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T Henriksen

Publications and source records attributed to T Henriksen.

At least 37 records · Page 2Linked to original sources
PubMed1998

[Pregnancy, essential hypertension and chronic renal disease].

Women with chronic hypertension or renal disease are at a particular high risk of developing pre-eclampsia or eclampsia. Pre-eclampsia is associated with an increased risk of fetomaternal complications. In women with uncomplicated mild and moderate hypertension, pregnancy is usually normal. Treatment of high blood pressure aims at reducing maternal cardio- and cerebrovascular catastrophies, and the benefit of the treatment must be weighed against possible harmful effects on the foetus. In some cases, antihypertensive treatment can be discontinued, or medication changed. Preconceptional counselling is important both for women with chronic hypertension and, even more so, for women with renal disease, since the outcome of the pregnancy may be affected by the underlying disease.

Female↗
PubMed1998

[Measurement of blood pressure in pregnancy].

The prevalence of hypertension in pregnancy is 4-10 percent. The most serious complication associated with hypertension in pregnancy is pre-eclampsia. In one out of ten pregnancies where pre-eclampsia is present very serious complications develop in the mother or the foetus, or both. Rising blood pressure remains the main indicator of impending pre-eclampsia. The reliability of blood pressure measurement is therefore of particular importance in pregnancy. This is emphasized by the following characteristics of hypertension in pregnancy: limited time to observe the patient; pre-eclamptic complications may be present at any stage where there is a rise in blood pressure, and the indications for and objectives of treatment of pregnancy hypertension are different from those employed in the general population. The measurement of antenatal blood pressure should be standardized. It should be carried out by a limited number of well-qualified health professionals, using only equipment of reknowned quality and technical standard. Rising blood pressure in pregnancy indicates pre-eclampsia until it has been disproved post partum. Because pre-eclampsia is a placental disorder, the foetus may be at risk at any stage in the development of the disease. The status of the foetus should therefore be monitored accordingly.

Blood Pressure Determination↗
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↗
PubMed1998

Hypertension in pregnancy and preeclampsia--diagnosis and treatment.

Women who have or develop high blood pressure during pregnancy are all at increased risk of complications antenatally, intrapartum and in the puerperium. The increased risk applies to the mother as well to the fetus. Preeclampsia is the most serious form of hypertensive pregnancy complications. Preeclampsia is, however, not primarily a hypertensive disease but a disorder induced by factors dependent on the presence of placenta. The prime target of the placenta dependent factors is the vascular endothelium. Therefore the complications are associated with the vascular system, i.e. intravascular coagulation, bleeding and organ failure following poor perfusion. The fetus is at increased risk due to growth retardation and hypoxia following placental damage. Treatment of the hypertension is first indicated if the blood pressure rises to a level of increased risk of cerebral vascular complications, i.e. above 105-110 mmHg. Delivery is the only causal treatment and is always indicated if severe maternal or fetal complications develop.

Female↗
PubMed1997

A new method for isolation of smooth muscle cells from human umbilical cord arteries.

A simple method is described for obtaining a large number of single smooth muscle cells by enzymatic digestion of heparin-perfused human umbilical cord arteries. The smooth muscle cell cultures exhibited the characteristic "hill and valley" growth pattern as seen by phase contrast and scanning electron microscopy. By using indirect immunofluorescence or alkaline phosphatase-anti-alkaline phosphatase techniques the cells were identified as smooth muscle cells by the presence of alpha smooth muscle actin and vimentin. The cultures were not contaminated by endothelial cells as demonstrated by the lack of von Willebrand factor immunoreactivity. This method makes it possible to study smooth muscle cells in primary cultures.

Cell Separation↗
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

[Oxidative stress and antioxidants].

Oxidative stress is a metabolic state where the cellular oxidative reactions are out of control. Under such conditions superoxide (O2.-) may accumulate, leading to formation of the hydroxyl radical, OH.. This is a free radical that abstracts hydrogen from the double bonds of unsaturated fatty acids. The fatty acid will then become a free radical which reacts easily with oxygen to form a peroxyradical. This will in turn abstract hydrogen from another fatty acid, establishing a perpetuating oxidative chain reaction. This may lead to peroxidation of cellular functions. DNA, proteins and carbohydrates may be oxidized too. There is good evidence that oxidative stress may play a role in the pathogenesis of cancer, atherosclerosis, ischemic tissue damage and inflammatory diseases. Possibly antioxidants can be used to limit oxidative stress. Recent reports indicate that high intake of vitamin E is associated with reduced risk of coronary heart disease.

Antioxidants↗
PubMed1994

Parathyroid hormone-related protein is produced by cultured endothelial cells: a possible role in angiogenesis.

Parathyroid hormone-related protein (PTHrP) is produced by various normal and neoplastic tissues. Even if the physiological function(s) of PTHrP is unclear, evidence suggests that the protein may participate in the local regulation of smooth muscle contractility. We show here that PTHrP is produced in endothelial cells cultured from human umbilical veins as demonstrated both at the mRNA and protein level. The expression of PTHrP can be upregulated by the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate, which is known to stimulate endothelial cell differentiation and angiogenesis in vitro. Unlike smooth muscle cells, the endothelial cells do not express the parathyroid hormone (PTH)/PTHrP receptor mRNA, nor could specific binding of the protein be detected. We therefore suggest that PTHrP produced by endothelial cells acts on smooth muscle cells and may be of importance for the growth and development of new vasculature.

Cells, Cultured↗
PubMed1994

Lipoproteins do not modulate the tissue factor activity, plasminogen activator or tumour necrosis factor production induced by lipopolysaccharide stimulation of human monocytes.

Upon stimulation with lipopolysaccharides (LPS), monocytes are able to produce tissue factor (TF), the most powerful physiological procoagulant substance known. In several assay systems LPS bound to lipoprotein has been reported to be less active than unbound LPS in stimulating monocytes. In the present study the LPS-induced TF activity was, however, not prevented by lipoproteins (VLDL, LDL, HDL). In fact, the very low density (VLDL) fraction further increased the TF inducing capacity of LPS. The lipoproteins per se mediated reduced plasminogen activator (PA) production in monocytes. LPS had an even more and significant depressing effect on PA production, which was not further decreased in the presence of lipoproteins. Furthermore, LPS-induced release of tumour necrosis factor (TNF), a marker of monocyte activity, was not inhibited by lipoproteins. Our experiments suggest that lipoproteins do not render LPS less effective in stimulating TNF release, procoagulant and fibrinolytic activities in human monocytes.

Cells, Cultured↗
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

[Urinary incontinence after apoplexy].

In a retrospective study, based upon doctors' and nurses' case records, urinary incontinence (UI) and its relation to the severity of strokes was studied in 156 stroke patients discharged from the department of neurology, Bispebjerg Hospital in 1988. A significant relationship was found between the presence of UI and stroke severity measured by length of hospital stay, circumstances of discharge and mobility (p < 0.0001). 44% of patients had some urinary incontinence on admission and on discharge 26% still had UI. Surprisingly, however, information about incontinence appeared in only 10% of doctors' records, whereas nurses, records had the relevant information concerning as many as 90% of patients. It appears that urinary incontinence in stroke patients has a low priority among doctors.

Aged↗
PubMed1993

Reduced contralateral hemispheric flow measured by SPECT in cerebellar lesions: crossed cerebral diaschisis.

Four patients with clinical signs of cerebellar stroke were studied twice by SPECT using 99mTc-HMPAO as a tracer for cerebral blood flow (CBF). When first scanned 6 to 22 days after onset, all had a region of very low CBF in the symptomatic cerebellar hemisphere, and a mild to moderate CBF reduction (average 10%) in contralateral hemispheric cortex. In all four cases clinical signs of unilateral cerebellar dysfunction were still present when rescanned 1 to 4 months later and the relative CBF decrease in the contralateral cortex of the forebrain also remained. The basal ganglia contralateral to the cerebellar lesion CBF showed variable alterations. A relative CBF decrease was seen in upper part of basal ganglia in all four cases, but it was not a constant phenomenon. A relative CBF increase in both early and late SPECT scans was seen at low levels of neostriatum in two cases. The remote CBF changes in cerebellar stroke seen in the forebrain are probably caused by reduced or abolished cerebellar output. The term "Crossed Cerebral Diaschisis" may be used to describe these CBF changes that would appear to reflect both decreased and increased neuronal activity.

Aged↗