[Hyperacute kidney transplant rejection: scanning electron microscopy of the intrarenal arteries].
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Biomedical subjects
Publications and source records attributed to H Sinzinger.
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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.
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.
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.
The aortas of 9 months aged Show Racer and White Carneau pigeons were examined for their PGE2, PGF2 alpha and 6-keto-PGF1 alpha synthesis from labelled arachidonic acid by radiothinlayer chromatography. The prostacyclin formation was estimated by means of Moncada's bioassay. PGE2 and PGF 2 alpha synthesis in the aorta of pigeons is higher than in rats, whereas less 6-keto-PGF1 alpha is formed in pigeon aortas. The susceptible White Carneau pigeons synthesitize more prostaglandins than the resistant Show Racer pigeons. PGI2 and 6-keto-PGF 1 alpha-formation is extremely low in avian arota. These data are in part contradicting to our findings im mammalians (where the atherosclerosis susceptible animals generate less PGI2) and warrants sequential measurements of prostaglandin synthesis in aorta to assess its significance during various stages of atherogenesis.
This study of 20 patients with monoclonal gammopathy (17 patients with multiple myeloma and 3 patients with Waldenström's syndrome) showed a decreased platlet aggregation induced by ADP and collagen, a reduced platlet retention and a prolonged bleeding time in 25% of the cases in comparison with 30 age- and sex-matched healthy controls. Using Wu and Hoak's technique as increased number of reversible platelet aggregates was observed. There was no relationship between the parameters of primary haemostasis and protein analysis. A disturbed mechanism of primary haemostasis is the main factor responsible for the bleeding diathesis in patients with monoclonal gammopathy.
The human gastric mucosa generates prostacyclin (22 +/- 6 ng PG I2/g). There is no age or sex difference in PG I2 formation by normal gastric mucosa. The properties of the substance are the same as reported in other tissues.
In eight chronically haemodialysed patients a significant increase of circulating platelet aggregates (method of Wu and Hoak) was observed immediately after starting haemodialysis. The number of aggregates decreased at the end of haemodialysis reaching the starting values after 360 min. The platelet interaction with the dialysis membrane surface might cause this phenomenon. Anticoagulation with heparin alone was insufficient in preventing aggregate formation during haemodialysis.
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The newly formed tissue of dacron vascular prosthetic grafts implanted in humans demonstrates prostacyclin generation and fibrinolytic activity comparable to that of the atherosclerotic artery in the vicinity. This provides some evidence that both activities important for haemostasis run parallel.
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Activated smooth muscle cells exhibit a statistically significant (p less than 0.025) higher prostacyclin production than the contractiles. It is concluded, that the proliferation of the metabolically activated cells, which is an early event in atherogenesis, could be due to prostacyclin regulation.
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