leak channels are involved in the Ca overload induced by metabolic inhibition or free radical exposure. The inhibitory effect of polycation may have important therapeutic implications for the treatment of ischemic cardiac heart disease.
J Mol Cell Cardiol 1995 Jan
PMID:Increase in calcium leak channel activity by metabolic inhibition or hydrogen peroxide in rat ventricular myocytes and its inhibition by polycation. 776 Mar 45


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