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B Lorentzen

Publications and source records attributed to B Lorentzen.

15 recordsLinked to original sources
PubMed1998

Plasma lipids and vascular dysfunction in preeclampsia.

The dominating hypothesis of the preeclampsia syndrome (PES) is that placentally derived factors are released to the maternal circulation. These factors are believed to alter endothelial properties resulting in disturbed vasomotor function, increased endothelial permeability, and activation of thrombogenic factors. However, the impact of placentally derived factors on the endothelial cells is influenced by another major variable: the "sensitivity" of the maternal endothelium to the placental factors. Several maternal factors may play a role in determining this sensitivity. They include chronic hypertension, diabetes, and hyperlipidemia. In this article we discuss the possible role of hyperlipidemia (especially high free fatty acids and hypertriglyceridemia) in the pathogenesis of preeclampsia, viewed from this perspective. Pregnancy in general, preeclamptic pregnancy in particular, is associated with a marked hyperlipidemia. We suggest a parallel to atherosclerotic diseases, wherein hyperlipidemia induces endothelial dysfunction, probably by promoting oxidative stress in the arterial wall. The hyperlipidemia of pregnancy may have a similar effect on the endothelial cells. When placentally derived endothelial disturbing factors, like lipid peroxides and trophoblastic components, are released into the maternal circulation, their effects on the endothelium may be enhanced because of hyperlipidemia-mediated activation or "sensitization" of the endothelial cells. Alternatively, placentally derived factors like peroxides may combine with lipoproteins, forming complexes that are more disturbing to cells than the placental factors or lipoproteins are individually. We also discuss the possible role of maternal hyperlipidemia in aggravating placental insufficiency caused by poorly transformed spiral arteries. The hemodynamic flow pattern may be markedly different in completely and incompletely transformed spiral arteries. By analogy to the fundamental role of hemodynamic factors in development of atherosclerosis, we pose the hypothesis that abnormally transformed spiral arteries have an "atherogenic" blood flow pattern that promotes lipid deposition and "acute atherosis".

Arteriosclerosis↗
PubMed1998

Glucose intolerance in women with preeclampsia.

BACKGROUND: We have previously shown that women with proteinuric hypertension of pregnancy (preeclampsia) have increased circulating levels of triglycerides and free fatty acids. Preeclampsia has, therefore, several features in common with the insulin resistance syndrome. The objective of the present study was to investigate the glucose tolerance and insulin response of women with preeclampsia compared to women with normal pregnancy. METHODS: Oral glucose tolerance test was performed in ten women with preeclampsia and eight healthy women with normal pregnancy. The glucose, insulin, C-peptide and free fatty acid responses were calculated. RESULTS: The mean fasting glucose concentration was significantly lower in preeclamptic women (3.3 vs 3.7 mmol/l; p = 0.02). Fasting serum triglycerides were increased in women with preeclampsia compared to normal pregnancy (3.3 vs 1.9 mmol/l; p = 0.003). Women with preeclampsia had also increased serum free fatty acids, 0.52 vs 0.36 mmol/l for normal pregnancy; p = 0.056). Log s-insulin and cholesterol were not different. The incremental area under the curve for the glucose (p = 0.001) and insulin (p = 0.02) responses to oral glucose tolerance test showed higher values for preeclampsia as compared to women with normal pregnancy. For free fatty acids the total area under the suppression curve was higher in women with preeclampsia (p = 0.03). CONCLUSIONS: These results support the concept that preeclampsia is associated with metabolic aberrations found in insulin resistance syndrome.

Adult↗
PubMed1996

Thrombin-inhibitor complexes in the blood during and after delivery.

Activation of coagulation leads to generation of thrombin which in turn is inactivated by the formation of thrombin-antithrombin (TAT) complexes, and thrombin-heparin cofactor complexes (T-HCII). These complexes were measured in plasma by ELISA methods. During normal delivery, the median TAT level in ten women increased from 4.1 to 7.8 times the median normal reference level. There was great individual variation, and levels 42 and 56 times normal median were found in two women shortly after normal delivery. The median T-HCII levels increased only moderately from 2.3 to 3.1 times median normal reference. D-dimer values were elevated in 28 out of the 30 samples. In blood sampled 1-2 days after delivery, the median TAT level was 2.5 times the median normal reference. The median T-HCII level was now 5.6 times the median normal reference value. The values were stable during the first 4 days post partum, and there was little difference between those delivered vaginally or by Caesarean section (C-section). D-dimer values were above normal reference in all women, and higher in women delivered by C-section. In conclusion, increasing TAT levels during labour and delivery indicated generation of thrombin which was mainly inactivated by antithrombin. The T-HCII levels increased less during delivery. In the early post partum period, the T-HCII levels were relatively more increased than the TAT levels. These results suggest that intravascularly generated thrombin is preferably inactivated by antithrombin, even in parturient women. In the post partum period, formation of T-HCII complexes was more evident, possibly reflecting extravascular inactivation of thrombin.

Adult↗
PubMed1995

Sera of preeclamptic women are not cytotoxic to endothelial cells in culture.

OBJECTIVE: The null hypothesis of this study was that sera of women with preeclampsia are not cytotoxic to endothelial cells in culture. STUDY DESIGN: Endothelial cells were incubated in the presence of sera (30% vol/vol) of either preeclamptic patients (n = 11) or normal pregnant women (n = 11). Release of chromium 51 from prelabeled cells was measured after exposure to the different sera. Viability of the cells was evaluated by trypan blue exclusion and plating efficiencies. Deoxyribonucleic acid and protein synthesis were studied by measuring incorporation of tritiated thymidine and leucine into deoxyribonucleic acid and proteins, respectively. Cell growth was determined by monitoring the number of cells per culture dish during a 5-day incubation period. RESULTS: Release of chromium 51 from endothelial cells incubated in the presence of sera from preeclamptic women was similar to controls (26.3% +/- 4.7% vs 26.7% +/- 2.5%). There was no difference in the number of trypan blue-positive cells in cultures incubated in the presence of sera from preeclamptic women and controls. Seeding the cells in either sera from preeclamptic or control women gave the same percentage of attached cells. Similarly, preincubation of endothelial cells with either one of the two sera resulted in the same number of attached cells when they were reseeded (45% +/- 6% vs 40% +/- 15%, respectively). Incubation of endothelial cells with sera from preeclamptic or control women affected neither deoxyribonucleic acid nor protein synthesis of the endothelial cells. Furthermore, cell proliferation was similar in cultures incubated with sera from preeclamptic women and controls. CONCLUSION: No evidence was found that sera of women with preeclampsia are cytotoxic to endothelial cells in culture.

Blood Physiological Phenomena↗
PubMed1995

Fatty acid pattern of esterified and free fatty acids in sera of women with normal and pre-eclamptic pregnancy.

OBJECTIVE: To determine the composition of esterified and free fatty acids in sera of women with normal and pre-eclamptic pregnancy. SETTING: Department of Obstetrics and Gynaecology, Aker Hospital, Oslo, Norway. SUBJECTS: Blood samples were taken from 510 healthy nulliparae at a gestational age of 17-19 weeks. Nineteen of these subsequently developed pre-eclampsia. Seventeen of these, for whom blood samples were still available, and a control group of 17 women taken from the same population and matched for age, body mass index, gestational age and parity, were later studied in detail. A further group of 29 women admitted to the hospital with pre-eclampsia were also studied, as was a matched control group of 29 women with normal pregnancies recruited from the antenatal clinic. METHODS: Blood samples were drawn after 8 to 10 h fasting. The patterns of serum free fatty acids and esterified fatty acids were determined by thin-layer chromatography combined with gas-liquid chromatography. Free fatty acids were also determined enzymatically. RESULTS: Among the circulating free fatty acids, the levels of palmitic (16:0), oleic (18:1 n-9) and linoleic acids (18:2 n-6) were significantly higher early in pregnancy in women who later developed pre-eclampsia. The same free fatty acids were also significantly increased in women with pre-eclampsia. The level and composition of the esterified fatty acids in phospholipids, triglycerides and cholesteryl esters did not, however, differ between the two groups early in pregnancy. In contrast, in women with pre-eclampsia, the relative content of oleic acid was increased in the phospholipid fraction, whereas linoleic acid was decreased in the phospholipid and triglyceride fractions. CONCLUSIONS: We observed that the level and composition of circulating free fatty acids were already altered 10-20 weeks before the clinical onset of pre-eclampsia. When the disease became overt there were changes in both esterified and free fatty acids.

Adult↗
PubMed1994

Effects of free fatty acids found increased in women who develop pre-eclampsia on the ability of endothelial cells to produce prostacyclin, cGMP and inhibit platelet aggregation.

Recently, we showed that levels of circulating free fatty acids are increased in women who later develop pre-eclampsia long before the clinical onset of the disease. Among the serum free fatty acids, oleic-, linoleic-, and palmitic acid were found to be increased by 37, 25 and 25%, respectively. In the present study we asked if these free fatty acids can interfere with endothelial cell functions. Cultured endothelial cells were exposed to linoleic-, oleic- and palmitic acid in concentrations ranging from 0.016 to 0.133 mumol ml-1, resulting in molar ratios of free fatty acids to albumin of 0.2-1.6. We found that among these fatty acids, linoleic acid reduced the thrombin-stimulated prostacyclin release by 30-60%, oleic acid by 10-30%, whereas palmitic acid had no effect. Endothelial cells incubated in presence of linoleic acid showed a concentration-dependent reduction in prostacyclin release in response to thrombin, and cells incubated with linoleic acid for up to 28 h, showed a reduced thrombin-induced prostacyclin release at every time point. Endothelial level of cGMP mainly reflected the synthesis of endothelium-derived relaxing factor/nitrogen monoxide (EDRF/NO), since blocking of the endogenous production of EDRF/NO with N-omega-nitro-L-arginine, resulted in about 90% reduction in cGMP-content of the endothelial cells. Incubation with linoleic acid reduced the endothelial cGMP level by 70%. Linoleic acid reduced the endothelial cells ability to inhibit platelet aggregation by 10-45%, (p = 0.0019). It was concluded that linoleic acid impedes the ability of the endothelial cells to produce prostacyclin and cGMP, and to inhibit platelet aggregation.

Cells, Cultured↗
PubMed1993

Increased lipolytic activity of sera from pre-eclamptic women due to the presence of a lysophospholipase.

Sera from pre-eclamptic women exhibit an increased lipolytic activity compared to sera of women with normal pregnancies. The null hypothesis of this study was that the increased release of free fatty acids (FFA) was due to hydrolysis of circulating triglycerides. The nature of the increased lipolytic activity was investigated by incubating sera from pre-eclamptic (PE) and normal pregnant women (C) with various lipid substrates radiolabeled in the FFA position. The release of FFA in PE-sera was not due to hydrolysis of triglycerides or diglycerides. Lysophosphatidylcholine, however, served as substrate for the enhanced lipolytic activity. By using lysophosphatidylcholine with radiolabeled FFA in the sn-1-position we found that 32 +/- 10 nmol FFA ml-1 h-1 was released in PE-sera, compared to 10 +/- 4 nmol FFA ml-1 h-1 in C-sera. This lysophospholipase activity appears independent of Ca2+ and other divalent cations. The increased release of FFA in sera of pre-eclamptic women can be explained by the presence of a lysophospholipase which releases the remaining fatty acid of lysophosphatidylcholine.

Antibodies↗
PubMed1992

[HELLP syndrome--4 case reports].

HELLP-syndrome (H - haemolysis, EL - elevated liver enzymes, LP - low platelet count) is a serious complication of pregnancy. It can be considered as a variant of severe preeclampsia, where haemolysis, hepatic damage (elevated liver enzymes) and thrombocytopenia (low platelets) are all present. Four case reports of HELLP-syndrome are described. HELLP-syndrome may develop within a few hours. It can be seen pre-, intra- and postpartum. Many patients do not exhibit a clinical picture of severe preeclampsia. Patients who develop HELLP-syndrome usually complain of malaise, nausea, epigastric pain and headache. The diagnosis is confirmed when haemolysis, elevated liver enzymes and thrombocytopenia are demonstrated. Patients with HELLP-syndrome require intensive care by a team of obstetricians, anaesthesiologists and haematologists.

Adult↗
PubMed1992

[The vascular endothelium--a multifunctional organ].

The authors summarize the role of the vascular endothelium in hemostasis, thrombosis, vasomotor regulation, inflammation and angiogenesis. Quiescent endothelium is antithrombogenic, whereas perturbed endothelial cells become thrombogenic. The endothelium produces both vasodilating substances like endothelial derived relaxing factor and prostacyclin and vasoconstrictive compounds such as the endothelins. The presence of leucocyte adhesion molecules on the endothelial surface allows specific interactions with circulating leucocytes. Surface expression of HLA-antigens class I and II further underscores the importance of the endothelial cells in the inflammatory process. In the recent years it has become evident that the endothelial cells play a major role in the pathogenesis of diseases such as atherosclerosis, preeclampsia, hemolytic uremic syndrome and certain vasculitides.

Arteriosclerosis↗
PubMed1992

Increased lipolytic activity and high ratio of free fatty acids to albumin in sera from women with preeclampsia leads to triglyceride accumulation in cultured endothelial cells.

OBJECTIVE: The null hypothesis of this study was that the triglyceride accumulation in endothelial cells exposed to sera from preeclamptic women was determined by the presence of triglyceride-rich lipoproteins in the sera. STUDY DESIGN: The accumulation of triglycerides in cultured endothelial cells was studied using incorporation of tritiated glycerol. RESULTS: Triglyceride-rich lipoproteins in the patient sera contributed little to the endothelial triglyceride accumulation. However, sera from preeclamptic women were found to have a higher molar ratio of free fatty acids to albumin compared with sera from women with normal pregnancies (1.6 +/- 0.5 vs 0.9 +/- 0.4, respectively, p less than 0.025). In addition, sera from preeclamptic women, compared with sera from normal pregnancies, showed enhanced lipolytic activity (release of free fatty acids 0.85 +/- 0.29 vs 0.17 +/- 0.16 mmol/ml per 24 hours, respectively; p less than 0.025) that further increased the free fatty acids/albumin ratio. CONCLUSION: Sera from preeclamptic women have both a higher ratio of free fatty acids to albumin and increased lipolytic activity, resulting in enhanced endothelial uptake of free fatty acids, which are further esterified into triglycerides.

Cells, Cultured↗
PubMed1991

Sera from preeclamptic women increase the content of triglycerides and reduce the release of prostacyclin in cultured endothelial cells.

UNLABELLED: The causes of the "endothelial dysfunction" accompanying preeclampsia are unknown. Women with preeclampsia have a marked hyperlipidemia which reflects altered lipid metabolism. We asked if the hyperlipidemic sera of preeclamptic women could cause altered endothelial cell properties. Cultured endothelial cells were incubated with sera from women with preeclampsia (PE) or normal pregnancies as controls. Fifty PE-sera were tested and in 45 cases the endothelial cells acquired a large number of sudanophilic granules which by electron microscopy had lipid appearance. In 31 incubations with 31 individual control sera cellular lipid granules were observed in 4 cases. The cellular triglyceride content was increased to 153 +/- 30 compared to 48 +/- 10 micrograms/mg cell protein in the control cells. Furthermore, the endothelial release of prostacyclin, measured as 6-keto PGF1 alpha, was 8.8 +/- 0.6 ng/mg cell protein in cells incubated with PE-sera as compared to 40.3 +/- 6.4 ng/mg in the control cells. CONCLUSION: The hyperlipidemic sera from preeclamptic women induced triglyceride accumulation in cultured endothelial cells. This was accompanied by altered endothelial function as demonstrated by reduced prostacyclin release.

6-Ketoprostaglandin F1 alpha↗
PubMed1976

A comparison between the release of fluoride from sodium fluoride lozenges and bone meal tablets.

The release of fluoride from a fluoride-containing bone meal tablet and a chewable sodium fluoride lozenge to 0.5 M perchloric acid, deionized water, and saliva was compared. In acid, all the fluoride was released from the bone meal tablet (0.25 mg F), while there was a poor release in water and saliva (2-10 %). The release from the sodium fluoride lozenge (0.25 mg F) was essentially complete in water and saliva as well as in acid. Following sucking and chewing on a sodium fluoride lozenge, the mean salivary fluoride concentration increased from 0.04 to 36 parts/10(6) 5 min after intake. Concentrations exceeding the preintake level were still recorded after 20 min. With the bone meal tablet, only a slight increase (to 0.2 parts/10(6)) in the salivary fluoride level was obtained.

Calcium Phosphates↗