Biomedical subjects
Publications and source records attributed to K Silberbauer.
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In six patients arterial blood samples were withdrawn during haemodialysis (HD) for the measurement of platelet microaggregates, platelet and leucocyte counts, pO2 and 6-oxo-PGF1 alpha (the stable metabolite of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.
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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.
In 8 oarsmen aged 19 to 31 years a symptom-limited rectangular-progressive bicycle stress test has been conducted. Venous blood was taken before and at the end of the test, and 30 and 60 minutes afterwards. pH, base excess, pCO2, platelet count and platelet count ratio (WU and HOAK) were measured or calculated, the last in order to quantify the tendency of the platelets to form reversible aggregates. At the point of exhaustion there is a highly significant (p < 0.001) decrease in the platelet cunt ratio (= increase in reversible platelet aggregates). A highly significant correlation exists between base excess and the platelet count ratio. The regression line does not fall below the normal value of the platelet count ratio until the delta-base excess is -4 mval/l. This means that an increase in the tendency to form reversible platelet aggregates is not typical of the range of aerobic metabolism but of muscular work in the anaerobic range with high exercise-induced metabolic acidosis. The basis for sudden death in sport due to internal reasons is not uncommonly an unknown and asymptomatic coronary disease and platelet aggregates. Persons aged over 30 years and sports in which competition is also inherent (soccer, tennis) are often involved. Acute cardiac death in sport is not very frequent. Nevertheless, the following recomendation seems to be warranted: persons aged over 30 years in bad condition should not start competitive sports or other intensive muscular exercise. Before they do so, low-intensive, controlled, aerobic endurance training is necessary.
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PGI2 synthesis was investigated in rectal mucosa of 8 patients with active ulcerative colitis, 4 in remission and 16 controls. Determinations were carried out using Moncada's bioassay. The results demonstrated enhanced PGI2 synthesis in rectal mucosa in active ulcerative colitis. Further clinical studies should clarify whether or not selective inhibiton of PGI2 synthetase might be a useful therapeutic approach in ulcerative colitis.
Species exhibiting a higher susceptibility to the development of atherosclerosis have a reduced prostacyclin (PGI2)-generation in the arterial wall, which differs in various parts of the vascular system. As the difference in PGI2-formation in various diseases is a generalized vascular effect, the changes can be detected in all vessels. This is a very important point for diagnostic purposes in humans.
In the presence of cimetidine, pentagastrin and somatostatin prostacyclin formation does not differ significantly from the value obtained with the buffer control, whereas cimetidine alone is able to inhibit ADP-induced platelet aggregation in vitro to a small degree. It is concluded that the in vivo action of the drugs if not primarily mediated by prostacyclin.
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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.
Unaltered human arterial tissue as well as different types of macroscopically and microscopically characterized atherosclerotic lesions were microdissected under a preparation microscope. The prostacyclin formation was examined using its potent platelet aggregation inhibition in vitro according to Moncada's bioassay. In contrast to different PGI2-formation in various experimental animal models the generation in the different lesion types in terms of wet weight was statistically significantly (p less than 0.001) diminished in comparison to normal control tissue. However, the PGI2- formation in different lesion types is comparable. Accepting the hypothesis delivered earlier by us, that the arterial wall is able to react upon exogenous noxes with a temporarily enhanced PGI2-formation, followed (after ceasing) by a decrease of PGI2-synthesis (exhaustion phenomenon) it can be concluded, that the critical stage is prior to the fatty streak formation, which is a preatherosclerotic lesion. Therefore, PGI2-generation-exhaustion might be mainly responsible for initiation and progression of atherosclerosis, probably before any detectable morphological alterations.
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The sudanophilic lesions around the aortic ostia of 10 fetus, 10 newborns and 10 children aged up to 1 year were studied using a polar coordinate mapping method. The periorificial sudanophilic lesions develop initially distal to the orifices and show a continuous increase with age in percentage and extent. In children the lesions nearly completely surround all the ostia with a significant distal peak. There was no sex difference; the involvement of the right and left side was comparable. The comparison of the morphological data from the parents and children with anamnestics showed no relationship.
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