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Query: UMLS:C0004153 (atherosclerosis)
 77,401 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

In a brief review the author presents selected results of endocrinological research, published in 1989 to 1990. In the sphere of peptide hormones he mentions findings on the reduced level of the endothelial relaxation factor in the blood stream in atherosclerosis, the classification of endothelin with neuropeptides and the existence of a vasopressin antagonist which causes polyuria after operations of the hypothalamus. Hybrid hormones (biotechnologically prepared combined molecules), mammastatins (inhibitors of proliferation of mammary cell cultures lacking in transformed cultures) and adipsin (a peptide factor lacking in some types of experimental obesity) are other recent advances. Findings on endogenous benzodiazepine substances (occupying receptors for diazepines) and of an endogeneous factor for receptors for tetrahydrocanabinols supplement the contemporary picture. Adrenocortex stimulating immunoglobulins may be the cause of hyperplasia of the adrenal cortex, similarly as TSI is the cause of Graves-Basedow's disease. In the latter evidence of a retroviral aetiology was provided.
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PMID:[Endocrinology 1989-1990]. 207 Mar 86

The majority of cases of central diabetes insipidus are still pathogenetically unclear (idiopathic). Atherosclerotic cholesterol emboli might be partly responsible for some of these idiopathic cases. A 54-year-old woman with known aortic valve stenosis and a history of a transitory ischemic attack presented with sudden-onset polyuria and polydipsia of up to eight l/d, which had started acutely with headaches. She had been treated with lithium for 3 years because of cyclothymic depression. Plasma sodium was in the upper normal range (142-148 mmol/l). Hypertonic saline infusion during lithium therapy revealed a normal threshold of thirst and resetting of vasopressin secretion (osmotic threshold > 300 mosmol/l), whereas vasopressin reserve was normal. Lithium withdrawal led to an even greater delay of vasopressin release upon hypertonic saline infusion (> 310 mosmol/l). Pituitary function tests revealed a normal anterior pituitary function. MR imaging of the hypothalamo-hypophyseal region showed a normal hypothalamic region and a highly intensive neurohypophyseal signal in the T1-weighted image. The patient responded well to desmopressin. We suggest that in this rare case clinical symptoms as well as biochemical findings like impairment of AVP release might be related to a minor structural hypothalamic damage by a vascular lesion, caused, for example, by an atheromatous (cholesterol) embolism in the hypothalamic region responsible for integration of osmoreceptor function and AVP-secretion. The patient's atherosclerosis and aortic stenosis might be responsible for this event.
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PMID:Atherosclerosis, aortic stenosis and sudden onset central diabetes insipidus. 928 11

Many studies, both national and international, have shown that tea has protective effects on many chronic diseases and their risk factors. In cancer prevention, our studies indicated that tea drinking could inhibit the carcinogenicity of various chemical carcinogens, including oral tumors induced by 7,12-dimethylbenz[a]anthracene (DMBA) in Golden hamsters, esophageal tumors in rats by blocking in vivo synthesis of N-Nitroso-methylbenzylamine (NMBzA), esophageal cancer induced by NMBzA in rats, precancerous liver lesions (r-GT and GST-P) induced by diethylnitrosamine (DENA) in rats, intestinal preneoplastic lesion (ACF) and intestinal tumors induced by 1,2-dimethyl-hydrazine (DMH) in rats, lung carcinoma induced by nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK) in A/J mice. Our studies have also shown that the protective effects of tea against cancer is a combined effects of various tea ingredients, among which the major ones are polyphenols and tea pigments. Based on animal studies, antioxidant properties, protection against DNA damage and modulation of immune functions were found to be the main mechanisms of anticancer effects of tea. In human trials, tea drinking showed protective effects against oxidative damage and DNA damage caused by cigarette smoking. Mixed tea drinking significantly blocked lesion progress in patients with oral mucosa leukoplakia, therefore, demonstrated its protective effects on oral cancer. Our studies have also shown effects of tea on prevention of cardiovascular diseases (CVD). For example, tea pigments was found to significantly inhibit LDL oxidation induced by Cu2+, Fe2+ in in vitro studies. In vivo studies showed that tea could prevent blood coagulation, facilitate fibrinogen dissolution, inhibit platelet aggregation, lower endothelin levels, enhance GSH-Px activities, protect against oxidated LDL-induced damage in endothelium cells, and prevent atherosclerosis of coronary arteries. The mechanisms of these protective effects of tea are possibly related to its antioxidant properties or its inhibition of lipid oxidation. Green tea and pigments was also found to inhibit cardiac hypertrophy induced by renal hypertension in rat models, whose mechanisms might, at least partly, involve its modulation on nitric oxide, angiotensin II and endothelin-1. Clinical intervention trials have indicated that tea and tea extracts decreased blood lipid, improved blood flow of coronary artery, and played an important role in atherosis inhibition and prevention. Our studies also showed that tea drinking has protective effects on diabetes. White tea drinking could significantly relieve symptoms including polyuria, polydipsia, polyphagia and weight loss in diabetic mice, decrease fasting plasma glucose level and improve glucose tolerance. In human trial, continuous white tea drinking could significantly improve symptoms of diabetic patients, such as relieve polydipsia, decrease plasma glucose levels, both fasting and 2 hours after meal, and increase insulin secretion. The effective rate for glucose lowering is 48% in clinical study.
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PMID:[Studies on tea and health]. 2227 81