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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intermittent electrical stimulation of the lateral hypothalamus of rats performed for 30 min to 6 hr, results in hyperlipidemia and endothelial cell damage of the aorta and coronary arteries. Hyperlipidemia is related to transient biliary obstruction elicited by hypothalamic stimulation and is characterized by elevation of the cholesterol, phospholipid, and triglyceride fractions. Endothelial cell damage is observed ultrastructurally as plasma membrane degeneration with detachment and the formation of large spaces ("vacuoles"). Thus, neural factors may be implicated in inducing conditions associated with early atherogenesis. Stimulation carried out for longer time intervals would be expected to produce more advanced lesions. However, the role of neural transmission per se (i.e., without hyperlipidemia) in producing arteriopathy is not clearly defined from these experiments. In rats, the lesser splanchnic nerve forms the major innervation of the abdominal aorta. In animals fed normal diets, chronic intermittent stimulation of this nerve (up to 3 weeks) resulted in advanced arteriosclerotic changes with intimal fibrosis and calcification. On histologic examination, lipid deposits appeared to be absent from these lesions. Animals stimulated for shorter periods of time exhibited earlier changes associated with atherogenesis, such as endothelial damage, elastic reduplication, and adherent microthrombi. Thus, direct neural transmission, especially if excessive, plays a role in producing arteriopathy. Hyperlipidemia, if persistent, could modify these lesions so that they would accumulate plasma lipids. Experiments to test this hypothesis are currently in progress.
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PMID:Neural factors in experimental degenerative arteriopathy. 20 81

An association between atherosclerosis, biliary obstruction and hyperlipidemia has been reported in the literature. In previous study from this laboratory, ultrastructural evidence of coronary artery endothelial damage was obtained in rats following ligation-induced biliary obstruction. In the present investigation, serum bile acids, total cholesterol and alkaline phosphatase levels were studied in association with similarly induced biliary obstruction and related to electron-microscopic observations of coronary artery endothelium. The results disclosed marked elevation of all serum parameters in as short a time as 24 hr following ligation compared with shamoperated controls. Animals exhibiting increases of serum bile acids and cholesterol also revealed severe configurational changes of endothelial cells which manifesed as buckling, detachment from the underlying internal elastic lamina, and vacuole formation. The role of elevated circulating bile acids and hypercholesterolemia as possible factors in producing arterial injury through membrane interaction is discussed. These observations suggest that biliary obstruction, even of short duration, may act as a potentially atherogenic mechanism in the experimental animal.
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PMID:Endothelial injury. Association with elevations of serum bile acid and cholesterol concentration in biliary-obstructed rats. 113 4

A 44-year-old man with uncontrolled diabetes and chronic pancreatitis presented with abdominal pain, jaundice and unintentional weight loss. Laboratory investigations were significant for hyponatraemia, an obstructive pattern of liver enzymes. Imaging was consistent with intrahepatic and extrahepatic biliary obstruction, and endoscopic evaluation revealed a long common bile duct stricture. Intravascular volume depletion, beer potomania and syndrome of inappropriate antidiuretic hormone (with concern for biliary or pancreatic malignancy) were considered in the work-up for the aetiology of the hyponatraemia. After 4 days of conventional treatment, hyponatraemia persisted. Lipid panel obtained revealed very high levels of total cholesterol. The patient underwent a successful biliary diversion and reconstruction surgery. Follow-up after 3 months showed a clinically stable patient with resolution of elevated liver enzymes, hyperlipidaemia and hyponatraemia. We illustrate this rare case of hyponatraemia secondary to hyperlipidaemia in obstructive biliary cholestasis. It is important for physicians to thoroughly investigate the aetiology of hyponatraemia at its onset.
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PMID:Pseudohyponatraemia secondary to hyperlipidaemia in obstructive jaundice. 2919 8