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Biomedical subjects

H Sinzinger

Publications and source records attributed to H Sinzinger.

At least 595 records · Page 33Linked to original sources
PubMed1979

Alterations of the internal elastic membrane in juvenile human arteries.

Quantitative changes in the internal elastic membrane (IEM) were studied in human arteries from different location in 31 males and 31 females, using an eight-criterion classification system. The IEM involvement shows a sex-dependent increase with age, and is more pronounced in arteries known to exhibit a more intensive atherosclerotic involvement. It seems that the IEM changes represent a true ageing phenomenon, which is sometimes influenced to a various degree by the atherosclerotic process.

Adolescent↗
PubMed1979

Platelet adhesion and platelet thrombus formation on subendothelium of human arteries and veins exposed to flowing blood in vitro. A comparison with rabbit aorta.

Subendothelium of blood vessel segments from elderly patients was exposed in a perfusion chamber to citrated blood under arterial blood flow conditions. The resulting platelet adhesion and thrombus formation was assessed morphometrically. The results show that the time course and the extent of platelet adhesion and aggregation were similar to the results obtained previously with subendothelium from rabbit arteries. The extent of surface-induced platelet aggregation was furthermore governed by both the properties of the exposed surface as well as those of the blood perfusate. No significant differences with regard to platelet reactivity were found between veins and arteries and the extent of surface-induced platelet aggregation was rather low.

Animals↗
PubMed1979

[Physiopathology of prostaglandin I2 synthesis in the human gastrointestinal mucosa].

1. PGI2 is synthetized in human gastrointestinal mucosa. 2. PGI2 seems to be responsible for pathophysiological conditions. 3. Disorders caused by an enhanced or diminished PGI2-synthesis could be treated in the future by inhibition of prostacyclin synthetase or exogenous synthetic PGI2 respectively. 4. In order to remove the problems with the unstable PGI2, synthetic analogs could be used for the treatment.

Adult↗
PubMed1979

Prostacyclin activity in rat kidney stimulated by angiotensin II.

Prostacyclin (PGx, PG12) activity can be found in renal tissue as indicated by platelet aggregation inhibition. The activity of the medullary tissue in terms of wet weight is significantly higher (P less than 0.01) than that of cortex. The activity decreases with time and has almost entirely gone within 1 h. Boiling for 30 s destroys the inhibitory effect of the prostacyclin on platelet aggregation. Angiotensin II is able to stimulate the prostacyclin availability of the tissue after incubation for 3 min. Addition of angiotensin II to platelet-rich plasma (PRP) has no significant effect on ADP-induced platelet aggregation. The spontaneous generation of prostacyclin as well as that stimulated by angiotensin II can be suppressed by previous incubation of the tissue with a prostaglandin synthetase inhibitor such as ketoprofen. Tissues which have only a small amount of basal release in buffer show an increased platelet aggregation inhibitory effect after addition to PRP. The difference between medulla and cortex is statistically significant. This different release of prostacyclin cannot be related to different endothelial surface area, because the endothelial surface in medulla and cortex is quite similar. It is suggested that prostacyclin has an important influence on the renal function. The different capacity of renal medulla and cortex in generation of prostacyclin could be of great importance for a fuller understanding of the physiology of renal function.

Angiotensin II↗
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↗