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Results for “HYPERLIPEMIA”

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At least 91 records · Page 5Linked to original sources
PubMed1984

Factitious methemoglobinemia caused by hyperlipemia.

Hyperlipemia in an acyanotic patient with diabetic ketoacidosis, alcoholism, and pancreatitis produced a falsely elevated concentration of methemoglobin (19 percent) and a lower-than-expected oxygen saturation measured with an automated spectrophotometer (IL-282 CO-Oximeter). In addition, there was a "normal" hemoglobin level despite a low hematocrit reading. In vitro studies showed that hyperlipemia corresponding to triglyceride levels of 500 mg/100 ml and greater produced erroneously high values for methemoglobin and total hemoglobin and "negative" values for carboxyhemoglobin. These abnormalities disappeared when the excessive lipids were removed by washing the erythrocytes in physiologic saline solution.

Adult↗
PubMed1999

[Preventing and treating effect of total oil of Microula sikkimensis (Hemsl.) on experimental hyperlipemia in rats].

OBJECTIVE: To study the effect of the total oil of Microula sikkimensis on an experimental hyperlipemia model of rat. METHOD: Using feeding method to set up the experimental hyperlipemia model and determining the biochemical criteria. RESULT: The total oil of Microula sikkimensis significantly decreased the contents of cholesterol, triglyceride and MDA in blood serum, and increased the rate between total cholesterol and high density lipoprotein. CONCLUSION: The study provides an important basis for exploiting and utilizing the total oil of Microula sikkimensis.

Animals↗
PubMed2004

[Effect of API 0134 on platelet membrane glycoprotein expression in patients with hyperlipemia].

OBJECTIVE: By observing the effect of API 0134, an active ingredient of green chiretta, on platelet membrane glycoprotein (GP) in patients with hyperlipemia to explore the mechanism of the anti-platelet aggregation effect of API. METHODS: The mean immunofluorescent intensity (MFI) of the platelet membrane glycoprotein GP II b/III a, GPIb, P-selectin (GMP-140) and von Willebrand's factor (vWF) in resting platelet, activated platelet (untreated or treated with API 0134 of different concentrations) were detected in 30 randomly selected patients with hyperlipemia, using immunofluorescent marker and flow cytometry. RESULTS: API of all concentrations (25 mg/L, 50 mg/L and 100 mg/L) could significantly decrease the MFI of GP II b/III a in a positive dose-dependent manner, as compared with that in activated platelet untreated with API; API of 50 mg/L and 100 mg/L could also reduce the MFI of GMP-140 and vWF in activated platelet (P < 0.01); but API of 100 mg/L showed insignificant influence on GPIb expression in activated platelet membrane. CONCLUSION: API 0134 exerts obvious anti-platelet GP II b/III a effect on activated platelets, middle or large dose of API also shows inhibiting effect on GMP-140 and vWF expression in platelet.

Aged↗
PubMed2005

[Effects of Qilan Tangzhining capsule on glucose and lipid metabolism in rats with diabetes mellitus and hyperlipemia].

OBJECTIVE: To study the effects of Qilan Tangzhining capsule on glucose and lipid metabolism in diabetes mellitus and hyperlipemia. METHOD: Rats were fed with high sugar and fat food for 2 months, then 2% streptozocin (STZ, 30 mg kg(-1)) was injected intraperitoneally to induce hyperglycemia and hyperlipemia. After the model rats were administrated drugs, the blood glucose, the serum lipids, and the histopathology of the liver and pancreas were observed. RESULT: Qilan Tangzhining capsule could decrease the FBG and the serum TC, TG, LDL-C, increase HDL-C, and improve the histopathologic injury of the liver and pancreas. CONCLUSION: Qilan Tangzhining capsule can not only adjust the blood glucose and lipid, but also improve the histopathology injury of the liver and pancreas.

Animals↗
PubMed2005

Effects of medicinal cake-separated moxibustion on plasma 6-keto-PGF1alpha and TXB2 contents in the rabbit of hyperlipemia.

Hyperlipemia rabbit models established with high cholesterol and fat diet were treated with direct moxibustion and medicinal cake-separated moxibustion. The post-treatment plasma 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) and thromboxane B2 (TXB2) contents were determined by radioimmunoassay. Results indicated that the plasma 6-keto-PGF1alpha content significantly increased, the TXB2 level decreased (P < 0.05) and the TXB2 /6-keto-PGF1alpha ratio also decreased (P < 0.01) in the medicinal cake-separated moxibustion group as compared with those in the model group respectively, but there was no significant difference between the medicinal cake-separated moxibustion group and the direct moxibustion group (P > 0.05), suggesting that both the medicinal cake-separated moxibustion and direct moxibustion can regulate the plasma 6-keto-PGF1alpha and TXB2 contents, and the TXB2/6-keto-PGF1alpha ratio with similar actions, and have a certain protective action on endothelial cells of the aorta in the rabbit of hyperlipemia.

6-Ketoprostaglandin F1 alpha↗
PubMed1976

[Hyperlipemia and diabetes].

There are several causes for hyperlipemia in the diabetic: (a) an increase in hepatic synthesis of prebetalipoproteins, and (b) reduced elimination of prebetalipoproteins and chylomicrons from the bloodstream, due to diminished activity of lipoprotein lipase in insulin deficiency. The role of heredity has been put in doubt by the observation that diabetes and hypertriglyceridemia are not transmitted by the same genetic factor. The shortterm and longterm implications of diabetic hyperlipemia are discussed, together with the treatment.

Chylomicrons↗
PubMedDate not supplied

[Hyperlipemia and lipoprotein blood spectrum of rabbits of different age with administration of cholesterol].

Hyperlipemia developing in impuberal, young and old rabbits with administered cholesterol is characterized by a considerable prevailence of the cholesterol level over the triglyceride one. The degree of shifts in lipids depends on the age, it is most pronounced in old animals and the least pronounced in impuberal ones. The amount of blood serum cholesterol bound with lipoproteids of high density lowers and most considerably in old rabbits. Separation of blood serum lipoproteids by electrophoresis in polyacrylamide gel detects in rabbits with hyperlipemia a sharp decrease as compared to the norm in the intensity of alpha-lipoproteids disc. This decrease is most pronounced in animals of older age groups. The presence of the intermediate fraction between pre-beta- and beta-lipoproteids is also found in the same animal by the separation especially often in old animals.

Aging↗
PubMed1978

The hypotriglyceridemic effect of chenodeoxycholic acid in type IV hyperlipemia.

The effect of chenodeoxycholic acid on the fasting serum triglycerides was studied in 30 patients with type IV hyperlipemia and in 20 patients with primary gout and associated endogenous hypertriglyceridemia, the triglycerides being determined before treatment and at monthly intervals for three months. Chenodeoxycholic acid treatment resulted in a significant lowering of the serum triglycerides in both groups of patients. The drug was well tolerated and there were no undesirable side-effects. Although the mechanism of action is still not known, the drug is thought to reduce triglyceride synthesis in the liver. Chenodeoxycholic acid appears to be electively indicated in type IV hyperlipemia treatment.

Adult↗
PubMed1990

[Effect of a mixture of Acanthopanax senticosus and Elsholtzia splendens on serum-lipids in patients with hyperlipemia].

The serum-lipids were determined in 31 hyperlipemia patients before and after treated with the mixture of Acanthopanax senticosus and Elscholtzia splendens. While the mean value of serum beta-lipoprotein decreased from 902 +/- 228 mg/dl to 608 +/- 189 mg/dl (P less than 0.001), the mean value of HDL-C increased from 52.6 +/- 12.5 mg/dl to 61.2 +/- 15.4 mg/dl (P less than 0.001). Thus the ratios of HDL-C to total cholesterol (HDL-C/TC) and to LDL-C (HDL-C/LDL-C) increased significantly, the arteriosclerosis index (AI) decreased significantly. The results indicate that the mixture of Acanthopanax senticosus and Elsholtzia splendens could improve the lipid-metabolism in hyperlipemia patients so that it might play a good role in preventing or alleviating arteriosclerosis.

Cholesterol↗
PubMed1989

[Alcohol-induced hyperlipemia. Hypertension and extreme hypercholesterolemia/hypertriglyceridemia in a patient with hidden alcohol abuse].

The article presents the case history of a 28 year-old male with alcohol-induced hypertension and extreme hypercholesterolemia (36 mmol/l) and hypertriglyceridemia (76 mmol/l). Blood pressure and blood lipids were completely normalized after a few months withdrawal from alcohol. Alcoholism is emphasized as a possible differential diagnosis for both hypertension and hyperlipemias. The upper referential value for alcoholic hyperlipemia should probably be adjusted in accordance with the values observed in the present case.

Adult↗
PubMedDate not supplied

Effects of SF-482 on bile, gallstones formation and experimental hyperlipemias.

The effects of 3 alpha, 7 beta-dihydroxy-12-cheto-cholan-24-oic acid (SF-482) were compared with those of ursodeoxycholic acid on bile flow and composition, on gallstones formation and on experimental hyperlipemias. SF-482, like ursodeoxycholic acid, increases the bile flow and residue in normal and ethynylestradiol-treated rats. The two compounds increase the biliary excretion of bile acids and phospholipids with a desaturation of bile cholesterol. SF-482 and ursodeoxycholic acid decrease the incidence of gallstones in mice; both compounds are active in Triton WR-1339, in olive oil and margarine hyperlipemias in rats and in ethanol intoxication in mice. In general, SF-482 is more active than ursodeoxycholic acid.

Alcoholic Intoxication↗
PubMed1987

A study of atherosclerotic lesion development in the injured pulmonary arteries of dogs with induced hyperlipemia.

Studies of experimental atherosclerosis in the dog demonstrate that many months at plasma cholesterol concentrations greater than 750 mg/dl are required to produce lipid containing atherosclerotic lesions. Since it has been recognized for many years that vascular injury in combination with hyperlipemia will result in rapid formation of atherosclerotic lesions, we attempted to combine vascular injury with hyperlipemia as a means of accelerating this process in the dog. Injury was produced in pulmonary arteries with experimental Dirofilaria immitis (DI or heartworm) infection. This filarial parasite produces characteristic lipid-free lesions containing smooth muscle cells and occasional monocytes and collagen. Plasma cholesterol was increased by feeding 10 dogs an essential fatty acid-deficient diet (EFAD) for 90 days. Five of the EFAD dogs were infected with 30 to 31 adult DI worms to produce pulmonary artery injury. The remaining 5 EFAD dogs were not subjected to any form of vascular injury. An additional 5 control dogs were not subjected to vascular injury nor to the EFAD diet. The arteries of dogs infected with DI developed myointimal proliferative lesions which contained smooth muscle cells and macrophages. In addition, the EFAD diet produced significant elevations in LDL but not VLDL plasma cholesterol in all 10 dogs fed the diet. However, the plasma cholesterol was less than 750 mg/dl in all EFAD-fed dogs. Although smooth muscle cells and macrophages in the pulmonary arteries of DI-infected dogs were focal points for lipid accumulation, cholesterol content of these injured arteries was not increased compared to noninjured EFAD dogs. The results suggest that even severe vascular injury does not reduce the threshold of 750 mg/dl required to produce significant lipid accumulation in canine arteries.

Animals↗
PubMed1979

[Grawitz's tumor and provoked hyperlipemia (author's transl)].

After reporting a case of a patient aged 69 years with an inoperable hypernephroma, in whom the presence of a polycythemia and a reduction in the provoked hyperlipemia curve was found to co-exist, the authors review the data in the published literature on the influence on the small intestine of cancers other than those in the gastro-intestinal system. Basing their comments on studies of hypernephromas, they stress that a reduction or delay in the hyperlipemia curve was found in 23 out of 28 patients. This abnormality can only be explained by hypotheses at the present time.

Adenocarcinoma↗
PubMed1979

[Pancreatitis and hyperlipemia].

Hyperlipemia was revealed in 3 of 26 patients who died from an acute destructive pancreatitis. The level of lipids was as high as 2000--5000 mg%. Hyperlipemia when combined with destructive pancreatitis should be considered to be a poor prognostic sign.

Adult↗
PubMed1981

[Etiologic mechanisms of carbohydrate-induced hyperlipemia].

Experiments on rats with hyperlipemia induced by carbohydrates have been shown that synthesis of apoprotein B by the liver and its relative content in very low-density proteins (VLDP) of the liver and blood increase. This is accompanied by accelerated metabolism of C-III in blood VLDP and by hyperinsulinemia suggesting that hyperinsulinemia may be regarded as one of the mechanisms by which there occurs hyperlipemia under high carbohydrate diets.

Animals↗
PubMedDate not supplied

[Carbohydrate metabolism and endogenous hyperlipemia].

The state of carbohydrate metabolism was studied under conditions of endogenous hyperlipemia induced by triton WR-1339. The data obtained testify to the fact that administration of triton WR-1339 to experimental animals intensifies lipogenesis from carbohydrates, that is confirmed by a decrease in the glycogen amount in the liver and by an activation of the pentose-phosphate pathway of carbohydrate oxidation which is important for cells intensely synthetizing fatty acids. Thus, there is a relation between disturbances in carbohydrate metabolism and development of hyperlipemia induced by the triton.

Animals↗
PubMed1980

Studies on the etiology of the hyperlipemia in rats fed an atherogenic diet.

The etiology of the hyperlipemia which occurs in cholesterol- and fat-fed hypothyroid rats was investigated. In hyperlipemic rats the disappearance rate of 125I-labeled chylomicron remnants was markedly prolonged (t1/2 of 13.1 +/- 0.9 min versus t1/2 of 2.1 +/- 0.5 min in controls). However the ability of isolated livers from these rats to remove remnants was not significantly different from that of control livers. This suggested that the delay in removal was due to an increase in the circulating remnant concentration without a removal defect. 125I-labeled VLDL from hyperlipemic rats was removed by isolated livers from normal rats at a rate similar to normal chylomicrons or hepatic VLDL and more slowly than normal remnants. This suggested that remnants were not the principal constituents of the VLDL in these animals. Moreover when these VLDL were injected into intact normal rats they were removed with a t1/2 (5.5 +/- 1.2 min) comparable to normal VLDL rather than remnants. Finally, livers from hyperlipemic rats were perfused and the composition of the VLDL secreted was examined Compared to controls or animals fed propylthiouracil, these livers secreted a particle which was triglyceride-poor and cholesteryl ester-rich. Thus, the etiology of the hyperlipemia has several components. There is both expansion of the remnant pool and secretion of an abnormal lipoprotein.

Animals↗