Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of low protein diet on cardiac metabolic and structural changes subsequent to an extremely high pressure load were investigated. Spontaneously hypertensive rats(SHR) were divided into four groups, and fed the following diets for four weeks: 1) Group A: regular diet (23% protein) and water, 2) Group B: regular diet and 1% saline, 3) Group C: low protein diet (10% protein) and water, and 4) Group D: low protein diet and 1% saline. Two weeks after the start of feeding, there was no significant difference in the left ventricular ultrastructures between the corresponding regular and low protein diet groups. Four weeks after, degenerative findings such as streaming of Z lines, dilatations of smooth endoplasmic reticulum, and disarrangements of myofilaments appeared Group D, while in Group B electron microscopic findings indicated hypertrophy. Incorporation of [14C] leucine into the myocardial myosin B in Group D was significantly low, with a resulting fall of the LVdP/dtmax per integrated isometric pressure (IIP) and a rise of the left ventricular end-diastolic pressure (LVEDP), as compared to that in Group C at four weeks after the start of feeding. These observations suggest that, in the heart with an extremely high pressure load, low protein diet hinders the development of hypertrophy to the load with resulting heart failure.
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PMID:Effect of low protein diet on cardiac function and ultrastructure of spontaneously hypertensive rats loaded with sodium chloride. 103 68

We report a case of hypocalcemic heart failure without underlying myocardial disease. Two-dimensional and Doppler echocardiography revealed dilatation and impaired contraction of the left ventricle, but did not show any valvular dysfunction. Cardiac catheterization showed a normal coronary artery, and cardiac muscle biopsy showed morphological changes in mitochondoria and endoplasmic reticulum, which may be due to metabolic changes. This patient was asymptomatic after the serum calcium concentration was normalized.
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PMID:A case of primary hypoparathyroidism complicated by heart failure. 180 49

A study was carried out on the evolution of histological and ultrastructural lesions of liver fragments harvested at different time intervals in the course of extracorporeal circulation in 62 patients operated for acquired and congenital heart disease, as well as that of serologic tests, pre-, intra- and postoperatively up to seven days. Morphologically, it is only the ultrastructural examination that detects the accentuation of preexisting hypoxic lesions within the framework of a state of "controlled shock", noting especially accentuated dilation of the endoplasmic reticulum, lysosomal activation, mitochondrial lesions and a tendency to ribosomal and glycogenic depletion. The lesions did not exceed the limits of reversibility, excepting the cases with advanced heart failure and cardiac cirrhosis. Lending support to these data is the decrease of proteinemia and the dynamics of LDH, SDH, G1DH, gamma GT and transaminases increase after 24 h, then fall to normal values within seven days.
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PMID:Contributions to the biology of the hypoxic liver. Note II. Histologic, electron microscopic and biochemical aspects in the course of open heart surgery under extracorporeal circulation. 214 7

The relationship between the abundance of specific Leydig cell organelles and daily sperm production (DSP) was determined. Testes from 10 men (26-53 years of age) were obtained at autopsy within 10 h of traumatic death or heart failure and fixed by vascular perfusion. Testicular tissue was processed for light and electron microscopy. DSP/testis and Leydig cell cytoplasmic volume/testis were determined by stereology of histologic sections. The Leydig cell organelle content was determined by point counting electron micrographs for smooth endoplasmic reticulum (SER), rough endoplasmic reticulum, mitochondria, lipofuscin pigment, lipid, Golgi bodies, and Reinke crystals. Men were divided equally into two groups based on DSP/testis. Men with low DSP/testis had less SER volume density (P less than 0.01) and lower SER volume per testis (P less than 0.05) than men with high DSP. Other organelles were unrelated to DSP. When all men were combined, the volume density of SER (r = 0.80; P less than 0.01), the volume SER per testis (r = 0.69; P less than 0.05), and the volume SER per Leydig cell (r = 0.84; P less than 0.01) were significantly related to DSP. Hence, there appears to be a significant relationship between Leydig cell SER and the level of spermatogenesis in men.
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PMID:Leydig cell cytoplasmic content is related to daily sperm production in men. 232 2

A study was carried out on the histological and ultrastructural aspects of liver fragments harvested from 62 patients with acquired or congenital heart disease before open heart surgery under extracorporeal circulation. Against a background of passive congestion in the pericentrolobular and mediolobular areas, various mitochondrial lesions and dilation of the endoplasmic reticulum with a reduced number of ribosomes, the presence of microbodies, biliary pigments, lipid vacuoles, lysosomol hyperplasia and activation, glycogen depletion could be seen, as well as extensive collagenization of Disse's spaces, fibroblast hyperplasia and Kupffer cell activation. These lesions are more reduced in the periportal zones. In the advanced stages of heart failure, there appeared a cirrhogenic organization due to extensive pericentrolobular and periportal fibrosis.
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PMID:Contributions to the biology of the hypoxic liver. Note I. Histological and electronmicroscopical aspects of the liver in chronic congestive heart failure. 253 65

To clarify whether diminished hepatic blood flow and portal endotoxaemia interact in the pathogenesis of hepatic dysfunction secondary to acute circulatory failure, such as shock, prolonged hypotension, or left-sided heart failure, the present study was undertaken in rats. Reduced hepatic perfusion, which was produced by partial obstruction of the portal vein, caused elevation of serum transaminase activities and electron microscopic abnormalities of hepatocytic structure, namely, disruption of plasma membrane, swelling of mitochondria, vesiculation and disruption of endoplasmic reticulum, etc. Portal endotoxaemia, which was induced by infusion of endotoxin into the portal vein, led to a rise of serum transaminase activities and random, focal coagulative hepatocellular necrosis. In contrast, massive hepatic necrosis and excessive elevation of serum transaminase activities, which are similar to those seen in patients with shock, etc., were produced when portal endotoxaemia was superimposed upon poor hepatic perfusion. These experimental results suggest that acute hepatic failure and massive hepatic necrosis secondary to acute circulatory failure may be induced by the coexistence of reduced hepatic blood flow and portal endotoxaemia.
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PMID:On the pathogenesis of hepatic dysfunction and necrosis following acute circulatory failure. 343 9

Patients with chronic heart failure (CHF) can often develop such diseases as hepatitis of viral etiology, alcoholic hepatitis, drug affection of the liver and other diseases masked as congestive liver. In most cases CHF concomitant liver diseases have an atypical course with a tendency to a chronic course. CHF is one of the important pathogenetic mechanisms lying in the basis of chronicity of concomitant liver diseases. Refractory CHF, inconsistency of the hemodynamic indices of persistent hepatomegaly must lead a physician to the detection of probable independent liver diseases complicating the syndrome of heart failure. CHF is a factor causing an enhanced fibrosing liver reaction. An important diagnostic test of fibrinogenesis lying in the basis of chronicity of liver diseases, is the determination of enzymatic markers reflecting synthesis and catabolism of the main substance of connective tissue. Change in the levels of haptoglobin, ceruloplasmin and glutamic acid dehydrogenase is an indirect sign of damage of the liver parenchymal endoplasmic reticulum. These indices can serve as differential criteria of the prevalence of cardiovascular disorders in the liver or concomitant independent liver diseases.
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PMID:[Pathogenetic mechanisms of chronicity in liver diseases in patients with circulatory failure]. 361 41

Intracellular Ca2+-release channels on the sarcoplasmic reticulum of striated muscle [ryanodine receptors (RyRs)] and on the endoplasmic reticulum of almost all types of cells [inositol 1,4,5-trisphosphate receptors (IP3Rs)] comprise a unique family of molecules that are structurally and functionally distinct from all other known ion channels. These channels play crucial roles in Ca2+-mediated signaling that triggers excitation-contraction coupling, T-lymphocyte activation, fertilization, and many other cellular functions. Three forms of RyR have been identified: RyR1, expressed predominantly in skeletal muscle; RyR2, expressed predominantly in cardiac muscle; and RyR3, expressed in specialized muscles and nonmuscle tissues including the brain. RyR channels are tetramers composed of four subunits each with a molecular mass of approximately 560,000 Da. The tetrameric structures of RyR1 and RyR2 are stabilized by a channel-associated protein known as the FK506 binding protein (FKBP). FKBP is the cytosolic receptor for the immunosuppressant drugs FK506 and rapamycin that inhibit the prolyl isomerase activity of FKBP and can dissociate FKBP from RyRs. Rapamycin and FK506 increase the sensitivity of RyRs to agonists such as caffeine and could be a cause of cardiac dysfunction associated with high-dose immunosuppressant therapy by promoting leakage of Ca2+ from the sarcoplasmic reticulum. The role of prolyl isomerase activity of FKBP in regulating RyR function remains uncertain, and several models have been proposed that could explain how the channel is modulated by its association with FKBP. Three forms of IP3Rs (types 1, 2 and 3) have been characterized by cDNA cloning. Most cells have at least one form of IP3R, and many express all three types. Like RyRs, the IP3R channels are tetramers composed of four subunits (approximately 300,000 Da each). IP3R1 function is regulated by at least two major cellular signaling pathways: the second messenger IP3 activates the channel, and phosphorylation by nonreceptor protein tyrosine kinases (e.g., Fyn) increase its open probability. During end-stage human heart failure, RyR2 mRNA and protein are downregulated, whereas IP3R1 is upregulated, suggesting that altered Ca2+-release channel levels may contribute to defects in Ca2+ homeostasis. Cells that are deficient in IP3R1 exhibit defective T cell-receptor signaling and thus cannot be activated by T cell-receptor stimulation. IP3R1-deficient cells are also resistant to induced apoptosis. Thus RyRs and IP3Rs play critical roles in fundamental and diverse signaling phenomena that include excitation-contraction coupling, T-cell activation, and programmed cell death.
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PMID:Intracellular calcium-release channels: regulators of cell life and death. 912 14

Although Ca(2+)/calmodulin-dependent protein kinase-II (CaMK) is known to phosphorylate different Ca(2+) cycling proteins in the cardiac sarcoplasmic reticulum (SR) and regulate its function, the status of CaMK in heart failure has not been investigated previously. In this study, we examined the hypothesis that changes in the CaMK-mediated phosphorylation of the SR Ca(2+) cycling proteins are associated with heart failure. For this purpose, heart failure in rats was induced by occluding the coronary artery for 8 weeks, and animals with >30% infarct of the left ventricle wall plus septum mass were used. Noninfarcted left ventricle was used for biochemical assessment; sham-operated animals served as control. A significant depression in SR Ca(2+) uptake and release activities was associated with a decrease in SR CaMK phosphorylation of the SR proteins, ryanodine receptor (RyR), Ca(2+) pump ATPase (SR/endoplasmic reticulum Ca(2+) ATPase [SERCA2a]), and phospholamban (PLB) in the failing heart. The SR protein contents for RyR, SERCA2a, and PLB were decreased in the failing hearts. Although the SR Ca(2+)/calmodulin-dependent CaMK activity, CaMK content, and CaMK autophosphorylation were depressed, the SR phosphatase activity was enhanced in the failing heart. On the other hand, the cAMP-dependent protein kinase-mediated phosphorylation of RyR and PLB was not affected in the failing heart. On the basis of these results, we conclude that alterations in SR CaMK-mediated phosphorylation may be partly responsible for impaired SR function in heart failure.
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PMID:Sarcoplasmic reticulum Ca(2+)/Calmodulin-dependent protein kinase is altered in heart failure. 1072 Apr 22

Sarcoplasmic reticulum (SR)-mediated Ca(2+) sequestration and release are important determinants of cardiac contractility. In end-stage heart failure SR dysfunction has been proposed to contribute to the impaired cardiac performance. In this study we tested the hypothesis that a targeted interference with SR function can be a primary cause of contractile impairment that in turn might alter cardiac gene expression and induce cardiac hypertrophy. To study this we developed a novel animal model in which ryanodine, a substance that alters SR Ca(2+) release, was added to the drinking water of mice. After 1 wk of treatment, in vivo hemodynamic measurements showed a 28% reduction in the maximum speed of contraction (+dP/dt(max)) and a 24% reduction in the maximum speed of relaxation (-dP/dt(max)). The slowing of cardiac relaxation was confirmed in isolated papillary muscles. The late phase of relaxation expressed as the time from 50% to 90% relaxation was prolonged by 22%. After 4 wk of ryanodine administration the animals had developed a significant cardiac hypertrophy that was most prominent in both atria (right atrium +115%, left atrium +100%, right ventricle +23%, and left ventricle +13%). This was accompanied by molecular changes including a threefold increase in atrial natriuretic factor mRNA and a sixfold increase in beta-myosin heavy chain mRNA. Sarcoplasmic endoplasmic reticulum Ca(2+) mRNA was reduced by 18%. These data suggest that selective impairment of SR function in vivo can induce changes in cardiac gene expression and promote cardiac growth.
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PMID:Impaired sarcoplasmic reticulum function leads to contractile dysfunction and cardiac hypertrophy. 1129 5


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