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Biomedical subjects

J Kaliman

Publications and source records attributed to J Kaliman.

At least 55 records · Page 3Linked to original sources
PubMed1987

Development of optimal infusion regimens for epoprostenol using radio labelled platelet uptake over atherosclerotic lesions in man.

1. Epoprostenol (prostacyclin, PGI2) has been evaluated in clinical trials in peripheral vascular disease and other conditions chiefly on the basis of its platelet inhibitory properties. These therapeutic evaluations have proceeded in the absence of evidence as to the optimum infusion regimen for epoprostenol and the choice of schedules of administration has been arbitrary. We have tried to establish an optimum infusion regimen in patients with peripheral vascular disease in terms of maximal inhibition of platelet deposition on atherosclerotic lesions in vivo together with maximal inhibition of platelet aggregation ex vivo. 2. One hundred and twenty three patients with atherosclerotic peripheral vascular disease and increased platelet uptake at atherosclerotic sites were selected. Epoprostenol was administered at a fixed dose of 5 mg kg-1 min-1 for 0.5-24 h daily for 3-7 days. 3. Infusion of epoprostenol for 6 h daily for up to 5 days caused maximum decrease in platelet uptake without tachyphylaxis and without loss of the inhibitory effect of epoprostenol on platelet aggregation responses. Longer daily infusion periods were associated with progressive loss of the anti-aggregatory effect of epoprostenol without any greater decrease in platelet uptake. Shorter daily infusion periods produced smaller decreases in platelet uptake.

Adenosine Diphosphate↗
PubMed1986

[A new method for the treatment of supraventricular rhythm disorders].

Initial experience of His-bundle ablation is presented in 12 patients with intractable supraventricular arrhythmias which were not amenable to treatment with conventional drugs. In 8 patients His-bundle ablation resulted in total AV-block and in 2 patients significant improvement without total AV-block was achieved. During long-term follow-up (mean 5.3 months) tachycardia recurred in 1 patient with total AV-block resulting in an overall success rate of 75%. A permanent pacemaker was implanted in 10 patients. 1 patient developed deep leg vein thrombosis as a direct result of this procedure and in 2 patients there were complications due to pacemaker implantation. His-bundle ablation appears to be a promising tool in the management of intractable supraventricular tachycardia.

Aged↗
PubMed1986

[Vasodilating effect of leukotriene C4 and D4 by stimulation of prostacyclin synthesis].

Since the original discovery and structural characterization of leukotrienes, these substances have attracted considerable interest due to their numerous biological activities. It is known that these substances exert a short lasting vasoconstrictory and a longer lasting vasodilatory response. However, the cause of this biphasic response is not clear as yet. Human coronary artery segments synthesize about 50 pg PGI2/cm2/min in vitro under pressure perfusion. At concentrations ranging from 1 to 100 ng leukotrienes C4 and D4 cause a dose-dependent increase in PGI2 generation. Inhibition by acetylsalicylic acid and 15-hydroxyperoxyarachidonic acid indicates the mechanism to be mediated via the cyclooxygenase. It is, therefore, concluded that the capacity of leukotrienes C4 and D4 to stimulate PGI2 formation might play a key role during acute inflammation at the site of white blood cell accumulation.

Coronary Circulation↗
PubMed1986

Imaging of human atherosclerotic lesions using 123I-low-density lipoprotein.

In patients suffering from clinically manifest atherosclerosis autologous LDL-labelling has been done using 123I. This technique allows localization of areas with an increased LDL entry as well as a monitoring of kinetics. Normally, no tracer uptake can be seen in the vascular system. Positive camera images, however, can be obtained in pathological areas as early as 60 min after LDL-reinjection. Experimental data and morphological control reveal a very good correlation to the gamma-camera findings. The technique seems to be very promising for diagnosis in patients suffering from atherosclerosis and hyperlipoproteinemia.

Aged↗
PubMed1986

Prostacyclin synthesis stimulating plasma factor in patients with primary hyperlipoproteinemia--effect of dietary and drug treatment.

Recent data have demonstrated a possible pathogenetic influence of the prostacyclin synthesis stimulating plasma factor (PF) in various diseases. Studying this PF in 26 patients with primary hyperlipoproteinemia (HLP) we examined patients suffering from types IIa (n = 8), IIb (n = 6) and IV (n = 12) classified according to Fredrickson. Plasma was withdrawn at the detection of the HLP, 4 weeks after a dietary intervention and again 4 weeks after the beginning of a drug treatment. Using various test models such as rat and minipig aortic tissue, human aorta and saphenous vein as well as cultured endothelial and smooth muscle cells, the data reveal an in part significant improvement of PF running parallel with the improvement of HLP. These findings suggest that even though a significant difference between healthy controls and patients suffering from severe atherosclerosis has not been found, there occurs a significant improvement of PF in hyperlipidemic patients after successful treatment. Thus, it can be concluded that normalization of PF is one of the many factors improving the hemostatic balance in patients undergoing beneficial dietary or drug treatment.

Adult↗
PubMed1986

Prostacyclin synthesis stimulating plasma factor in coronary heart disease.

Evidence has been presented that the prostacyclin synthesis stimulating plasma factor might be altered under various clinical conditions and thereby influence in a positive or negative way the hemostatic balance. Therefore, we studied angiographically verified coronary heart disease patients with a combination of various risk factors. Different test systems like cultured endothelial and smooth muscle cells, rat aorta, human coronary artery, minipig abdominal aorta and aorta of streptozotocin-induced diabetic rat have been used. With an increasing number of risk factors being present, the plasma factor activity shows a trend towards a decrease, however, in none of the groups was the difference statistically significant. It is thus concluded that changes in plasma factor activity are too small to be of clinical importance by influencing hemostatic regulation in humans.

Animals↗
PubMed1986

Effect of leukotrienes C4 and D4 on prostaglandin I2-liberation from human lymphatics.

Whereas prostaglandin I2 (PGI2), a major metabolite of human lymphatics, does not itself affect lymphatic contractility significantly, it is able to counterbalance the contractile response to thromboxane and leukotrienes. We now demonstrate that leukotrienes C4 and D4 evoke a dose-dependent increased production of PGI2 from human lymphatics. It is likely that leukotrienes either exert a contractile rhythmic effect on human lymphatics or, alternatively, evoke increased PGI2-formation which relaxes human lymphatics. These mechanisms may be of local importance in regulating lymphatic "tone" at sites of inflammation as leukotrienes are liberated from activated white blood cells.

Adolescent↗
PubMed1986

Enhanced prostaglandin I2-formation of human lymphatics during pulsatile perfusion.

Previous studies demonstrate that prostacyclin (prostaglandin I2, PGI2) is the main arachidonic acid product in human lymph vessels. Pulsatile perfusion increases and prolongs PGI2-formation as do leukotrienes (LT) such as LTC4. Thus, physical activity besides local mechanical and biochemical influences on lymph pressure and flow also stimulates local lymphatic PGI2 synthesis, a prime counterbalancing factor in lymphatic constriction induced by other eicosanoids.

Adolescent↗
PubMed1985

[Accelerated degradation of prostacyclin in diabetic plasma--a further factor in the impairment of hemostatic balance?].

Prostacyclin is degraded in human plasma in vitro with an average half-life of 10 minutes. The degradation in plasma of patients suffering from type II diabetes mellitus is significantly enhanced. However, the inactivation of prostacyclin in plasma in patients with clinical manifestations of atherosclerosis, such as peripheral vascular disease, is unchanged. Methodological studies reveal that storage of plasma at various temperatures up to investigation, repeated freezing and thawing, as well as the addition of thromboxane-synthetase inhibitors do not exert any effect on plasmatic degradation of PGI2. In addition, no differences are found in plasmatic degradation in diabetics in accordance with the mode of treatment. The presence of a factor in human plasma in diabetics capable of increasing PGI2 degradation or the loss of a possible stabilizer could be one further important parameter, amongst others responsible for the development of either macro- or microangiopathy in diabetes mellitus.

Aged↗
PubMed1985

[Defects in the prostaglandin system. II. Familial platelet-prostacyclin receptor defect (Wien-Hietzing defect)--pathogenetic significance for (early) development of atherosclerosis?].

A case is reported of a 10 year-old girl admitted to hospital because of severe intermittent claudication. Occlusion of the left popliteal artery was diagnosed. Since successful surgical intervention the patient has been symptom-free. No causative factor was detected for this premature occlusion. During intensive laboratory check-up an extreme diminution in sensitivity of the platelets to prostacyclin and a receptor defect were discovered. This defect seems to be genetically determined. The extent to which this as yet unreported platelet defect might have contributed to the development of atherosclerosis at such an early age is discussed.

Arteriosclerosis↗
PubMed1985

Platelet sensitivity to antiaggregatory prostaglandins (PGE1,D2,I2) in patients with peripheral vascular disease.

Platelet sensitivity to antiaggregatory prostaglandins (PGI2, PGE1, PGD2) was studied in 143 patients (122 male) with angiographically proven peripheral vascular disease and compared with age-matched clinically normal controls. Patients had a significantly lower platelet sensitivity to PGI2, PGE1, and PGD2 than controls. Clinical stages had no significant influence on the platelet sensitivity to PGI2 and PGE1. Patients with stage IIa had a lower sensitivity to PGD2 than patients with stage IV, the difference not being significant. Analyzing the influence of risk factors like diabetes, hyperlipoproteinemia, or smoking, there seemed to be an inverse relation between risk factors and platelet sensitivity to PGI2 and PGE1. Smokers especially, together with smokers exhibiting an additional risk factor, exhibited the highest prostaglandin consumption (PGI2, PGE1) and therefore the lowest platelet sensitivity. However, it has to be emphasized that the differences were not significant. There was a significant correlation between platelet sensitivity to PGI2 and PGE1, whereas this was not the case between the respective sensitivities to PGI2 and PGD2. This supports the hypothesis that both these prostaglandins (PGI2, PGE1) share the same receptor on the platelet surface, whereas PGD2 has its own receptor.

Adenosine Diphosphate↗
PubMed1985

The prostacyclin synthesis stimulating plasma factor is unchanged during acute angina pectoris.

Earlier studies have demonstrated that the levels of prostacyclin synthesis stimulating plasma factor are changed during various clinical situations thus leading to disturbances in hemostatic balance. Therefore, we studied the plasma factor in 20 patients undergoing acute anginal attacks in order to see whether there is any influence or a timedependent change after the event. The patients were subdivided into males or females as well as into those with or without maturity onset diabetes and who were smokers or no-smokers. As in-vitro test systems the rat abdominal aorta, human coronary artery and cultured endothelial and smooth muscle cells obtained from minipigs were used. Our findings demonstrate that incubating the different tissue samples in plasma leads to a significant increase of prostacyclin formation or of its stable breakdown 6-oxo-PGF1 respectively, in comparison to buffer control incubation. However, in none of the groups was a change observed during an anginal attack or in rate 60 and 120 minutes thereafter. These findings suggest that the prostacyclin synthesis stimulating plasma factor is not involved in hemostatic dysregulation, which has been observed to occur during and immediately after a coronary anginal attack.

Adult↗