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Biomedical subjects

W Rücker

Publications and source records attributed to W Rücker.

At least 19 recordsLinked to original sources
PubMed1990

Influence of the acyl-coenzyme A:cholesterol--acyltransferase inhibitor octimibate on cholesterol transport in rat mesenteric lymph.

The effect of the new inhibitor of acyl-coenzyme A:cholesterol-acyltransferase, octimibate (sodium 8-[1,4,5-triphenyl-1H-imidazole-2yl)-oxy)octanoate), on the cholesterol transport in rat mesenteric lymph was evaluated. During intraduodenal infusion of a triglyceride-phospholipid emulsion, volume and triglyceride concentration of lymph collected from a mesenteric lymph fistula remained constant in control and treated rats. After addition of 3.75 mg 3H-cholesterol/h to the intraduodenal infusion, cholesterol content of lymph increased to about double the basic concentration in control rats. Yet there was no significant change of lymph cholesterol in treated animals, which had received 40 mg octimibate followed by ca. 120 mg/24 h x kg body weight octimibate added to the intraduodenal infusion. Up to 35% of the infused dose of 3H-cholesterol were recovered in lymph of control rats, in contrast to only 23% in lymph of treated rats. It is concluded that the inhibition of the intestinal acyl-coenzyme A:cholesterol-acyltransferase by octimibate may prevent the increase of cholesterol in mesenteric lymph induced by dietary cholesterol.

Animals↗
PubMed1989

[Diagnosis of very early arteriosclerosis vascular changes using Duplex sonography].

The technical evolution of ultrasonic equipment provides a high resolution imaging analysis of the vessel wall and thereby offers new possibilities in diagnosing very early atherosclerotic changes. The typical B-mode image in human and animal arteries shows parallel wall contures enclosing a hypoechoic space. In this study in Vitro- and in Vivo-experiments in rabbit aortas document the distance between these contures correlating histologically with a high cholesterol diet caused a broadening of the hypoechoic space in the rabbit aortic vessel wall. The data demonstrate that high resolution Duplex Sonography is a usefull noninvasive approach for the detection of very early atherosclerotic changes in arterial vessel walls in a stage before plaques can be identified.

Animals↗
PubMed1988

Antiatherosclerotic and antihyperlipidemic effects of octimibate sodium in rabbits.

Octimibate sodium (8-[(1,4,5-triphenyl-1H-imidazol-2-yl)oxy]octanoic acid, sodium salt; NAT 04-152) was investigated for its antihyperlipidemic and antiatherosclerotic activities in New Zealand White rabbits. Hypercholesterolemia and atherosclerosis were induced by feeding a diet containing 0.3% cholesterol for 8 weeks. In addition, repeated injections of bovine serum albumin (BSA) were used to enhance the experimental atherosclerosis. Octimibate sodium, 10.0 and 30.0 mg/kg p.o., reduced both the increase in serum cholesterol levels and the aortic plaque-formation (by about 50% in the higher dose group) as compared to control animals. Serum triglyceride levels were not influenced. Biochemical and histological examinations of the aortas showed reduced cholesterol contents in the higher dose group and a dose-dependent inhibition of pathological changes in the aortas.

Animals↗
PubMed1984

Prolonged infusion of prostacyclin in patients with advanced stages of peripheral vascular disease: a placebo-controlled cross-over study.

Twelve patients (age 33-77 years, mean age 68.4 years) with peripheral vascular disease (PVD) stage III-IV received continuous intravenous infusions of 5 ng prostacyclin (PGI2)/kg/min and physiological saline for 7 days. The administration was randomized and double-blind with an interval of 7 days between the infusions. During PGI2 infusion systolic blood pressure fell significantly from 147.8 +/- 4.8 mm Hg to 140.6 +/- 4.0 mm Hg (P less than 0.01) and returned to 144.5 +/- 4.9 mm Hg post infusion. Transcutaneous pO2 (tcpO2) measured on the instep of the affected limb increased significantly by 8.9 +/- 3.8 Torr during PGI2 infusion and remained elevated during the subsequent week. A significant reduction of pain was observed from the 5th day of PGI2 infusion, lasting for at least the following observation period. Platelet cAMP increased from 18.8 +/- 1.5 pmol/10(8) platelets to 24.7 +/- 1.6 pmol/10(8) platelets on the 3rd day of PGI2 infusion (P less than 0.01). Spontaneous platelet aggregation was also significantly reduced during PGI2 infusion. However, 7 days after the infusion thromboxane B2 (TXB2) in plasma and spontaneous platelet aggregation significantly increased in comparison with the preinfusion values, indicating a rebound phenomenon. The clinical outcome was favorable in 9 of 12 patients, was unchanged in two patients, while progressing to limb amputation in one patient.

Adult↗
PubMed1984

Cardioprotective actions of pentoxifylline in an animal model of acute myocardial ischaemia.

The action of pentoxifylline on some of the consequences of acute myocardial ischaemia was studied in cats in vivo. Occlusion of the left anterior descending coronary artery (LAD) for 5 h resulted in a significant elevation in the ST-segment of the ECG, a reduction in free platelet count in right atrial blood and a loss of creatine phosphokinase (CK) and cathepsin D activities in homogenates of the severely ischaemic myocardium as compared to non-ischaemic myocardium. Intravenous infusions of pentoxifylline (0.30 mg kg-1 min-1 for 1 h and 0.15 mg kg-1 min-1 for the remainder of the 5 h observation period, starting 0.5 h after LAD occlusion) significantly reduced the loss of enzymes from the ischaemic myocardium, prevented any further increase in the ST-segment and restored the platelet count to its control level. There were no significant changes in plasma immunoreactive 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) and thromboxane B2 (TXB2), although a tendency for a reduction in TXB2 levels was observed. Pentoxifylline seems to affect, beneficially, the myocardium in this animal model of acute myocardial ischaemia. The reason for this cardioprotective action remains to be elucidated. It is, however, noteworthy that the overall profile of action of pentoxifylline resembles that of PGI2 administration in this model.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

RCS from human platelets: is it only thromboxane?

To determine if inhibition of a rabbit aorta contracting substance (RCS) corresponds to inhibition of thromboxane synthetase human washed platelets were stimulated with thrombin. RCS formation was bioassayed on rabbit aorta strips in Tyrode solution containing selective blocking agents and thromboxane (TX)B2 in the same probes by specific radioimmunoassay. Dazoxiben inhibited the formation of TXB2 but not of RCS, whereas indomethacin inhibited both RCS and TX formation. The data indicate that the rabbit aorta cannot be used alone to predict inhibition of TX formation with specific TX synthetase inhibitors.

Animals↗
PubMed1983

Evidence for high affinity prostacyclin binding sites in vascular tissue: radioligand studies with a chemically stable analogue.

Prostacyclin-specific binding sites are described in the muscularis of pig aorta using [3H]ZK 36374, a chemically stable prostacyclin analogue, as radioligand. Under standard incubation conditions [300 micrograms membrane protein in 350 microliter Tris buffer (50 mmoles/l., pH 7.4) containing 3 mM Ca2+ at 37 degrees for 10 min] both association and dissociation were complete within 30 sec, thus not allowing the determination of association or dissociation rate constants. The Scatchard plot was upward convex, whereas the Hill plot was linear, having a slope of 1.9. The equilibrium dissociation constant (KD) was 22.4 nmoles/l. and the specific binding was saturated at 360 fmoles [3H]ZK 36374/mg protein. The reversibility of binding was demonstrated by displacement of bound ligand with ZK 36374, its 5-(Z)-stereoisomer (ZK 36375), PGI2 and PGE1, but not with PGF2 alpha. The data suggest high affinity binding sites for ZK 36374 in the smooth muscle cells of pig aorta for which PGI2 may be the physiological ligand. They also demonstrate a possible co-operativity with two molecules binding simultaneously to two interacting sites.

Animals↗
PubMed1982

[Iodine deficiency in Salzburg in spite of iodized table salt prophylaxis].

Urinary iodine excretion was determined in 293 medical technical and nursing students in hospitals of the province Salzburg. The average urinary iodine excretion amounted to 46.6 +/- 18 micrograms iodine per gram creatinine. 67.6% of the students showed a deficiency of iodine II, whilst 98.3% had a deficiency of iodine I according to WHO criteria. Urinary iodine levels and natriuria are closely correlated, indicating that iodized table salt probably constitutes the most important source of iodine. 73 of the students had a palpable giotre, 10 of these being nodular. Our investigations, together with those of Innsbruck, Graz and Vienna, demonstrate the existence of generalized iodine deficiency in spite of iodized salt prophylaxis, which has been legally enforced in all of Austria since 1963. Iodized table salt prophylaxis has, thus, led to a drastic decrease in goitres in children, but is not sufficient to eliminate iodine deficiency in adults. An increased level of iodization of table salt, as has been put into force in Switzerland, must be called for in Austria, too.

Adolescent↗
PubMed1980

Effects of PGI2 and PGI analogues on cAMP levels in cultured endothelial and smooth muscle cells derived from bovine arteries.

PGI2 increased cAMP levels in cultured endothelial cells derived from bovine aortas in the presence of isobutylmethylxanthine (IBMX). Stable PGI analogues were more effective, while PGE1 was without effect. In cultured smooth muscle cells from bovine aortas, PGI2, pGE1 and the stable PGI analogues dose-dependently increased cAMP levels in the absence and presence of IBMX. The data confirm the stimulatory effect of PGI2 on cAMP content in bovine coronary artery rings and suggest that the effect is mainly due to the stimulatory action of PGI2 on cAMP in smooth muscle cells.

1-Methyl-3-isobutylxanthine↗
PubMed1979

Effects of dipyridamole in vivo on ATP and cAMP content in platelets and arterial walls and on atherosclerotic plaque formation.

In rabbits receiving an atherogenic diet for 2 months, the ATP content of platelet rich plasma (PRP) and arterial tissue was significantly elevated as compared to normal rabbits. This increase in ATP levels of platelets from atherosclerotic rabbits was paralleled by higher basal as well as PGI2-induced cAMP levels. In arterial tissues, an increase was only obtained in PGI2-stimulated cAMP content. Treatment with dipyridamole (DPD) for 4 weeks resulted in a reduction of the ATP content in platelets and arterial tissue from atherosclerotic rabbits to values seen in normal animals. Again, the reduction of ATP content was reflected in a decrease of basal as well as PGI2-induced cAMP levels in platelets, whereas in arterial tissue a decrease was only obtained in PGI2-induced cAMP content. At the same time, DPD treatment enhanced atherosclerotic plaque formation in the aortic wall. The enhanced atherosclerotic plaque formation seen in DPD treated atherosclerotic rabbits may be linked to the inhibition of adenosine uptake, resulting in a decrease of the adenine nucleotide pools of arterial wa-l cells. The decrease also caused a reduction in PGI2-induced cAMP content. This effect may be linked to altered proliferative activity, since in many cell types, stimulation of cAMP levels results in reduced proliferation rates.

Adenosine Triphosphate↗
PubMed1979

PGI2 enhanced cAMP content in bovine coronary arteries in the presence of isobutylmethylxanthine.

Incubation of bovine coronary artery (BCA) rings with isobutylmethylxanthine (IBMX) resulted in a time-dependent increase of cAMP content. This effect was blocked, when the rings were preincubated with indomethacine or 15-hydroperoxy-arachidonic acid for 5 min, indicating that the IBMX-induced increase in cAMP content may depend on endogenous PGI2 formation. PGE2 did not increase the cAMP content in BCA rings. Dipyridamole did not effect cAMP content, when used as a substitute for IBMX. It is suggested that PGI2 stimulates cAMP formation in arterial walls, but that this effect only becomes visible in the presence of a phosphodiesterase inhibitor.

1-Methyl-3-isobutylxanthine↗
PubMed1979

Prostacyclin-dependent differences in TXA2 formation by platelets from normal and atherosclerotic rabbits.

Intact platelets from atherosclerotic rabbits release more thromboxane B2 (TXB2) and 12-hydroxyeicosatetraenoic acid (HETE) than platelets from normal rabbits following incubation with [14C]arachidonic acid (AA). In contrast, no difference is found between homogenates of platelets from normal and atherosclerotic animals. PGI2 stimulates cAMP accumulation and inhibits TXB2 formation more potently in intact platelets from atherosclerotic than from normal rabbits, but has no effect on AA metabolism in homogenised platelets.

Animals↗
PubMed1979

Effects of dipyridamole in experimental atherosclerosis. Action on PGI2, platelet aggregation and atherosclerotic plaque formation.

Experimental atherosclerosis in rabbits induced by feeding a standard atherogenic diet for 4 months resulted in an increased sensitivity of platelets to the proaggregatory action of collagen and ADP. Treatment with dipyridamole (3 x 10 mg/day i.m.) for 4 weeks normalized platelet loss in atherosclerotic rabbits and abolished the increased sensitivity to proaggregatory collagen, but not to ADP. Dipyridamole treatment lowered basal as well as PGI2-induced cAMP levels below values seen in platelets from normal rabbits, but the stimulation by PGI2 relative to basal cAMP levels was not affected or even increased by dipyridamole treatment. Dipyridamole did not affect the increased sensitivity of platelets from atherosclerotic rabbits to the antiaggregatory action of PGI2, indicating that dipyridamole decreased absolute cAMP levels, probably due to reduction of the adenine nucleotide pool in platelets without affecting the adenylate cyclase function. Dipyridamole enhanced atherosclerotic plaque formation in arterial walls. Basal as well as PGI2-stimulated cAMP content was lower in homogenates from atherosclerotic than from normal aortic tissue. Dipyridamole-treated animals showed a further decrease in basal as well as PGI2-stimulated cAMP content of the aortic tissue, suggesting that this decrease in cAMP content may be linked to the enhanced proliferative activity seen in artherosclerotic plaque formation.

Adenosine↗
PubMed1979

Atherosclerosis decreased prostacyclin formation in rabbit lungs and kidneys.

Metabolism of arachidonic acid (AA) was studied in perfused lungs and kidneys of normal and atherosclerotic rabbits by determination of PGE2, PGF2 alpha and the stable metabolites of PGI2 (6-keto-PGF1 alpha) and TXA2 (TXB2). PGI2 was the main AA metabolite formed by normal lungs and kidneys. Atherosclerosis reduced the formation of PGI2 by about 50 % in both organs. TXA2 formation was similarily decreased in lungs. In kidneys, the decrease in PGI2 formation was accompanied by an increase in PGE2 formation.

Animals↗
PubMed1979

Prostaglandins and fibroblast functions in vitro.

Secondary embryonic mouse fibroblasts synthesise mainly E-type PG. The formation of PGF2 alpha is about 10 times lower. No PGI2 formation was observed. Secondary embryonic mouse fibroblasts possess an adenylate cyclase which is stimulated by E-type PGs, but little by PGF2 alpha or PGI2. PGE1-induced stimulation of cAMP levels is dose-dependently linked to an increase in biosynthetic activity of the cells, visible in increased GAG biosynthesis and PG formation. cAMP-dependent enhancement of GAG biosynthesis does not alter the carbohydrate spectrum of the secreted GAG, indicating that only the amount, but not the quality of the secreted GAG is affected by PGE1 or cAMP. Steroidal as well as non-steroidal antirheumatic agents can affect either basal or PGE1 stimulated cAMP levels or other components of the adenylate cyclase system independent of their inhibitory action on PG formation. These effects are always reflected in a decrease or increase of GAG biosynthesis. PGE1-induced stimulation of cAMP levels is related to an inhibition of fibroblast proliferation. Reduction of endogenous PG formation for prolonged periods does not result in a prolonged decrease of intracellular cAMP followed by a decrease in GAG biosynthesis or an increase in proliferation. The initial effect of reduced endogenous PG formation is compensated for by an increased sensitivity of the cells to PG's, resulting in maintenance of basal cAMP levels and an increased sensitivity to exogenous PGE1. These effects on cAMP levels are also reflected in GAG biosynthesis and proliferative activity of the cells.

Animals↗
PubMed1979

[Plasma levels of PGE2, PGA2 and PGF2 alpha during spontaneous labour].

Plasma levels of PGE2, PGA2 and PGF2 alpha were determined by radioimmunoassay in maternal venous blood during different phases of uterine contractions. Mean prostaglandin levels during labor were: PGE2 = 2,25 +/- 1,3 ng/ml (mean +/- SD), PGA2 = 2,86 +/- 1,55 ng/ml and PGF2 alpha = 0,58 +/- 0,37 ng/ml. The approximate ratios between the prostaglandin concentrations were: PGE2:PGA2: PGF2 alpha = 1:1-3:0,3. No changes of PGE2 levels were found in the course of concentrations during the first and second stage of labor. At delivery and at the contraction followed by the expulsion of the placenta, PGE2 concentrations rose from the beginning of the contraction (2,21 +/- 0,07 ng PGE2/ml) to the maximum of the contraction (4,31 +/- 0,56 ng PGE2/ml). PGA2 levels did neither show a correlation to the course of contractions nor to the different stages of labor, but were considerably different between patients during the first stage of labor (e.g. 1,9 +/- 1,1 ng PGA2/ml) and during the second stage of labor (3,36 +/- 2,8 ng PGA2/ml). Mean PGF2 alpha concentrations were between 0,21 +/- 0,12 ngPGF2 alpha/ml (1st stage) and 0,81 +/- 0,11 ng PGF2alpha/ml (highest value obtained, 1st stage of labor, too). There was no correlation between PGF2 alpha concentrations and the course of contractions during the different stages of labor.

Female↗