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Query: UMLS:C0023890 (cirrhosis)
42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arteriosclerotic and nonarteriosclerotic rats were treated with carbon tetrachloride (CCL4) to induce cirrhosis of the liver. Massive myocardial infarction was then induced in intact and CCL4-treated animals. During acute necrosis (Days 1 thru 3), animals were killed at 4, 8, 12 and 24 h on Days 1 and 2, and during myocardial repair on Days 4, 5 and 8. During the induction of cirrhosis, animals developed polydypsia, polyuria, and hyperglycemia; during myocardial infarction, the arteriosclerotic + cirrhotic animals developed severe and persistent congestive heart failure, i.e., hydrothorax. Adrenal and thymus gland weights and corticosterone levels indicated that cirrhosis per se increased pituitary--adrenal activity, particularly in arteriosclerotic animals. Enzyme levels of SGOT and SGPT demonstrated severe hepatic damage due to cirrhosis and acute myocardial infarction. Blood triglycerides and cholesterol responded abnormally in cirrhotic animals during acute myocardial ischemia due to their entrapment within hepatic cells. The cirrhotic animals manifested poor myocardial repair with persistent foci of necrosis, calcification, and a high incidence of large, occlusive, atrial thrombi. It is suggested that cirrhosis interferes with lipid metabolism and adrenal steroid conjugation leading to abnormal levels of mineralocorticoids which favor congestive heart failure, poor myocardial repair, and atrial thrombosis.
Atherosclerosis 1979 Mar
PMID:Effect of CCL4-induced cirrhosis on the pathophysiologic course of acute myocardial infarction in nonarteriosclerotic vs arteriosclerotic male rats. 46 16

Tests on 100 alcoholic patients revealed increased lipoprotein levels in 24%. Type IV was the most frequently ecountered (80%), followed by type II or V. The average plasma triglyceride level of the alcoholic group was significantly increased in comparison with a control population. The causal mechanism of alcoholic hyperlipoproteinemia remains poorly understood. The combination of a genetic defect of lipid metabolism, nutritional factors and acute alcohol excess may have an essential bearing on the incidence of hyperlipoproteinemia. Acute excessive intake of alcohol was significantly increased in comparison with alcoholic subjects wihtout hyperlipoproteinemia. The critical dose may be a daily ethanol consumption of about 200 gm. There appeared to be no correlation between acute pancreatic injury or active liver disease and serum lipid elevation. On the other hand, the observation was confirmed that alcoholic patients with hepatic cirrhosis usually do not develop hyperlipoproteinemia. Ethanol-induced hyperlipoproteinemia may be a risk factor for the development of atherosclerosis and pancreatitis.
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PMID:[Alcohol-induced hyperlipoproteinemia]. 91 92

Hypercholesterolemia was induced in rats by feeding them a high cholesterol olive oil diet. The livers were homogenized in modified Krebs-Ringer medium and centrifuged at 35,000 x g. The supernatants from livers of both hypercholesterolemic and normal rats were found to stimulate collagen synthesis in freshly isolated embryonic chick-tendon fibroblasts. However, this was significantly greater in the supernatants from fatty livers. The stimulating principle proceed to be dialyzable, non-lipid and heat-stable. There were at least two factors involved, the more effective of which was trypsin-sensitive, with a molecular weight below 2,000. The results suggest that a mediator is formed in the livers of hypercholesterolemic rats which might be responsible for the enhanced collagen synthesis of fibrotic processes vivo, e.g., in atherosclerosis and liver cirrhosis.
Atherosclerosis
PMID:Factors stimulating collagen synthesis from the livers of hypercholesterolemic rats. 94 25

Two artificial estrogens, ethinyl estradiol and mestranol, were found to cause cirrhosis in the rabbit liver during a study of atherosclerosis. These drugs showed protective effects against atherosclerosis in cholesterol-fed rabbits when administered orally (1 ppm in diet). These drugs and two naturally occurring estrogens, estrone and estradiol, were similarly effective when administered intramuscularly (1.5 mg per rabbit per week) to rabbits fed a diet lower in cholesterol. Reduction by estrogens of plasma cholesterol did not fully account for the reduction of extent of aortic atherosclerosis. Also, no differences in aortic or platelet eicosanoid production from exogenous arachidonic acid were found to explain the effect on atherogenesis. The 2 artificially modified estrogens, ethinyl estradiol and mestranol, caused portal fibrosis with biliary proliferation (even in rabbits not fed cholesterol). Estrone, estradiol, and testosterone were not injurious in this regard at the dosages used. Only the unmodified estrogens reduced atherosclerosis without damaging the rabbit liver.
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PMID:Estrogen protection against atherosclerosis and synthetic estrogen production of cirrhosis in the rabbit. 157 Apr 4

Small-diameter vascular grafts woven from bioresorbable lactide/glycolide copolymers have been successfully interposed into aortas of normal NZW rabbits. The current study examines the histologic and functional reactions to these bioresorbable grafts in severely hypercholesterolemic rabbits, a standard animal model of atherosclerosis. Sixty rabbits were placed on a 2% cholesterol, 6% peanut oil atherogenic diet. Baseline serum cholesterols and triglycerides were measured and repeated at operation 3 months later. Woven polyglactin 910 (PG910) grafts were interposed into infrarenal aortas. Fifty-two rabbits died on the diet or within 3 days of surgery and eight survived operation (normal NZW rabbit operative mortality is less than 10%). Cholesterol levels rose from 63 to 1989, p less than .001. Of the eight survivors, five died after 3 weeks, and one died after 2 1/2 months. Two were sacrificed at 2 and 4 months. Four aortic disruptions with retroperitoneal hematomas, one pseudoaneurysm, and one diffuse aneurysm were observed, greater than in normal rabbits, p less than .001. Inspection revealed severe atherosclerosis. Histologically, 3-week explants showed only small areas of neointima with myofibroblasts and endothelial cells; the outer capsules were infiltrated by lipid-laden macrophages. Graft material in 2- to 4-month explants was replaced by tissue with histologic atherosclerosis. More severe atherosclerosis was observed in native aortas at the perianastomotic areas than the more distant aortic segments. Abundant intracellular lipid was seen also in splenic histiocytes and hepatic cells with evidence of micronodular cirrhosis. Macrophages phagocytizing bioresorbable prostheses may release growth factors mediating the formation of a cellular tissue conduit. Severe hypercholesterolemia may alter monokine release from macrophages resulting in a weakened prosthesis/tissue complex.
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PMID:Effects of hypercholesterolemia on healing of vascular grafts. 191 76

This study evaluates the correlation between long-term weight history and health risks. One thousand three hundred and sixteen male subjects of normal weight (-5%(-)+5% by Broca's obesity index) at age twenty, were studied. The average age of the subjects was 43.7 +/- 6.5 (M. +/- S.D.) years old. According to their long-term weight history, the subjects were classified into four groups: weight lost (N = 35), weight stable (N = 502), mild weight gain (N = 187), severe weight gain (N = 592). Odds ratios for systolic blood pressure, diastolic blood pressure, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, gamma glutamyl transpeptidase, uric acid, fasting blood sugar, total cholesterol, triglyceride, shortness of breath, hyperperspiration, angina pectoris, and hypertension were significantly higher in the severe weight gain group than in the stable weight group. Stepwise logistic regression analysis was performed by choosing weight history, obesity index, age, and smoking and drinking habits as the independent variables. Weight history was shown to be a significant variable in systolic blood pressure, diastolic blood pressure, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, gamma glutamyl transpeptidase, fasting blood sugar, total cholesterol, triglyceride, shortness of breath, chronic hepatitis and liver cirrhosis. Odds ratios for factors suspected of promoting atherosclerosis were significantly higher in the severe weight gain group. Results of this study indicate that a weight gain of over 7 kilograms appears to be the critical level that is associated with health risks.
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PMID:[Health risk assessment of long-term weight history]. 213 52

A male to female ration of coronary disease of 2:1 has been a consistent finding. This differential persists event when the classic risk factors for coronary disease--hypertension, smoking, obesity, diabetes, and hyperlipidemia--are controlled for gender. The most likely ultimate cause of this phenomenon is male-female differences in sex hormone patterns. Clinical studies in this area have either compared the sex hormone profiles of men and women with and without coronary disease or computed the relative prevalence of disease in populations that differ in their sex hormone patterns. In general, research findings have disputed the hypothesis that persons with coronary disease have low levels of a protective factor such as estrogen or progesterone and high levels of testosterone. Coronary disease patients actually have elevated estrogen levels and low testosterone levels; endogenous progesterone levels are normal before infarction but show a stress-mediated increase in the immediate postinfarction period. Findings of a low prevalence of coronary disease in premenopausal women, a loss of protection after menopause, and a low prevalence of coronary disease in men with cirrhosis-related hyperestrogenemia suggest that natural estrogens are antiatherogenic. The protective effect of pregnancy against myocardial infarction, despite concomitant potentially thrombogenic levels of estrogen at the time, seems to indicate that progesterone, whose levels are also extremely high during pregnancy, plays a major anti-infarction protective effect distinct from that of estrogen. Studies of women oral contraceptive (OC) users and men taking estrogens for brief periods have found that these exogenous hormones produce coronary thrombosis but not atherosclerosis. Finally, the finding of increased coronary disease risk in long-term OC users indicates that synthetic estrogens favor coronary atherosclerosis by suppressing natural estrogen and progesterone production.
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PMID:Sex hormones and coronary disease: a review of the clinical studies. 223 42

The liver participates in the turnover rate of free fatty acids (FFA) with a third. A severe disruption of liver function that occurs in cirrhosis leads therefore to a pathogenetic relevant hyperlipacidaemia respectively increases that. With regard to its clinical relevance a survey is given of the FFA metabolism of the liver. The factors are described which influence the FFA uptake by this organ. In this connection the metabolic fate of the FFA in dependence on the hormonal nutritive state is depicted. The author deals with the relation of the hepatic FFA metabolism to that of triglycerides, cholesterol, ketone bodies, carbohydrates, amino acids and insulin. The importance of these relatons for the caloric homeostasis and for the pathogenesis of various acute and chronic functional disturbances (ketoacidosis, negative nitrogen-balance, hyperlipoproteinaemia, hyperinsulinism, atherosclerosis) is described.
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PMID:[The metabolism of free fatty acids in the liver]. 266 56

Cirrhosis is associated with several circulatory abnormalities. A hyperkinetic circulation characterized by increased cardiac output and decreased arterial pressure and peripheral resistance is typical. Despite this hyperkinetic circulation, some patients with alcoholic cirrhosis have subclinical cardiomyopathy with evidence of abnormal ventricular function unmasked by physiologic or pharmacologic stress. Florid congestive alcoholic cardiomyopathy develops in a small percentage, but the concurrent presence of cirrhosis seems to retard the occurrence of overt heart failure. Even nonalcoholic cirrhosis may be associated with latent cardiomyopathy, although overt heart failure is not observed. Tense ascites is associated with some cardiac compromise, and removing or mobilizing ascitic fluid by paracentesis or peritoneovenous shunting results in short-term increases in cardiac output. Cirrhosis also appears to be associated with a decreased risk of major coronary atherosclerosis and an increased risk of bacterial endocarditis. Small hemodynamically insignificant pericardial effusions may be seen in ascitic patients. The release of atrial natriuretic peptide appears to be unimpaired in cirrhosis, although the kidney may be hyporesponsive to its natriuretic effects.
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PMID:Cardiac abnormalities in liver cirrhosis. 269 Apr 63

Patterns of mortality among members of the Seneca Nation of Indians between January 1, 1955, and December 31, 1984, were investigated. The study cohort consisted of all members of the Seneca Nation residing in New York State who were listed in the tribal rolls as of January 1, 1955 (n = 3,262). Deaths among cohort members were identified through a computer match against New York State vital records files. Sex-specific standardized mortality ratios (SMRs) were calculated on the basis of mortality patterns exhibited by the general population of New York State, exclusive of New York City. Seneca Nation males demonstrated an excess of deaths from all causes (SMR = 124), while all-cause mortality among Seneca Nation females did not differ from that expected (SMR = 106). Both males and females exhibited excess mortality from infectious diseases, diabetes mellitus, cirrhosis of the liver, and accidents and injuries. Excess mortality was also noted among males for deaths due to atherosclerosis and hernia/intestinal obstruction and among females for deaths due to pneumonia, chronic nephritis, and homicide. Both sexes exhibited a deficit of deaths due to malignant neoplasms and circulatory diseases. Findings from this study will be useful to those responsible for the planning and implementation of health care programs among the Seneca Nation of Indians and other Native American groups.
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PMID:Mortality in a northeastern Native American cohort, 1955-1984. 292 27


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