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Results for “HYPERCHOLESTEREMIA”

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At least 19 recordsLinked to original sources
PubMed1996

[Effect of hypercholesteremia on vascular endothelial function and albumin excretion rate in patients with diabetes mellitus].

Tissue-type plasminogen activator (tPA) is an endothelium-derived vasoactive substance which is released to the blood stream by exercise, blood occlusion, and desmopressin (DDAVP). The increased capacity of the plasma tPA level raised by these factors is thought to reflect in vivo endothelial function. On the other hand, endothelial dysfunction has been reported in patients with hypercholesteremia as well as in those with diabetes mellitus. Therefore, diabetic patients with hypercholesteremia were administered 5 mg of simvastatin daily for one month and plasma tPA responses evoked by DDAVP were examined before and after treatment for hypercholesteremia. While the treatment of simvastatin for one month significantly reduced serum cholesterol levels from 257 +/- 12 mg to 206 +/- 10 mg (no change in HbA1c was observed during the study), plasma tPA levels and % delta vWF (von Willebrand factor) following DDAVP infusion significantly increased from 11.4 +/- 1.2 ng/ml to 13.4 +/- 1.4 ng/ml and from 69.3 +/- 23.4% to 126.5 +/- 47.4%, respectively. However, neither increase in plasma levels of guanosine 3', 5'-cyclic monophosphate (cGMP) nor change in the depressive response of blood pressure was observed following DDAVP infusion after the treatment of simvastatin. In addition, no change in urinary albumin excretion rate was observed with the treatment of hypercholesteremia. Therefore, it was suggested that improvement in hypercholesteremia may ameliorate vascular endothelial dysfunction in diabetic patients with hypercholesteremia and that hypercholesteremia may enhance endothelial dysfunction in these patients.

Albuminuria↗
PubMed1976

Cholesterol contents of various tissues of chickens with exogenous or endogenous hypercholesteremia.

Cholesterol contents of 16 different tissues were determined in 12 normal roosters, 12 roosters with diet-induced, exogenous hypercholesteremia, 10 actively laying hens with minimal endogenous hypercholesteremia, and 12 nonlaying hens with hereditable extreme hyperlipidemia. The tissue cholesterol contents of the normal roosters were strikingly similar to that of the corresponding tissues of the mammals except for a low cholesterol content of the brain in chickens. The hypercholesteremia in the roosters fed a 2% cholesterol diet for 2 months was associated with an increase of cholesterol content in all tissues except the brain, muscle, and adipose tissue. The actively laying hens, on the other hand, had a decreased cholesterol content in most tissues, despite the persistence of a minimal hypercholesteremia for 18 months and significant aortic cholesterol accumulation with mild atherosclerosis. The nonlaying hens developed extreme hypercholesteremia and severe atherosclerosis but only a moderately expanded cholesterol pool in most tissues. The results indicated a remarkable difference in tissue response to diet-induced exogenous hypercholesteremia and endogenous hyperlipidemia associated with laying activity in chickens and the propensity of their aortas to accumulate excessive cholesterol in the presence of either endogenous or exogenous hyperlipidemia.

Animals↗
PubMed2005

[Effect of chronic enhanced external counterpulsation on arterial endothelial cells of porcine with hypercholesteremia].

OBJECTIVE: To verify whether chronic enhanced external counterpulsation (EECP) may repair artery endothelial cells (ECs) damage resulted from hypercholesteremia in pigs. METHODS: EECP was performed for 36 hours in pigs with hypercholesteremia and the left descending artery (LDA) was isolated for scanning electron microscopy (SEM). The ECs were collected from the thoracic aorta and analyzed by proteomic technique. RESULTS: The ECs of hypercholesteremia pigs showed irregular arrangement with obvious desquamation of coronary ECs and formation of atherosclerotic plaque, and these lesions were milder in EECP-treated pigs. Six over-expressed proteins were detected in the endothelial cells in EECP-treated pigs in comparison with those of the hypercholesteremia pigs. CONCLUSION: Chronic EECP helps restore cell morphology and repair functional damage of ECs resulted from hypercholesteremia by regulating endothelial protein expressions, and consequently improves cell adhesion and intracellular metabolism and reduces EC apoptosis.

Animals↗
PubMed2001

[Rat hearing loss and hearing organs mitochondrial DNA4834 deletions associated with hypercholesteremia].

OBJECTIVE: To determine whether or not the rat hypercholesteremia contributes to hearing organs mtDNA4834 deletion and involves in the development of hearing loss. METHODS: The rat hypercholesteremia model (n = 38) was established by feeding with high cholesterol diet and the control group (n = 22) with common diet for 6 months. The rats were tested for auditory sensitivity using auditory brainstem response (ABR). Twenty-one left cochleae and 27 left cochlear nuclei from experimental group and 10 left cochleae and 13 left cochlear nuclei from control group were harvested. The total DNA of them was extracted. mtDNA was amplified by nest PCR to examine the presence of mtDNA4834 deletion. RESULTS: Our result showed: (1) There is a significant increase in serum cholesterol level and ABR threshold in the experimental group. (2) The mitochondrially-encoded tRNA and ND1 segments were amplified from all samples, as well as mtDNA4834 deletions. (3) The incidence of mtDNA4834 deletions in hearing organs of hypercholesteremia rats was significantly higher than that of the control group (P < 0.05). CONCLUSION: Extended hypercholesteremia can induce hearing loss, and mtDNA4834 deletion in hearing organs may be one of the pathogenic mechanisms.

Animals↗
PubMed1952

Observations concerning the production and excretion of cholesterol in mammals. V. The relation of biliary retention of cholesterol, distention of the biliary tract, the shunting of bile to the vena cava, and the removal of the gastro-intestinal tract to the hypercholesteremia consequent on biliary obstruction.

Plasma cholesterol was observed to fall after release of biliary obstruction without any concurrent change in biliary excretion of cholesterol. Excision of the nerve trunks accompanying the hepatic artery did not change the degree of hypercholesteremia following biliary obstruction. No significant change in the cholesterol content of hepatic tissue occurred following biliary obstruction. Animals with gastro-intestinal systems removed exhibited no significant change in plasma cholesterol, whereas those subjected to gastro-intestinal removal plus biliary obstruction exhibited a marked hypercholesteremia. Anastomosis of the bile duct to the inferior vena cava resulted in a hypercholesteremia similar to that occurring after obstruction of the bile duct.

Animals↗
PubMed1983

Effects of hypertension and hypercholesteremia on the permeability of fibrinogen and low density lipoprotein in the coronary artery of rabbits. Immunoelectron-microscopic study.

In an attempt to elucidate the effects of hypertension and/or hypercholesteremia on atherogenesis, with special reference to permeation and deposition of fibrinogen and low density lipoprotein (LDL) in the coronary artery, we studied electron-microscopically the localization of fibrinogen and LDL. In the untreated control rabbits, fibrinogen was localized in the caveolae and vesicles of the endothelial cells and in very small amounts in the subendothelial spaces of the coronary artery. Hypertension or hypercholesteremia was related to an enhanced insudation of fibrinogen into the subendothelial spaces of the coronary artery. The insudation of fibrinogen seemed to have occurred by way of vesicular transport and, to some extent, by junctional transport. LDL was localized only in the caveolae and vesicles of the endothelial cells of the coronary artery in the untreated control rabbits. LDL was deposited in the subendothelial space of the hypercholesteremic rabbits, with or without hypertension. Despite the lack of clear-cut and direct evidence, the insudation of LDL into the intima appeared to be enhanced by way of vesicular transport.

Animals↗
PubMed1953

The mechanism responsible for the hypercholesteremia induced by triton WR-1339.

Injection of triton WR-1339 into rats leads to a rapid increase in the cholesterol, cholate, and various lipid fractions of their blood. The increase in cholesterol is confined to the blood itself. The cholesteremic effect of triton was not dependent upon a prior accumulation of cholate in plasma. The liver was found to be the source of the excess cholesterol but the rate of cholesterol synthesis, the excretion of cholate, and the cholesterol content of the liver were not changed by injection of triton. The cholesteremic effect of triton is not due to alteration in the intestinal excretion of cholesterol. Transfer of blood between "tritonized" and normal rats leads to a disappearance of the hypercholesteremia in the former and its appearance in the latter animals. The plasma proteins of rats injected with triton are markedly changed qualitatively. Heparin was found to inhibit the hypercholesteremic effect of triton. The hypercholesteremia following triton injection appears to be due to a fundamental physicochemical change in the plasma proteins produced by injection of this detergent.

Animals↗
PubMed1979

Inhibition of host resistance by nutritional hypercholesteremia.

Previous experiments showed that nutritionally induced hypercholesteremia in mice caused an increase in susceptibility to coxsackievirus B, with a marked suppression of cellular infiltrates in infected tissues and an increased mortality. The present studies demonstrated that a hypercholesteremic diet was associated with an inhibition in host resistance as measured by susceptibility to Listeria monocytogenes infection and the growth of two transplanted syngeneic murine tumors. Moreover, the ability of Corynebacterium parvum to induce regression of a transplanted methylcholanthrene-induced fibrosarcoma was inhibited in hypercholesteremic hosts, as was the histiocytic infiltration normally accompanying C. parvum inoculation. In contrast, the peritoneal macrophages from C. parvum-treated hypercholesteremic mice were indistinguishable from similarly treated macrophages from normal mice with respect to their in vitro tumoricidal activity and the presence of a cell surface antigen associated with activated macrophages. Hypercholesteremia was also associated with a decreased antibody response to sheep erythrocytes in vivo, but dit not appear to exert a detrimental effect on B- or T-cell blastogenesis when tested in vitro. The findings that the hypercholesteremic diet was associated with an impairment in the host immune response and increased susceptibility to viral, bacterial, and tumor cell challenge are discussed with respect to virus-lipid interactions in the pathogenesis of atherogenesis and diabetes mellitus.

Animals↗
PubMed1975

Youthful hypercholesteremia: its associated characteristics and role in premature myocardial infarction.

Hypercholesteremic medical students were different from their normocholesteremic classmates in a variety of ways. When students are grouped by cholesterol level in medical school, gradients across the means of biological, physiological, physical, and psychological characteristics are found. The hypercholesteremic students were older, shorter, and heavier, with younger mothers, less depression, less anxiety and less overall nervous tension under stress. Compared with their normocholesteremic classmates, youthful hypercholesteremics were more than 30 times as susceptible to episodes of acute myocardial infarction occurring 13 to 21 years after the high cholesterol levels were measured. Ten male medical students who subsequently sustained a myocardial infarction, most of whom were known to have had hypercholesteremia in youth, were significantly different at the outset from their 103 hypercholesteremic classmates who have not had such an episode. On the average, the precoronary individuals in medical school were shorter in stature, were older, had more overall nervous tension under stress, were more tired on awakening and had lower academic standing. The combination of hypercholesteremia and a personality profile denoting sensitivity and vulnerability to stress best characterizes this group of ten subjects who sustained a myocardial infarction at an early age. These findings suggest that it may be possible to differentiate young hypercholesteremics who are highly susceptible to myocardial infarction from their hypercholesteremic peers with relatively low susceptibility on the basis of personality profile.

Adult↗
PubMed2002

[Comparative analysis of calcium accumulation in tissues of the brain and the liver in alimentary hypercholesteremia].

Some mechanisms of changing calcium content in brain and liver at alimentary hypercholesteremia were studied. Dynamics of calcium accumulation in tissues of the organs under exploration has proved its contribution to an adaptive reaction of the organism at alimentary stress and reflected peculiarities of its different stages. Similar and simultaneous dynamic changes in calcium accumulation in both organs (liver and brain) seem to be induced by stereotypical pathogenic mechanisms. The results contribute much to the current ideas of the pathogenesis of alimentar hypercholesteremia.

Animals↗
PubMedDate not supplied

Investigation of the role of prolonged emotional stress in the genesis of hypercholesteremia and hypertension.

In experiments on freely moving rabbits, exposed to prolonged (for 2 h) interrupted stimulation of negative emotiogenic zones of the hypothalamus through implanted electrodes daily for 4 months, the development of a lasting endogenous hypercholesteremia and of a mild but lasting hypertension was observed. Changes in the cholesterol concentration were greater if stimulation continued in conjunction with daily feeding of the rabbits with small doses of methylthiouracil.

Animals↗