Binding of Plasmodium falciparum to CD36 can be shielded by the glycocalyx
BACKGROUND Strategies targeting the protection of the vascular barrier, in particular the endothelial glycocalyx, are subjects of current research. Antithrombin III and hydrocortisone have been shown to reduce shedding of the glycocalyx following ischaemia/reperfusion. Platelet adhesion to endothelial cells is one consequence of ischaemia/reperfusion. OBJECTIVE Our goal was to evaluate the effect of pharmacological protection of the glycocalyx on platelet adhesion. DESIGN An experimental interventional animal study. SETTING The study was carried out in a basic science laboratory at the University of Munich. ANIMALS Eighty male guinea pigs (250 to 300 g) were used for the experiment. MAIN OUTCOME MEASURES The effect of preischaemic treatment with hydrocortisone 10 μg ml(-1) or antithrombin 1 IU ml on adherence of platelets was evaluated in isolated, beating guinea pig hearts (Langendorff model). Hearts were subjected to warm ischaemia (20 min at 37 °C) and consecutive reperfusion. Platelets were injected at the beginning of reperfusion via the aortic cannula and platelet concentration was measured in the effluent (after passing through the coronary vascular system). RESULTS Ischaemia and reperfusion led to significant shedding of the endothelial glycocalyx. Coronary venous release of syndecan-1 increased nine-fold, and heparan sulphate showed a 20.3-fold increase after ischaemia/reperfusion (both P < 0.01). Pretreatment with hydrocortisone or antithrombin III reduced endothelial glycocalyx shedding significantly (P < 0.05). Adherence of platelets to the coronary vascular bed increased more than 2.5-fold when they were injected during reperfusion. About 40% of this increase was blocked by pretreatment of hearts with hydrocortisone or antithrombin. CONCLUSION Pretreatment with hydrocortisone or antithrombin III can reduce platelet adhesion during reperfusion after warm ischaemia by protection of the endothelial glycocalyx.