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Biomedical subjects

C Leithner

Publications and source records attributed to C Leithner.

At least 55 records · Page 3Linked to original sources
PubMed1981

Platelet microaggregates and release of endogenous prostacyclin during the initial phase of haemodialysis.

In six patients arterial blood samples were withdrawn during haemodialysis (HD) for the measurement of platelet microaggregates, platelet and leucocyte counts, pO2 and 6-oxo-PGF1 alpha (the stable metabolite of prostacyclin). During the initial phase of HD the plasma concentrations of 6-oxo-PGF1 alpha increased, indicating an increased release of endogenous prostacyclin. Coincidentally to this phenomenon, hypoxaemia, reduction in platelet and leucocyte counts, and an increase in number of platelet microaggregates could be observed. Since prostacyclin is able to resolve platelet aggregates, we interpret the increased prostacyclin release to be in part a self protection mechanism against embolisation of microaggregates released from the dialyser into lung and peripheral vascular systems.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

[Prostacyclin as a protective factor for blood vessels].

Prostacyclin is a very unstable prostaglandin, which is continuously synthetized and released by blood vessels. It fulfills 2 main functions, namely strong inhibition of platelet aggregation and vasodilation. Thus it acts as an important defense mechanism of the vascular wall, which is directed against overwhelming platelet aggregation and against the development of atherosclerosis. Besides endogenous prostacyclin is an important antihypertensive factor. In several diseases, as diabetes mellitus, obliterative arteriopathy and haemolytic-uraemic syndrome, the reduced prostacyclin-synthesis is thought to be a key mechanism for the development of vascular lesions. On the other hand the haemorrhagic diathesis of uraemics is seen in connection with an increased vascular prostacyclin release. Synthetic prostacyclin is now under trial for therapy in peripheral obliterative arteriopathy and extracorporeal circulation, as haemodialysis and cardiopulmonary bypass.

Arteriosclerosis↗
PubMed1980

Enhanced 6-oxo-PGF1 alpha levels in plasma during hemodialysis.

The activation of platelets due to foreign surface interaction is a well known fact. Earlier, we found an increase of circulating platelet microaggregates (method of Wu and Hoak) during hemodialysis. Since this phenomenon might cause a PGI2-release by lung and/or vascular tissue, we studied the plasma 6-oxo-PGF 1 alpha-levels in 6 patients during hemodialysis. We found an initial increase of plasma 6-oxo-PGF 1 alpha. Coincidently, hypoxemia, fall in platelet and lekocyte count and a decrease in platelet count ratio were observed. An effect of heparin was excluded in a control group. The findings support the hypothesis that PGI2 acts as a defense mechanism against platelet deposition on vascular wall by a temporary increased synthesis which could be monitored by a temporarily enhanced plasma 6-oxo-PGF 1 alpha-level during the initial phase of hemodialysis.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

[Age dependence of vascular prostacyclin formation in man (author's transl)].

The synthesis of prostacyclin (PGI2), the most potent known inhibitor of platelet aggregation, varies with age. After 30 years the production decreases, but increases again in the 6th and 7th decade. Contrary to these physiological variations patients suffering from juvenile onset diabetes or peripheral angiopathy show a markedly decreased prostacyclin synthesis. Since the prostacyclin system in thought to be an important blood vessel protector, the pathological low level of PGI2-synthesis could be a key position in development or progression of vascular complications.

Adult↗
PubMed1980

Influence of proteoglycans (PG) and glycosaminoglycans (GAG) on ADP-, collagen- and thrombin-induced platelet aggregation.

PGs and GAGs have been isolated from fresh bovine aortas according to the method of Hascall and chemically characterized. These PGs and GAGs had only little effects on ADP- and collagen-induced platelet aggregation, but had very potent inhibitory action on thrombin-induced platelet aggregation and prolonged thrombin-clotting-time. Of the standard GAGs investigated hyaluronic acid, chondroitin-4-sulfate and chondroitin-6-sulfate had only little inhibitory action on thrombin-induced platelet aggregation, whereas heparin was very potent in this respect. The unsaturated disaccharides originating after degradation of GAGs with chondroitinases had no effect on platelet aggregation. No differences between PGs and GAGs in inhibiting thrombin-induced platelet aggregation could be detected.

Adenosine Diphosphate↗
PubMed1980

Effect of proteoglycans (Pg) and glycosaminoglycans (GAG) on prostacyclin (PGI2) and PGI2-formation of rat arteries.

Heparin had no effect on PGI2-activity if heparin and PGI2 have been incubated-together in an ice bath for 3 minutes. But heparin was able - unlike the other Pg or GAG - to abolish PGI2-activity if it had been incubated with PGI2 in an ice bath for 15 minutes. Pg and GAG, which had been isolated from bovine aortas according to the method of Hascall, and commerically available GAG (hyaluronic acid, chondroitin-40-sulfate, chondroitin-6-sulfate and heparin) had no effect on PGI2-formation of rat aortas in short time incubation (3 min). After long time incubation (15 min) or rat aortas in heparin less PGI2 was detectable compared to a buffer incubation. These data suggest that Pg and GAG do not influence PGI2-formation of arteries. The diminished PGI2-activity after long time incubation should be due to the PGI2-degrading effect of heparin.

Animals↗
PubMed1980

Aortic response to renovascular hypertension.

In the early phase of malignant renal hypertension induced by aortic ligature, a transient activation of transmural aortic permeability is observed. The transmural permeability shows its maximum during the first week of hypertension returning in the third week to normal or even subnormal values, whereas the blood pressure is still rising. The permeability disturbance precedes the structural transformation of the arterial wall. Although the aortic segments above and below the ligature are exposed to different blood pressure and hemodynamic stresses their patterns of permeability disturbance are the same. If the kidney below the aortic ligature is removed no permeability disturbance can be observed. Aortic wall PGI2-formation both above and below the ligature is elevated in the first phase of hypertension. The PGI2-synthesis returns to normal values during the 5th week. Our data suggest that in the early phase of renovascular hypertension there is an increased aortic antiaggregatory activity and that PGI2 is probably not the compound responsible for increased transmural permeability. Moreover, the blood pressure and the hemodynamic forces have no decisive importance in the induction of the aortic transmural permeability disturbance.

Animals↗
PubMed1980

Enhanced prostacyclin synthesis in acute human kidney transplant rejection.

In acute and chronic kidney transplant rejection renal cortical and medullary tissue samples were examined for their prostacyclin (PGI2) generation by bioassay and compared with normal tissue. In acute rejection PGI2 formation was significantly enhanced, particularly in the cortex. In chronic rejection the PGI2 formation was comparable with control tissue. Since PGI2 is a very potent platelet aggregation inhibitor and vasodilator, it is concluded that the increase in PGI2 generation in acute rejection might be a self protecting mechanism which is, however, overwhelmed in irreversible rejection.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

[Interaction between blood platelets and capillary kidney in haemodialysis (author's transl)].

In haemodialysis an interaction between platelets and the dialysator membrane occurs, which is not prevented by heparin. This can be demonstrated by parietal depositions of platelets in the capillaries of the artificial kidney by scanning electron microscopy, as well as in a marked increase of reversible platelet microaggregates during the first phase of dialysis. Some patients are prone to develop thrombosis of the capillary kidneys in spite of a high-dose heparinization. In these cases the use of diclofenac, a cyclooxygenase inhibitor, prevents these adverse platelet reactions.

Adolescent↗
PubMed1979

[Thrombocyte function and systemic effect of prostaglandin I2 inhalation].

After inhalation of prostaglandin I2 minimal effects on lung function and the cardiovascular system could be observed in healthy volunteers. Platelet function, however, decreased significantly. In the future the application of the prostaglandin I2 may be a new approach in the treatment of thromboembolic disorders in man.

Adult↗
PubMed1978

Scanning electron microscopic study of hyperacute rejection in the inbred rat.

Twenty skin-presensitised Lewis rats received kidney transplants from (Lewis X BN)f1 rats. Two grafts each were withdrawn at intervals from 1--120 min and examined using a scanning electron microscopic (SEM). A series of Lewis to Lewis isografts served as control. In hyperacute rejection at just 1 min spider-like fibrin fibres and platelets could be observed in small arteries, where the endothelium was severely altered. In these regions at 2 and particularly 5 min a fibrin network often contained platelet aggregates, mechanically altered erythrocytes as well as different kinds of leucocytes. This coagulation process progressed with time and resulted in a complete vascular occlusion at 30--60 min.

Animals↗
PubMed1978

Enhanced prostacyclin availability of blood vessels in uraemic humans and rats.

Recently prostacyclin (PHI2), an unstable prostaglandin with a strong inhibitory effect on platelet aggregation, has been demonstrated in the wall of blood vessels. We estimated the PGI2 availability of arteries and veins in 10 uraemic patients and 12 nephrectomised rats. The production of PGI2 after long-term incubation of the vessels was markedly enhanced and prolonged. This alteration is probably one key mechanism for the deterioration of haemostasis in uraemics. Preliminary results of further studies indicate that substances in uraemic plasma--presumably middle molecules--may enhance the PGI2 availability of normal vessels in vitro.

Animals↗
PubMed1976

[Renal thrombohemolytic microangiopathy (author's transl)].

The clinical findings in three patients with renal thrombohemolytic microangiopathy are presented. The triad of microangiopathic hemolytic anemia, disseminated intravascular coagulation and microangiopathic changes of the kidney leading to renal insufficiency is the characteristic feature of this disease. Beside the usual classification based on etiological factors (distinguishing between primary and symptomatic forms) a topographical classification (distinguishing between generalized forms and localized forms occuring in isolated organs) is suggested. The pathogenesis and therapy of this disorder are discussed.

Adolescent↗