Review Article

The Endothelium, A Protagonist in the Pathophysiology of Critical Illness: Focus on Cellular Markers

Table 4

Overview on endothelial microparticles in acute brain injury, SAH, and TBI.

Study groupStudy populationDetection methodPhenotype EMPMain findings

Lackner et al. [35]Case-control
spontaneous SAH ( )
Flow cytometry
plasma
CD105+/Annexin V+ or −
CD62E+/Annexin V+ or −
CD54+/Annexin V+ or −
CD106+/Annexin V+ or −
(i) Increased number of all EMP phenotypes studied in SAH versus healthy
(ii) In patients with Doppler detected cerebral vasospasm increased CD105+/Annexin V+ and CD62E+/Annexin V+
(iii) CD105+/Annexin V+ associated with cerebral infarction

Morel et al. [36]Case-control
TBI ( )
Capture technique
PFP and CSF
Annexin V+
CD31+
(i) Increased MP number in plasma and CSF at D0, decreased D3, D5, D10
(ii) High proportion of EMP

Sanborn et al. [37]Case-control
SAH ( )
Flow cytometry
Frozen plasma samples
CD146+/Annexin V+(i) Elevated EMP after SAH, and remained high until D10
(ii) Negative correlation EMP and infarction at D14

CSF: cerebral spinal fluid; EMP: endothelial microparticles; MP: microparticle, PFP: Platelet free plasma; SAH: subarachnoid hemorrhage; TBI: traumatic brain injury.