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Biomedical subjects

H R Baumgartner

Publications and source records attributed to H R Baumgartner.

At least 91 records · Page 5Linked to original sources
PubMed1977

Platelet interaction with collagen fibrils in flowing blood. II. Impaired adhesion-aggregation in bleeding disorders. A comparison with subendothelium.

Anticoagulated whole blood from patients and control subjects was circulated through an annular perfusion chamber in which the fibrillar collagen of alpha chymotrypsin-digested subendothelium and intact subendothelium were exposed. The blood flow conditions corresponded to those in arteries (830 sec-1 wall shear rate). Platelet surface interaction was measured morphometrically. Decreased adhesion to fibrillar collagen associated with normal spreading and normal adhesion-induced formation of platelet thrombi was found with blood of patients with von Willebrand's disease and the Bernard Soulier Syndrome, indicating a defect in the initial attachment reaction of platelets with collagen. Platelets of patients with thrombasthenia did normally adhere to the collagen fibrils and also lost their subcellular organelles during this reaction, but they totally failed to adhere to each other. In storage pool disease platelet thrombus formation was consistently inhibited whereas adhesion and spreading was inhibited in some patients and normal in others. In contrast adhesion was always normal after ingestion of aspirin which consistently caused a marked inhibition of platelet thrombi. These findings correspond -- in essence -- to those previously described on intact subendothelium. However, the observed defects are more pronounced on the fibrillar collagen than on intact subendothelium.

Animals↗
PubMed1977

Platelet interaction with collagen fibrils in flowing blood. I. Reaction of human platelets with alpha chymotrypsin-digested subendothelium.

The subendothelial surface of rabbit aorta and alpha chymotrypsin-digested subendothelium were exposed to anticoagulated human blood in an annular flow chamber. The wall shear rate was similar to that observed in large arteries (830 sec-1) and exposure times varied from 2 1/2 to 40 min. The platelet reactive substrate of alpha chymotrypsin-digested subendothelium consists of a three-dimensional meshwork of collagen fibrils which form islands of variable size and height in a matrix of virtually unreactive elastin. Collagen-induced aggregation in the aggregometer was similar with or without prior alpha chymotrypsin-digestion of a highly dispersed preparation of fibrillar collagen. The rate of platelet adhesion was decreased on the fibrallar collagen of alpha chymotrypsin-digested subendothelium as compared to intact subendothelium. On the other hand the rate of aggregation was increased once platelets adhered to the fibrillar collagen. Mural thrombi (aggregates) disappeared on subendothelium whereas they grew progressively on the fibrillar collagen. Thus the fibrillar collagen of alpha chymotrypsin-digested subendothelium appears to be a more thrombogenic surface. It is suggested that physical (loose three-dimensional meshwork versus a comparatively solid surface) and/or chemical (number of platelet reactive sites per unit surface area) differences between the two surfaces may explain the platelet-surface-interaction patterns which are characteristic for each surface.

Adult↗
PubMed1976

Effects of anticoagulation on the interaction of human platelets with subendothelium in flowing blood.

The subendothelial surface of rabbit aorta was exposed to a laminar stream of native human blood using a perfusion chamber. The blood was drawn at a constant flow rate and 37 degrees C from a cubital vein through the annular space of the chamber by means of a roller pump. Platelet interaction with subendothelium and fibrin deposition were measured morphometrically. Native blood and blood anticoagulated with 15 mM citrate obtained from the same donor was investigated at arterial blood flow conditions. Platelet adhesion was significantly increased by the anticoagulation. In contrast, platelet spreading and adhesion-induced aggregation were significantly inhibited by citrate. The extent of fibrin deposition varied greatly from one donor to another and did not correlate with platelet adhesion. It is concluded that initially, the two hemostatic systems platelet adhesion-aggregation and coagulation function independently.

Animals↗
PubMed1976

Enzymatic removal of ADP from plasma: unaltered platelet adhesion but reduced aggregation on subendothelium and collagen fibrils.

Subendothelium of rabbit aorta and fibrillar collagen were exposed to citrated human or rabbit blood which was circulated through a perfusion chamber under flow conditions similar to those found in arteries. The resulting platelet adhesion and subsequent formation of platelet microthrombi on the exposed surfaces were measured in 0.8 mum thich sections by a morphometric technique using light microscopy. Removal of plasma ADP by the substrate-enzyme combination CP-CPK (creatine phosphate-creatine phosphokinase; 3 mM and 90 U/ml blood) did not affect the initial attachment and spreading of platelets on subendothelium, whereas platelet thrombus formation was strongly inhibited. On free collagen fibrils CP-CPK was much less inhibitory on platelet thrombus formation but platelet adhesion again was not affected. It is concluded that platelet aggregation induced by thrombogenic surfaces in the presence of arterial blood flow is at least partially governed by ADP released from adhering platelets. Platelet adhesion to the examined surfaces, however, does not seem to be mediated by plasma ADP.

Adenosine Diphosphate↗
PubMed1976

Platelet adhesion, release and aggregation in flowing blood: effects of surface properties and platelet function.

Platelet adhesion to natural and artificial surfaces and adhesion-induced aggregation were investigated in vitro using an annular perfusion chamber. The surfaces were exposed to anticoagulated blood under identical flow conditions (approximately arterial shear rates). The initial attachment of platelets (contact) appeared less surface specific than spreading and release. Fibrillar collagen was the most powerful inducer of platelet degranulation whereas elastin, microfibrils and epon were virtually inactive. Fibrillar collagen caused release also in the absence of spreading. Surface coverage with platelets did not exceed 25% unless spreading occurred. Perfusion with platelet-free plasma or platelet-poor blood did not remove adhering platelets. However, platelets were translocated from mural thrombi to the surface by such perfusion. In addition, platelets which detached from mural thrombi adhered more readily to elastin or microfibrils than platelets from the circulating blood. The initial attachment of platelets to subendothelium was inhibited in von Willebrand's disease, the Bernard-Soulier syndrome and at high concentrations of dipyridamole; spreading was inhibited in storage pool disease of rats, at low temperature (20 degrees C), with EDTA (3 MM) and Prostaglandin E1 (1 muM); and adhesion-induced aggregation was inhibited in thrombasthenia, storage pool disease and after ingestion of sulfinpyrazone or Aspirin. It is concluded that the initial attachment (contact) of platelets, spreading and surface-induced release of platelet constituents are at least partially indendent phenomena, the latter two being highly surface specific. At flow conditions which cause the disappearance of platelet adhesion appears as an irreversible process.

Animals↗
PubMed1975

[Adhesion and aggregation in the subendothelium: hereditary platelet function disorder].

Platelet adhesion to a thrombogenic surface and adhesion-induced aggregation were investigated using a perfusion system at a blood flow rate similar to that observed in arteries. Morphometric measurements revealed diminished adhesion of platelets but normal surface-induced aggregation with blood of patients with von Willebrand's disease and with Bernard-Soulier syndrome. In contrast, surface-induced aggregation was defective with blood of patients with storage pool disease, thrombasthenia and with blood of healthy volunteers after Aspirin ingestion. These findings may explain the defective hemostasis in these patients. They suggest that platelet adhesion and aggregation are governed by different mechanisms.

Aorta↗
PubMed1975

Impaired interaction (adhesion-aggregation) of platelets with the subendothelium in storage-pool disease and after aspirin ingestion. A comparison with von Willebrand's disease.

Possible defects in the interaction of platelets with the subendothelial surface were evaluated in six patients with storeage-pool disease, nine patients with von Willebrand's disease and seven normal subjects who ingested aspirin. Citrated blood was perfused through a chamber containing everted segments of rabbit aorta previously denuded of endothelium by means of a ballon catheter. With normal blood, 83.3 +/- 1.9 per cent (S.E.M.) of the surface was covered by adherent platelets. Platelet adhesion was normal after aspirin ingestion (89.7 +/- 4.6 per cent) and decreased in some patients with storage-pool disease. The most striking defect in both circumstances was the virtual absence of platelet thrombi. In contrast, decreased adhesion (57.3 +/- 3.4 per cent), but normal thrombus formation, was characteristic of von Willebrand's disease. These types of defects in platelet adhesion and aggregation may account for the hemostatic defects in a variety of bleeding disorders. The findings further suggest the possible usefulness of aspirin as an antithrombotic agent.

Adenosine Diphosphate↗