Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolonged ingestion of ethanol may lead to a cardiomyopathy, and studies in the experimental animal have demonstrated alterations in protein metabolism. These changes include depression of protein synthesis with acetaldehyde in the acute experiment, in vitro, and after chronic ethanol ingestion in vivo. The present studies were initiated to see if the inhibition of protein synthesis following prolonged ethanol ingestion involved myocardial contractile proteins. Newly weaned guinea pigs, weighing 350 g, were placed on a regimen of normal laboratory diet with 10% ethanol in the drinking water. Calorie-matched controls, drinking dextromaltose in the water, were simultaneously run. After 40 weeks of ingesting 10% ethanol in the drinking water, hearts from growing guinea pigs were removed and synthesis of myocardial contractile proteins (myosin heavy chains, light chains (LC1, LC2), actin, and tropomyosin) assayed in vitro with 3H-labeled amino acids. With aging, there was a decrease in the rates of synthesis of all the contractile proteins. After 40 weeks of ethanol ingestion, the synthetic rates of myosin heavy and light chains and tropomyosin were the same as in calorie-matched controls, but the synthetic rate of actin was significantly decreased by 20% (p less than 0.01). This decrease in actin synthesis may be the first indication of ultimate inhibition of synthesis of all the contractile proteins which may lead to myofibrillar disorganization and vacuolization reported after chronic ethanol ingestion.
 ...
PMID:Prolonged feeding of ethanol to the young growing guinea pig. III. Effect on the synthesis of the myocardial contractile proteins. 354 78

Cardiomyopathy and plastic contractile myocardial insufficiency were simulated in Wistar rats by an anthracycline antibiotic rubomycin. The myocardium in conditions of DNA-dependent RNA synthesis suppression was studied using polarization, electron microscopy and the method of cardiomyocyte isolation. During anthracycline cardiomyopathy in the absence of necrotic and necrobiotic myocardial injuries there was a smaller depression of cardiomyocyte population and their nuclei in the right ventricle (23 and 22% respectively) than in the left ventricle (38 and 39% respectively). It was concluded that a smaller amount of cardiomyocyte population was in the phase of intensive protein synthesis in the right than in the left ventricular myocardium.
 ...
PMID:[Morphological manifestations of anthracycline cardiomyopathy in the ventricular myocardium of the rat]. 362 Jun 38

Biochemical investigations were performed on cardiac muscle samples from seven dogs with cardiomyopathy and on cardiac muscle from a varied selection of normal dogs. Biochemical examination of cardiac muscle from clinical cases of cardiomyopathy revealed that the concentrations of three enzymes were significantly altered. These were, catalase, succinic dehydrogenase and malate dehydrogenase. Depressed enzyme concentrations were recorded from both ventricles but were significant only on the left for catalase, on the right for malate dehydrogenase and in both ventricles for succinic dehydrogenase although the depression in this case was also greater on the right.
 ...
PMID:Biochemical investigations of cardiomyopathy in the dog. 362 75

To investigate still uncertain aspects of the diagnosis of ischemic heart disease (IHD) in women, between 1969 and 1984, repeated exercise studies were performed in 706 asymptomatic women (between the ages of 17 and 63 years). On observation of pathologic ST-segment depression of more than 0.1 mV, the exercise study was repeated after administration of 0.8 mg nitroglycerin. Pathologic ST-segment depression was seen in 310 women (44%). In 217 patients (31%), nitroglycerin had no effect (NTG negative); in 93 women (13%), there was normalization of the ST-segment changes (NTG positive). Additionally, in selected subgroups of patients, pulmonary artery pressure was measured at rest and during exercise and ECG mapping performed (n = 114); radionuclide ventriculograms (n = 64) and 201-thallium scintigrams (n = 99) were obtained and coronary angiography (n = 85) was performed. In the NTG-negative women, ejection fraction, myocardial perfusion and coronary arteries were normal. NTG-positive women had lower mean ejection fractions but still within normal limits and indications of impaired myocardial perfusion. High-grade coronary stenoses were found in 25%. No patient with pathologic ST-segment depression had mitral valve prolapse. NTG-positive women had significantly more risk factors than NTG-negative women. In the former group, pulmonary artery pressure measurements showed pathologic exercise hemodynamics, only in 25% of whom IHD with significant stenosis was found to be the cause. For this condition, differential diagnostic considerations include cardiomyopathy or small vessel disease.
 ...
PMID:[New aspects in the diagnosis of ischemic heart disease in females]. 365 37

R-wave amplitude (RWA) depends to a large extent on the left ventricular filling volume. Changes of RWA are attributed to the Brody-effect. Exercise has been shown to induce a decrease of RWA in a healthy population and an increase in patients with coronary artery disease (CAD). No clear data exist for cardiomyopathy (CMP). Controls (n = 12), patients with CMP (n = 32) and CAD (n = 58) were compared. Alterations of RWA (Wilson lead V5) were correlated with parameters of a bicycle exercise test including resting and exercise hemodynamics and parameters of LV-function including EF, LVEDV and LVEDP. CMP compared to CAD had smaller RWA at rest (0.78 +/- 0.47 vs 1.32 +/- 0.72 mV, P less than 0.01). During comparable levels of exercise CMP (EF 35 +/- 14%) showed no significant changes of RWA. CAD (EF 57 +/- 16%) presented an increase of RWA by +0.11 +/- 0.23 mV (P less than 0.01), while controls showed a straight decline of RWA (-0.31 +/- 0.24 mV). In patients with CAD delta RWA (RWA max exercise - RWA rest) was a more sensitive parameter for detection of disease (assuming delta RWA greater than or equal to +0.1 mV, 36/58 patients) than maximal ST-segment changes (ST-segment-depression in lead V5 greater than or equal to 0.2 mV at 0.08 sec after J-point, 22/58 patients). Precordial leads V2, V4, V5 and V6 showed similar changes. This paper supports the theory that changes of wall thickness or changes in the amount of air respective to the amount of fluid in the lungs are responsible for RWA changes. These changes are clearly dependent on the severity of the disease and on left ventricular function. Therefore measurement of RWA changes during exercise may offer additional information in patients with CAD as well as in patients with CMP.
 ...
PMID:R-wave amplitude changes during exercise stress testing: patients with dilative cardiomyopathy compared to patients with coronary artery disease. 365 98

This study examined the effects of ethanol and hereditary cardiomyopathy on sodium and water excretion by golden Syrian hamsters of both sexes. Ethanol (4 g/kg) or the isotonic saline vehicle were injected IP into 60-70-day-old hamsters of normal and cardiomyopathic (BIO 14.6) strains. Urine and blood were collected after 90 or 350 min in different groups. Cardiomyopathic hamsters more quickly lost their righting responses, eliminated ethanol more slowly, and had lower urine volume and sodium excretion than normal hamsters after ethanol injections. Plasma creatine kinase levels were normal in all animals tested, indicating no active skeletal or cardiac lesioning in the cardiomyopathic hamsters at the time of the experiment. Some factors which could contribute to the increased CNS and renal sensitivity to ethanol in cardiomyopathic hamsters include impaired ethanol metabolism, enhanced myocardial depression, and reduced atrial content of natriuretic peptides. The results do not owe to decompensated heart failure. Thus, the genetic mutation which causes skeletal and cardiac myopathy in these hamsters may also affect the metabolism and sensitivity to ethanol.
 ...
PMID:Ethanol in cardiomyopathic hamsters: Na and water excretion and righting response. 371 87

The treadmill exercise test with the Bruce protocol was performed in three patients with post-myocarditic myocardial hypertrophy (PMH) and ten patients with cardiomyopathy, including three with dilated cardiomyopathy (DCM), five with hypertrophic obstructive cardiomyopathy (HOCM), and two with hypertrophic and nonobstructive cardiomyopathy (HCM). The endurance time was below the normal level in all but one case and was normal or near normal in the three cases with PMH. ST depression was observed in five cases, none of which were of HCM. A marked increase in amplitude of the negative phase of the P wave in V1 was observed in one patient with DCM. The response of blood pressure during the exercise was abnormal in patients with DCM and HCM but was normal in PMH.
 ...
PMID:Treadmill exercise test in children with cardiomyopathy and postmyocarditic myocardial hypertrophy. 372 84

The clinical and pathologic findings in 12 patients with medium-chain acyl CoA dehydrogenase deficiency and three patients with long-chain acyl CoA dehydrogenase deficiency are summarized. Although these inborn errors of intramitochondrial beta-oxidation of fatty acids present with similar findings to Reye's syndrome, there are clinical, laboratory and hepatic histologic differences. Younger age at presentation, history of unexplained sibling death, a previous episode of lethargy, hypoglycemia or acidosis precipitated by fasting stress and only mildly elevated serum transaminases with normal or only mildly prolonged prothrombin time may all suggest an acyl CoA dehydrogenase deficiency. Long-chain acyl CoA dehydrogenase deficiency is differentiated from medium-chain acyl CoA dehydrogenase deficiency by younger age at presentation, more profound cardiorespiratory depression, evidence of cardiomyopathy, and sequelae of muscle weakness, hypotonia and developmental delay. Definitive diagnosis is made by assay of medium-chain or long-chain enzyme activity in cultured skin fibroblasts or in leukocytes. Hepatic light microscopic alterations are essentially limited to steatosis, which may be either macro- or microvesicular. The cases with microvesicular steatosis can be differentiated morphologically from Reye's syndrome by electron microscopy, showing the absence of the mitochondrial changes characteristic of Reye's. Four of seven cases of acyl CoA dehydrogenase deficiency showed some variations from normal in the appearance of the hepatocyte mitochondria. The relationship of these variations to the basic metabolic defect(s) remains to be determined.
 ...
PMID:Medium-chain and long-chain acyl CoA dehydrogenase deficiency: clinical, pathologic and ultrastructural differentiation from Reye's syndrome. 379 3

Wilson's disease is a multisystem disorder. Heart involvement in Wilson's disease, however, has rarely been recognized. A prospective study was undertaken of 53 consecutive patients (28 men and 25 women, mean age of 21.4 years) with Wilson's disease. Electrocardiographic abnormalities occurred in 18 of 53 patients (34 percent), including left ventricular hypertrophy, biventricular hypertrophy, early repolarization, ST depression and T inversion, premature atrial or ventricular contractions, atrial fibrillation, sino-atrial block, Mobitz type 1 atrioventricular block, and tremor artifact. In contrast, 26 medical students and 14 carriers of Wilson's disease as control subjects (mean age of 22.6 years) all showed normal ECG. Eight out of 43 patients (19 percent) demonstrated asymptomatic orthostatic hypotension. An abnormal response to the Valsalva maneuver occurred in six of 18 patients (33 percent). There were two cardiac deaths; one died of repeated ventricular fibrillation (the copper content in the myocardium was 2.28 micrograms/g, and in the bundle of His 1.21 micrograms/g wet weight in the autopsy specimen); and the other, of dilated cardiomyopathy. It is concluded that four modes of cardiac manifestations in Wilson's disease include arrhythmias, cardiomyopathy, cardiac death, and autonomic dysfunction. Such possible cardiac involvement should be added to the clinical picture of Wilson's disease involving the hepatic and central nervous system.
 ...
PMID:Cardiac Wilson's disease. 382 52

Diabetes mellitus is associated with a specific cardiomyopathy. This is evident from the clinical-pathological work and the epidemiologic data from the Framingham study. Noninvasive studies of diabetics have shown alterations in systolic and diastolic function that may ultimately lead to clinical heart failure. The relationship of these cardiac changes to the type of diabetes, its duration, and its severity is not settled. However, a correlation between changes in heart function and other complications of diabetes has been demonstrated. Insufficient prospective data is available from noninvasive studies to establish the frequency of progression from subclinical cardiac dysfunction to overt congestive failure. The pathogenesis of this disorder is still uncertain. Pathological studies have shown changes in the intramural arteries, arterioles, and capillaries but their functional significance is uncertain. Experimental studies have shown interstitial changes leading to an apparently less compliant left ventricle in the diabetic dog and monkey. In the diabetic rat reversible changes were found in myocardial function, related to changes in contractile proteins and intracellular calcium metabolism. In both species, the response to anoxia or ischemia was altered in the presence of diabetes. However, irreversible depression of the contractile element was not found in most animal studies of isolated diabetes. In contrast, the combination of hypertension and diabetes leads to substantial cardiac damage and circulatory congestion, both in clinical and experimental investigations. Clearly much more work must be carried out to understand the pathogenesis, treatment, and ultimately the prevention of diabetic cardiomyopathy.
 ...
PMID:Diabetic cardiomyopathy. 388 Sep 19


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>