Phenol and certain phenyl compounds affect someof the stagesof blood coagulation and fibrinolysis. It is, therefore, of interest to study the uptake of phenol by tissues, particularly the vascular wall. Basically the method used was as follows (with controls to allow for possible decomposition). Brain thromboplastin or finely minced vascular tissue (0.3 g) was inserted into a sacmade of Visking tubing (diameter 8 mm) and immersedin 10ml of 0.5% phenol in 0.9 % NaCl. This was incubated for 1 hr at 37” followed by 20 hr at 4”, and then the concentration of phenol remaining in solution was estimated. Brain tissue removed 14-17 mg of phenol while the aortic tissue adsorbed 8-9 mg. In terms of fresh-tissue weight, the amount of phenol adsorbed by the vascular wall is estimated at approximately three to three and a half times that removed by brain tissue. However, when related to the thromboplastic activity in wet material it is calculated to be about 300-350 times. From further experiments the following points also emerge. 1. Contrary to expectation, the protein moiety, rather than the phospholipid component, is mainly responsible for this uptake of phenol. 2. There is a certain relation betweenphenol concentration and the amount adsorbed on the thromboplastic tissue (Table 1). TABLE
1
A COMPARISON BETWEEN PHENOL ADSORPTION ON THE VASCULAR WALL AND BRAIN TISSUE Milligrams of phenol removed by 0.3 g:’ Concentration of phenol (%)
Brain tissue
Vascular tissue
2b 1 0.5 0.25 0.125 0.06
2626 20-26 14-17 7.5-10 1.5-2.5 l-l.5
11-15 11-13 8-9 4-8 l-2 0
’ Range in 10 experiments. b Higher concentrations appeared to produce denaturation.
3. The adsorption appears to be reversible; dialysis against a large volume of water or saline removed almost completely the adsorbed phenol. 4. Incubation at 37” hastensthe adsorption process; however, its prolonged usemay also lead to rapid decomposition of the tissueswhich would invalidate the investigation. 224
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In considering the implications of this high affinity of the vascular wall to phenol, it is worth noting that (a) certain oestrogenic phenols have a catalytic action, and cigarettes have a high concentration of phenols, and (b) there is evidence to suggest that the occurrence of thrombosis in women receiving oral contraceptives (containing oestrogens)is potentiated by smoking. These observations, together with the fact that certain phenols evolve (activate) blood factor XII, accelerate thrombin-fibrinogen interaction, retard clot retraction, and inhibit plasmin, raise for consideration the possibility that some phenolic compounds may play a part in the pathogenesis of thrombosis. Further investigations are now in progress. F. NOUR-ELDIE: Shenley Hospital, Herefordshire, England. Received November 7,1969