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J F Koster

Publications and source records attributed to J F Koster.

At least 37 records · Page 2Linked to original sources
PubMed1993

Malondialdehyde and glutathione production in isolated perfused human and rat hearts.

A number of studies show the relation between oxygen-derived free radicals and cardiac ischemia/reperfusion injury. However, little is known about oxidative stress in the human heart, which can be measured by oxidized glutathione (GSSG) and malondialdehyde (MDA) formation. Furthermore, data on MDA production by rat hearts are controversial, possibly because of the use of the aspecific thiobarbituric acid assay. Therefore, GSSG and MDA were measured, with colorimetric and high-performance liquid chromatographic assays, respectively, in buffer-perfused explanted human hearts and normal rat hearts made temporarily ischemic. Human hearts received cardioplegia; rat hearts were studied in a control and an ischemic group with or without cardioplegia. Baseline GSSG release was < 0.01 nmol.min-1.g wet wt-1 in both species. During reperfusion, GSSG release from human hearts and from ischemic and cardioplegic/ischemic rat hearts peaked at 0.24 +/- 0.12, 1.1 +/- 0.4, and 0.19 +/- 0.04 nmol.min-1.g-1, respectively. MDA was undetectable (< 0.02 nmol.min-1.g-1) in the effluent of both species and in human hearts (< 4 nmol/g protein). Rat heart reduced glutathione levels decreased 32% as a consequence of cardioplegia and ischemia. Cardioplegia induced a 41% (P = .08) decrease in rat heart MDA content, whereas cumene hydroperoxide increased it 3.6 times (P < .01). Thus, after ischemia human and rat hearts release GSSG, indicating that oxidative stress has occurred. Apparently, lipid peroxidation takes place in normal rat hearts, decreases after cardioplegia, but does not increase after ischemia/reperfusion. Human hearts lack MDA under normoxic and ischemic conditions. This novel finding seems to reflect a low MDA-forming potential in both situations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Leukocyte adhesion molecules on the vascular endothelium: their role in the pathogenesis of cardiovascular disease and the mechanisms underlying their expression.

It is well known that granulocytes increase infarct size after reperfusion of the ischemic myocardium, and that monocytes promote atherogenesis. Those cells are also believed to play a contributory role in pathogenesis of coronary restenosis as response to arterial injury during balloon angioplasty. The adhesion of those leukocytes to the vascular endothelium is a prerequisite for their recruitment and accumulation in the lesion. Inflammatory mediators likely to occur under those conditions, e.g., histamine, thrombin, oxygen-derived free radicals (ODFR), interleukin (IL)-1, tumor necrosis factor (TNF)-alpha, and activated complement factors, induce in a distinct time course the (transient) expression of the leukocyte adhesion molecules P-selectin, E-selectin, intercellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1 on the endothelium. Only VCAM-1 is specific for monocytes; the others mediate the binding and subsequent extravasation of both monocytes and granulocytes. The response to the relevant inflammatory mediators, except for extracellularly produced ODFR, is coupled via specific receptors on the surface of the endothelium to specific signal transduction pathways and, except for P-selectin (early response), is directly dependent on protein synthesis (intermediate and late response). Protein kinase-C-induced phosphorylation of transcription factors is often shown to be involved. Protein synthesis is preceded by increased transcription of mRNA that is regulated in part by the transcription factor NF-kappa B. Indications have been obtained that intracellularly produced ODFR may be involved in the translocation of this transcription factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Studies on the interaction of leucocytes and the myocardial vasculature. I. Effect of hypoxia on the adherence of blood granulocytes.

Granulocytes play an important role in increasing the infarct size after ischemia and reperfusion by the release of oxygen-derived free radicals (ODFR) and lysosomal enzymes. It has been shown that the number of granulocytes adhering to the vascular endothelium increases after occlusion of the coronary artery, and that the area of myocardial damage can be reduced by preventing granulocyte adherence with monoclonal antibodies directed against adhesion receptors. The underlying mechanism of granulocyte activation under these conditions is not yet known. We have investigated whether granulocytes can be activated directly by reduced oxygen tensions. Granulocytes were suspended in a hypoxic buffer and incubated on fibronectin and gelatin coated microtitre plates at 1-3% ambient oxygen to study their ability to adhere to these matrices. The results showed that the adherence of granulocytes to fibronectin was dependent on the duration of hypoxia. After 30 min of incubation under hypoxia granulocyte adherence increased 1.3 to 1.8 fold compared to the normoxic control. The adherence to fibronectin could be inhibited partially by anti-CD18 antibody, a monoclonal antibody to the common beta chain of a class of extracellular matrix receptors. This direct activation of granulocytes due to hypoxic conditions may have implications for the interaction of these cells with the vascular endothelium in vivo.

Antibodies, Monoclonal↗
PubMed1992

Low molecular weight iron and the oxygen paradox in isolated rat hearts.

Little is known about changes in the amount of iron in the intracellular low molecular weight pool, which catalyzes the Fenton reactions during reperfusion after ischemia. In this study a new approach is presented to measure low molecular weight iron and it is applied to normal hearts during ischemia and to iron-loaded hearts during anoxia and reoxygenation. The results of this study show that (a) during ischemia in normal hearts a progressive 30-fold increase occurs in low molecular weight iron after 45 min of ischemia, whereas (b) during 45 min of anoxic perfusion the low molecular weight iron does not increase. This means that the reductive release from the storage protein ferritin is greatly enhanced by the acidification that occurs during ischemia. (c) Anoxic perfusion of iron-loaded hearts does increase low molecular weight iron and there is a further increase upon reoxygenation, which is prevented by (+)-cyanidanol-3. Based on these findings it is concluded that oxygen deprivation enhances the susceptibility of rat hearts to oxygen radicals by increasing the amount of catalytic, ferrous iron in the low molecular weight pool.

Animals↗
PubMed1992

Nitrofen-induced diaphragmatic hernias in rats: pulmonary antioxidant enzyme activities.

We developed an experimental rat model of congenital diaphragmatic hernia (CDH) to elucidate the etiology and pathogenesis of this serious congenital anomaly in humans and in particular to study the effects of a short period of artificial ventilation on the CDH lung in relation to antioxidant defense mechanisms. CDH was induced in about 60% of the offspring by maternal exposure to 2,4-dichlorophenyl-p-nitrophenylether (Nitrofen) during pregnancy. This herbicide resembles thyroid hormone in chemical structure. The lungs of fetal rats (d 19, 20, 21, and 22) were examined for protein and DNA content and activity of superoxide dismutase, catalase, and glutathione peroxidase (GPX). The same parameters were assessed in tracheotomized newborn rats after pressure-controlled artificial ventilation with either room air or pure oxygen during a short period of 5 h. In both CDH rats and controls, wet lung weight increased during gestation. At term, CDH rats had significantly lower mean lung weights than controls. Neither group differed in protein and DNA content per mg lung or superoxide dismutase, catalase, and GPX activity before and at birth. After artificial ventilation of neonates with air and pure oxygen, superoxide dismutase activity tended to decrease, whereas catalase activity remained virtually unchanged in the CDH lung. However, GPX activity in the CDH lung was reduced to 80% of initial activity at term after ventilation with air and to 70% with pure oxygen. The present finding of a decline in GPX activity in this animal model after a short period of artificial ventilation may indicate that the CDH rat neonate is at risk to develop oxygen-related lung damage.

Animals↗
PubMed1991

Patients with combined hypercholesterolemia-hypertriglyceridemia show an increased monocyte-endothelial cell adhesion in vitro: triglyceride level as a major determinant.

Hypercholesterolemia (HC) is one of the primary risk factors for atherosclerosis. Patients with familial hypercholesterolemia (FH) or combined hypercholesterolemia-hypertriglycerinemia (CHH) are at risk to develop premature atherosclerosis. Animal models have revealed that diet-induced HC in vivo leads to an increased adhesion of monocytes to the endothelium of the vessel wall. Changes in the monocytes, endothelial cells, or serum components may lead to the increased monocyte adhesion that results in atherosclerotic plaque formation. In the present study, we investigated the binding of the monocyte in an in vitro system. Incubation of freshly isolated monocytes from CHH patients with cultured human umbilical vein endothelial cells (HUVEC) gave a significant 60% increase in monocyte adhesion when compared with monocytes from healthy subjects. No such increase was observed using monocytes from nontreated FH patients. These data suggest that CHH results in in vivo alterations of the monocytes that lead to an increased in vitro adhesion to HUVEC, and that an increased level of plasma triglycerides is the major determinant, since HC alone does not induce this alteration.

Cell Adhesion↗
PubMed1991

Contradictory effects of superoxide dismutase after global or regional ischemia in the isolated rat heart.

The effect of superoxide dismutase was investigated in two different models of ischemia and reperfusion in the isolated rat heart: global and regional ischemia. The results of this comparison show that reperfusion arrhythmias after 10 and 15 min of regional ischemia, induced by occlusion of the left coronary artery, can be prevented by SOD confirming the results of other investigators. Paradoxically SOD was without effect after 10 min of global ischemia, obtained by stopping coronary flow completely. After 15 min of global ischemia, SOD induced ventricle fibrillation. Apparently the effect of SOD depends on the model of ischemia and reperfusion that is used.

Animals↗
PubMed1991

Differential stimulation by oxygen-free-radical-altered immunoglobulin G of the production of superoxide and hydrogen peroxide by human polymorphonuclear leucocytes.

1. The effect of free-radical-altered IgG (monomer and polymer u.v.-irradiated IgG), compared with that of native and heat-aggregated IgG, on the production rate of superoxide anion and hydrogen peroxide by granulocytes (polymorphonuclear leucocytes) from normal blood and granulocytes obtained from the blood and synovial fluid of patients with rheumatoid arthritis was studied. 2. Similar rates of superoxide production by granulocytes from normal blood at rest and in the presence of any form of IgG were found. In contrast, the rate of hydrogen peroxide production could be stimulated in a dose-dependent fashion by monomer or polymer u.v.-irradiated IgG. 3. The stimulatory effect of free-radical-altered IgG on the rate of hydrogen peroxide production did not occur in the presence of 2-deoxyglucose, which deprives the NADPH:O2 oxidoreductase of its substrate NADPH by inhibition of glycolysis and the pentose phosphate pathway. This points to a stimulatory effect on the direct divalent reduction of oxygen without intermediate superoxide production by this enzyme complex. 4. Granulocytes obtained from the blood and synovial fluid of patients with rheumatoid arthritis reacted differently to polymer u.v.-irradiated IgG. In the presence of this stimulus the rate of release of both superoxide and hydrogen peroxide was increased. Furthermore, these granulocytes synthesized superoxide and hydrogen peroxide at a higher rate than did granulocytes from normal blood in the presence of serum-treated zymosan but not in the presence of phorbol myristate acetate. 5. Taken together, these results indicate that the rate of superoxide and hydrogen peroxide production by the granulocyte NADPH:O2 oxidoreductase depends on the pathological condition of the donor and the type of stimulus used.

Adult↗
PubMed1990

Iron status in the acute phase and six weeks after myocardial infarction.

In a case-control study of 84 myocardial infarction patients and 84 population controls we investigated the association between iron status parameters and myocardial infarction during the acute phase and after six weeks. Immediately after the infarction mean ferritin levels were significantly higher, whereas iron levels and iron saturation of transferrin were significantly lower in cases than in controls. Six weeks after the infarction, serum iron levels were still significantly lower in cases than in controls. Neither serum ferritin levels nor serum iron levels did show a clear association with the size of the ischemic tissue damage as estimated by creatine phosphokinase levels. Our results indicate that serum ferritin and iron levels are influenced by the traumatic effects of the myocardial infarction. Possibly, these transient changes are an acute effect, as seen in infections. An increased uptake of iron in the reticulo-endothelial system for synthesis of ferritin, may account for the lowered serum iron level and the iron saturation of transferrin.

Aged↗
PubMed1990

Cumene hydroperoxide, an agent inducing lipid peroxidation, and 4-hydroxy-2,3-nonenal, a peroxidation product, cause coronary vasodilatation in perfused rat hearts by a cyclic nucleotide independent mechanism.

STUDY OBJECTIVE - The aim of the study was to determine whether cumene hydroperoxide, a substance known to induce lipid peroxidation through free radical action, and 4-hydroxy-2,3-nonenal (4-hydroxynonenal), a major aldehyde formed during lipid peroxidation, induce coronary vasodilatation by changing cyclic nucleotide levels. DESIGN - The study involved Langendorff perfused rat hearts, using different concentrations of cumene hydroperoxide and 4-hydroxynonenal, with sodium nitroprusside for comparison. Coronary flow was measured indirectly as retrograde aortic flow, with constant perfusion pressure. Information about the precise localisation of cyclic guanosine monophosphate (cGMP) in the heart was obtained by immunocytochemistry, using a new cGMP antiserum. EXPERIMENTAL MATERIAL - Hearts were from male Wistar rats, body weight 200-250 g. MEASUREMENTS and RESULTS - Both cumene hydroperoxide and 4-hydroxynonenal caused a dose dependent and reversible increase in coronary flow comparable with sodium nitroprusside. With sodium nitroprusside there was a good correlation between extent of vasodilatation and total heart cGMP concentration. Vasodilatation induced by cumene hydroperoxide or 4-hydroxynonenal was not accompanied by increase in total heart cGMP or cAMP (cyclic adenosine monophosphate) concentration. Isoprenaline was used as a positive control for cAMP. cGMP immunostaining was found in coronary vascular smooth muscle after vasodilatation with sodium nitroprusside, but no immunostaining was found in vascular smooth muscle after vasodilatation with cumene hydroperoxide or 4-hydroxynonenal. CONCLUSIONS - Cumene hydroperoxide and 4-hydroxynonenal can provoke reversible coronary vasodilatation in isolated perfused rat hearts by a cyclic nucleotide independent mechanism.

Aldehydes↗
PubMed1990

Rat heart perfusion as model system for enzyme replacement therapy in glycogenosis type II.

Cardiac failure and skeletal muscle weakness are the main clinical features of glycogenosis type II, a lysosomal storage disorder caused by acid alpha-glucosidase deficiency. In our study, we have investigated in a rat heart perfusion-recirculation system whether acid alpha-glucosidase can be taken up from the vascular system into cardiomyocytes. When rat hearts were perfused with mannose 6-phosphate-containing acid alpha-glucosidase purified from bovine testis, a 3- to 4-fold increase of enzyme activity was obtained. Perfusion with human placental acid alpha-glucosidase not containing the mannose 6-phosphate recognition marker did not have such an effect. The presence of bovine testis acid alpha-glucosidase in heart tissue was demonstrated by immunoblotting. Immunocytochemistry provides evidence for uptake of the exogenous enzyme in lysosomes of the cardiomyocytes. The relevance of these findings for enzyme therapy in glycogenosis type II is discussed.

Animals↗
PubMed1990

Diminished superoxide production of synovial fluid neutrophils in patients with rheumatoid arthritis following piroxicam treatment.

Superoxide production by polymorphonuclear leukocytes (PMNs) and macrophages was inhibited by piroxicam and other non-steroidal anti-inflammatory drugs both in vitro and in vivo. Hitherto, data have only been available on blood PMNs and macrophages. In order to investigate the situation in the joint, PMNs were isolated from synovial fluid before and after 24 h of piroxicam treatment in patients with rheumatoid arthritis. Isolated PMNs were stimulated with PMA and serum-treated zymosan. The capacity of synovial fluid PMNs to produce superoxide decreased by 30% after piroxicam treatment. A similar decrease was found for blood PMNs. No difference in superoxide production was found between blood PMNs and synovial fluid PMNs which were obtained simultaneously. From the fact that the piroxicam concentration in synovial fluid was 40% of the serum value, it can be concluded that piroxicam probably became bound to PMNs before they entered the joint cavity. These results indicate that at the site of the inflammation the superoxide production by PMNs is inhibited by piroxicam treatment. The inhibition of superoxide production is probably important in the effect of piroxicam and other non-steroidal anti-inflammatory drugs in rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1989

Reappraisal of the e.p.r. signals in (post)-ischaemic cardiac tissue.

The present study was designed to measure directly, using e.p.r. spectroscopy, oxygen-derived free radicals in (post)-ischaemic or (post)-anoxic rat hearts. Rat hearts were rapidly freeze-clamped at 77 K under normoxic, anoxic, ischaemic or reperfusion conditions. The samples were measured at three different temperatures (13, 77 and 115 K) and at several microwave power levels, and were compared with isolated rat heart mitochondria. Samples were prepared both by grinding and as tissue cuts. The two preparation techniques gave identical e.p.r. results, which excludes the occurrence of grinding artifacts. No free radical signals linked to reperfusion injury were detected. Several electron transfer centres known in the mitochondrial respiratory chain were measured. The signals previously assigned to post-ischaemic reperfusion injury were found to originate from electron transfer centres of the respiratory chain, predominantly the iron-sulphur cluster S-1 in succinate dehydrogenase. The differences in signal intensity between normoxic, ischaemic and reperfused hearts were found to result from the different redox stages of these centres under the various conditions tested. These findings do not necessarily imply that oxygen-derived free radicals are not formed in cardiac tissue during (post)-ischaemic reperfusion. The constitutive background of paramagnetism from the respiratory chain, however, seriously hampers the direct detection of comparatively low concentrations of free radicals in cardiac tissue. It is therefore expedient to focus future experiments in this field on the use of spin-trapping agents.

Animals↗
PubMed1989

Xanthine oxidase-catalysed oxidation of paracetamol.

Paracetamol was polymerized in a reaction mixture containing xanthine oxidase, xanthine and paracetamol. This polymerization reaction was not inhibited by allopurinol or KCN, indicating that neither the molybdenum sites nor the iron-sulphur centres of the enzyme were involved in this catalytic activity. Removal of the flavin centres from the enzyme, however, completely abolished paracetamol oxidation. Spectroscopic measurements suggested that in the simultaneous presence of both paracetamol and H2O2 a peroxyflavin intermediate was formed, which is presumably responsible for the paracetamol polymerization reaction.

Acetaminophen↗
PubMed1989

Inhibition of enzymes and oxidative damage of red blood cells induced by t-butylhydroperoxide-derived radicals.

The effects of t-butylhydroperoxide (tBHP), its alkoxyl radical (tBuO.) and its peroxyl radical (tBuOO.) in model systems and on red blood cells were studied. Glyceraldehyde-3-phosphate dehydrogenase was strongly inhibited by tBHP via a direct reaction of the hydroperoxide with an essential sulfhydryl group in the enzyme molecule. Several other enzymes were unaffected by tBHP. Alcohol dehydrogenase was strongly inhibited by tBuO. but was much less sensitive to tBuOO.. Lysozyme, lactate dehydrogenase and trypsin, on the other hand, were very sensitive to the peroxyl and not, or much less, to the alkoxyl radical, whereas acetylcholinesterase was very sensitive to both radicals. tBuOO. caused covalent binding of tryptophan, tyrosine, histidine and methionine to serum albumin. The corresponding alkoxyl radical was ineffective in this respect. Conversely, tBuO. caused peroxidation of linolenic acid, whereas tBuOO. did not. Incubation of human erythrocytes with tBHP caused lipid peroxidation and K+ leakage. Both effects were caused by tBHP-derived radicals generated in a reaction of the hydroperoxide with hemoglobin. With radical scavengers it was possible to dissociate tBHP-induced lipid peroxidation and K+ leakage, demonstrating that these two processes are not causally related. Experimental results indicate that tBuO. causes lipid peroxidation, whereas tBuOO. is responsible for K+ leakage.

Amino Acids↗
PubMed1989

Studies on ferritin in rat liver and spleen during repeated phlebotomy.

1. The ferritin content of liver and spleen in normal and iron-loaded rats decreased during repeated phlebotomy. 2. During increased iron demand, ferritin is degraded in toto. 3. With the ESI and EELS technique the iron distribution was followed in different cell types and cellular compartments. 4. We have demonstrated two methods of iron mobilisation: (a) catabolism of lysosomal ferritin in toto and (b) delivery of ferritin from parenchymal cell into the bile and degradation of ferritin in toto.

Animals↗
PubMed1989

Peroxidative stress and in vitro ageing of endothelial cells increases the monocyte-endothelial cell adherence in a human in vitro system.

Adherence of monocytes to the endothelium is an early event in atherogenesis. Changes in the endothelium are probably involved in this process. We have investigated the influence of peroxidative stress and in vitro ageing of endothelial cells on the subsequent adherence of monocytes using an in vitro system. Treatment of young human umbilical vein endothelial cells (HUVEC) with 60 microM cumene hydroperoxide (Chp) resulted in a 2.1-fold increase in monocyte adherence. This increase was not dependent on de novo synthesis of membrane antigens. No such increase upon Chp treatment was observed using young human umbilical artery endothelial cells (HUAEC) and in vitro aged HUVEC and HUAEC. As compared with "young" HUVEC, a higher spontaneous adherence of monocytes to "young" HUAEC (1.8 times), "aged" HUVEC (2.5 times) and "aged" HUAEC (2.7 times) was observed. Furthermore, fibroblasts showed an about 3 times higher monocyte adherence, whereas an 8 times higher adherence was observed to endothelial extracellular matrix. These data suggest that the spontaneous monocyte adherence to "young", intact endothelium can be increased by peroxidative damaging and by ageing of the endothelial cells. A denudation and subsequent exposure of the extracellular matrix may further stimulate this process. The possible physiological vector for endothelial peroxidation is discussed.

Arteriosclerosis↗