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Biomedical subjects

G V Born

Publications and source records attributed to G V Born.

At least 91 records · Page 5Linked to original sources
PubMed1981

Aggregation of platelets in damaged vessels.

The only certain physiological function of platelets is their aggregation in injured vessel walls as haemostatic plugs. The association of thrombocytopenia with petechial haemorrhages suggests that platelets are somehow required for the functional integrity of small vessels, but no mechanism has yet been established. The pathological aggregation of platelets as thrombi in atherosclerotic arteries is commonly, if not always, initiated by haemorrhage. In artificial vessels, platelets tend to aggregate on the walls wherever blood flow is non-laminar. The mural aggregation of platelets is not prevented by unphysiologically high wall-shear forces. The facts suggest, on the contrary, that the process depends in some way on abnormal haemodynamic conditions. This contribution is mainly concerned with questions about how haemodynamic conditions in and around vascular leaks affect arriving platelets that aggregate there, and about the chemical agents responsible for making the platelets reactive. The effects of these agents are known mainly from in vitro experiments in which aggregation can be quantitatively correlated with biochemical effects by simple and reproducible methods; the relevance to their reactions in haemostasis and thrombosis is uncertain. It is difficult to devise quantitative methods for analysing these processes in vivo because of the very low concentrations at which endogenous agents can activate platelets and haemostasis factors in the plasma; the rapidity with which platelets aggregate in a damaged blood vessel; and the complexity and inconstancy of the haemodynamic situation. All these factors must be accounted for in hypotheses of haemostasis. New experimental approaches towards analysing the haemostatic mechanism in vivo are described.

Adenosine Diphosphate↗
PubMed1981

The embolization of bone wax from sternotomy incisions.

We discuss our study on the effects of discontinuation of the usage of bone wax as a hemostatic agent in sternotomy incisions. In 1976, we abandoned use of bone wax because it was suspected of causing several cases of Mycobacterium fortuitum sternal osteomyelitis. In a retrospective study involving 400 patients, we found that this step did not increase postoperative bleeding as measured by drainage from the chest tube and by the need to return patients to the operating room because of bleeding. It also was observed that there was an appreciable simultaneous drop in pulmonary complications. To test our theory that the wax pressed into the bone marrow can embolize to the lung, radioactively tagged bone wax was pressed into the cut sternum in animal models, and a search was made for radioactive deposits in the peripheral lung tissue. Shortly after the application of the wax, there was evidence of large radioactive deposits in the lungs. It is probable that this embolization occurs also under clinical conditions and may play a role in pulmonary complications following open-heart operations.

Animals↗
PubMed1981

Dependence of purine loss from human erythrocytes on external pH.

Human red cells were incubated at 37 degrees C in physiological saline at pH 7.4 with 8-3H-adenine to label the adenine nucleotides. After washing, the cells were incubated in similar salines which were buffered to different values of pH. The loss of radioactivity from cells into medium was very slow below pH 7.4 and accelerated greatly with increasing pH up to about 7.8. At that pH the loss increased for at least 3 h when it represented more than 30% of the initial radioactivity of the cells. The loss could not be accounted for by haemolysis which remained minimal. The extracellular radioactivity was present mostly in hypoxanthine and some inosine. The loss of purine did not depend on oxygenation of the cells. These results, together with the high-affinity uptake system for adenosine, could provide a partial explanation of the turnover of adenine nucleotide purines of red cells which is many times faster than that of the cells themselves.

Adenine↗
PubMed1981

The influence of blood flow on the behaviour of blood cells with particular reference to thrombosis.

Blood platelets can initiate arterial thrombosis by aggregating on atheromatous lesions and by accelerating the intrinsic coagulation system. The conversion of unreactive to reactive platelets (platelet activation) may be due to contact with vessel wall collagen and/or haemodynamic abnormalities in narrowed arteries, increasing the physical and chemical interactions with erythrocytes. Platelet activation is difficult to demonstrate and quantify in vivo. Proposed parameters include appearance of procoagulant (platelet factor 3) activity and other platelet-derived aggregating agents, notably prostaglandin endoperoxides and thromboxanes; appearance of "spontaneous" aggregates in the blood; alterations in ultrastructure, e.e., fewer dense inclusion bodies indicating the release reaction; and appearance of other released materials, e.g., platelet factor 4 which neutralises heparin and beta-thromboglobulin, both measurable by radioimmunoassay. Investigations of the biomedical mechanisms underlying platelet activation has brought up inhibitors of their reactions to aggregating agents in vitro and in vivo. Increases in bleeding time caused by such agents indicate that one or other may, if otherwise acceptable, be effective therapeutically against platelet-dependent thromboses. The recent discovery of prostacyclin and its biological effects may explain some of the problems besetting the outcome and interpretation of clinical trials so far.

Adenosine Diphosphate↗
PubMed1980

Activation time of blood platelets.

Blood platelets react rapidly in their hemostatic function. Determination of the reaction or activation time of individual platelets is difficult because it requires that physical and/or chemical effectors of activation are nonlimiting. Analysis of experimental conditions shows that the best estimate of mean activation time comes from in vivo measurements. Thus, the constancy of height-to-length ratio of a growing thrombus, and its change with flow rate, provide additional evidence for the activation time hypothesis.

Animals↗
PubMed1980

Uptake of purine bases and nucleosides in African trypanosomes.

Uptake of radioactivity labelled purine bases and nucleosides by suspensions of Trypanosoma brucei and Trypanosoma congolense in bicine buffer was determined at 37 degrees C. With T. brucei, the rate of uptake of adenosine was much greater than that of the other compounds tested, the uptake of which decreased in the order adenine, inosine, guanosine and hypoxanthine. With T. brucei, adenosine uptake increased with concentration in a manner suggesting two mechanisms, one with high and the other with low affinity for adenosine. The uptake of adenine increased with concentration only up to about 1.5 microM while the uptake of guanosine increased little with concentration and that of inosine and hypoxanthine not at all. In both species adenosine strongly inhibited the uptake of both of the other nucleosides and of both purine bases. In T. brucei, guanosine and inosine caused small increases in adenosine uptake which was, however, inhibited by them in T. congolense. In T. brucei, each of the purine bases adenine and hypoxanthine inhibited its own uptake maximally but that of each other less effectively. Hypoxanthine was more effective than adenine in inhibiting the uptake of the nucleosides guanosine and inosine, but neither base effected marked inhibition of adenosine uptake. The uptake of adenosine by T. brucei was inhibited by dipyridamole and its analogue, compound RA--233, strongly at 100 microM and slightly at 10 microM. The other dipyridamole analogues, VK--744 and VK--774, were ineffective.

Adenine↗