SummaryThe ADP-induced platelet adhesiveness has been investigated under experimental various conditions by the in vitro method of Hellem. The platelet, adhesiveness was found to be proportional to the logarithm of the ADP concentrations between 0.025—0.2 μg/ml in citrated and heparinized plasma. The effect of ADP on platelets decreased with increasing concentrations of citrate. In contrast, increasing amounts of heparin did not alter the platelet adhesiveness significantly, except when extremely high concentrations were used. Variations in the temperature highly influenced the result of the estimations when suboptimal concentrations of ADP were used. The reason for this probably inactivation of ADP by plasma enzymes, which have an optimal activity at about 37° C. This may explain why estimation at 20° C gives higher values of the platelet adhesiveness than at 37° C. If too high concentrations of ADP are used, this effect is not detectable. This may be the reason why O’Brien (1962) did not find any inactivating property of platelet poor plasma. Washing of platelets in buffered saline leads to a marked release of ADP, indicating that washed platelets are damaged. Repeated resuspension of platelets even in their own plasma gives release of ADP. When studying the mechanism of the ADP-induced reaction all the above variations must be taken into account.
SummaryIn a group of 25 patients with insulin-treated diabetes mellitus a marked increase in the ADP-induced platelet adhesiveness was demonstrated. This phenomenon was due to a plasmatic factor. In vitro-plasma from these patients restored the decreased ADP-induced platelet adhesiveness in von Willebrand’s disease.The factor was also effective in vivo, since transfusion of 450 ml diabetic plasma to a patient with von Willebrand’s disease normalized the decreased platelet adhesiveness and shortened the prolonged bleeding time. The role of this factor in the ADP platelet reaction as a cofactor together with calcium is stressed.
All 87 known cases of bacteraemia due to Streptococcus pyogenes (beta-haemolytic group A streptococci) occurring during the peak of a nationwide outbreak in Norway (population 4.2 million) between January and June 1988 were reviewed. Clinical features varied widely and appeared largely to be dependent on the patients' age. The case fatality rate ranged from 11% in the age group under 30 years to 44% in patients over 60 years. Clinical complications such as shock, severe renal or respiratory failure or serious local infection occurred particularly in 30-to 59-year old individuals. Shock was manifest in 32% of the patients and carried a 68% case fatality rate. Chronic heart disease in the elderly and pneumonia seemed to be associated with a fatal outcome. In the 25 patients (29%) who died the disease showed a fulminant course, 80% dying within 48 hours after admission. However, 56% of the patients had experienced symptoms for more than two days before admission, suggesting that early diagnosis and treatment might possibly have prevented the development of a serious disease. This study revealed a wide spectrum of clinical manifestations in bacteraemia cases in a unique epidemiological situation caused largely by a single serotype of Streptococcus pyogenes; 89% of the 27 preserved bacteraemia strains carried the M-1 antigen. The observations call attention to the ability of these organisms to cause fulminant clinical illness, indicating a probable increase in both invasiveness and toxicity of group A streptococci responsible for the epidemic.
SummaryAn attempt to clarify the ADP platelet reaction has been done by investigating the effect of substances which inhibit the reaction in vitro. The inhibitors used may be divided into two groups. Monoiodo acetic acid, molecular iodine, para-chloro mercuribenzoic acid and potassium ferricyanid lead to noncompetitive inhibition. Substances containing free -SH groups and adenine conjugates show competitive inhibition.The primary bleeding time is prolonged when wounds are flushed with solutions of these compounds.It is shown that adenosine tetraphosphate aggregates platelets in the same manner as ADP.Based upon these observations an attempt is made to explain some of the steps involved in the ADP platelet reaction.
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