A.G. Herman – författare

2 The free internal Ca+ concentration in human red cells is set according to the leak­ 2 and-pump principle: There is a finite passive Ca+ influx at the physiological 2 2 Ca+ -gradient across the membrane which is compensated by Ca+ pumping in the outward direction with a rate given by the degree of saturation of the A TP-fuelled Ca­ 2 pump at the steady-state internal Ca+ concentration. Simons (1982) recently devised a method allowing the measurement of the steady­ 2 2 state internal Ca+ concentration. Cells are suspended in media of different Ca+ con­ 2 2 tent whose Ca+ concentration is monitored by a Ca+ -selective electrode. When the cells are lysed (by digitonin) there is an upward or downward deflection of the elec­ 2 trode signal. At the point of zero deflection, the cellular Ca+ concentration equals that 2 of the medium. The result is, that in fresh human red blood cells the Ca+ concentra­ tion is ;;;; O.4,uM (this is an upper estimate; the true value may be considerably lower).

2 The free internal Ca+ concentration in human red cells is set according to the leak­ 2 and-pump principle: There is a finite passive Ca+ influx at the physiological 2 2 Ca+ -gradient across the membrane which is compensated by Ca+ pumping in the outward direction with a rate given by the degree of saturation of the A TP-fuelled Ca­ 2 pump at the steady-state internal Ca+ concentration. Simons (1982) recently devised a method allowing the measurement of the steady­ 2 2 state internal Ca+ concentration. Cells are suspended in media of different Ca+ con­ 2 2 tent whose Ca+ concentration is monitored by a Ca+ -selective electrode. When the cells are lysed (by digitonin) there is an upward or downward deflection of the elec­ 2 trode signal. At the point of zero deflection, the cellular Ca+ concentration equals that 2 of the medium. The result is, that in fresh human red blood cells the Ca+ concentra­ tion is ;;;; O.4,uM (this is an upper estimate; the true value may be considerably lower).

The rapid development in the knowledge about the synthesis and metabolism of the various products derived from arachidonic acid is a continuous chal- lenge for those who intend to measure these substances in biological fluids. The confusion which still exists about their possible role in some physiolo- gical and pathological situations is partly due to the methodological pro- blems related to the estimation of these metabol ites in subnanogram quanti- ties. This concern has inspired the Commission of the European Communities to sponsor a first workshop on the "Clinical Application of Assay Methods for Prostaglandins "which was held in Brussels at the end of 1976. During that meeting it became clear that progress in the qualitative and quantitative analysis of the prostaglandins could only be made by a permanent reevalua- tion of the existing techniques and therefore the possibility should be r created for experts in the field to meet regularly and to discuss the value of the newly developed assay methods.Since then exciting new discoveries have been made in this rapidly ex- r panding area: in October 1976 the birth of the prostacycl in area was an- nounced and in May 1979 a possible structure and biosynthetic pathway for slow-reacting substance of anaphylaxis (SRS-A) was presented.

A number of exciting new developments have occurred during the last few years concerning the platelet-vessel wall interaction. Although they may be obvious and clear to the specialist in the field, for the clinician the area has become rather confusing. Time has come to review current knowledge on the pathophysiology of the platelet-vessel wall interaction and show how this knowledge can constitute the rationale for pharmacotherapeutic interventions. A symposium was organized in Antwerp during which a number of outstanding speakers gave an overview of what is new on a particular topic and how this information can be translated to possible clinical applications. The proceedings of the symposium are not only of interest to the practising physician, but contain enough new fundamental data to be of use for all those who are interested in the role of platelets in the etiopathogenes ofcardiovascular diseases. Arnold G. Herman Antwerp, July 1-991 vii ListofContributors A.G. Herman DepartmentofPharmaceutical Sciences M.R.Buchanan University Hospital DepartmentofPathology Universiteitsplein I McMaster Clinic B-261O ANTWERP (Wilrijk) Hamilton General Hospital Belgium 237 Barton Street East HAMILTON, Ontario G. Homstra Canada L8L 2X2 DepartmentofHuman Biology UniversityofLimburg Co-author: SJ. Brister P.O. Box 616 6200MD MAASTRICHT J.-P. Cazenave The Netherlands Regional Centre ofBlood Transfusion 10, Rue Spielmann J.F. Martin F-67085 STRASBOURG Cedex Department ofMedicine France King's College School ofMedicine and Dentistry Co-authors: C. Gachet and F. Lanza LONDON SE5 9PE U.K.