Impairment of Blood-Brain Barrier Integrity during Carotid Surgery as Assessed by Serum S-100B Protein Concentrations

Abstract

During carotid endarterectomy (CEA) the internal carotid artery is cross-clamped for a period of several minutes. This maneuver may cause cerebral hypoperfusion and/or impairment of the blood-brain barrier (BBB) even in cases where clinical signs are absent. The aim of the present study was to examine whether such alterations could be detected by monitoring the cerebral marker S-100B protein concentrations during and after CEA in the serum. Twenty-five consecutive patients (17 M/8 F, mean age: 64.2 years, range 47-79 years) undergoing elective CEA at our department were studied. All of these patients were without perioperative neurological deficit. Intraoperative samples were collected from internal jugular and peripheral venous blood: 1) before carotid cross-clamping; 2) immediately before declamping; 3) after clamp release. Postoperative samples were taken from peripheral blood at 6 and 24 h, respectively. S-100B was assayed in sera using an immunoluminometric technique. During carotid cross-clamping, S-100B protein concentrations in the ipsilateral jugular serum significantly (p < 0.02) increased to pre-clamp values. After declamping, however, S-100B returned to the baseline level. No differences were seen between the responses of hypertensive and normotensive patients. There was no correlation between carotid occlusion time and S-100B protein concentrations. In the peripheral venous serum no significant changes in S-100B concentrations were detected during or after CEA. We presume that the elevation of S-100B protein concentration during CEA in patients with no neurological deficits indicates the transient opening of the BBB elicited by carotid cross-clamping.

Seizure‐Promoting Effect of Blood–Brain Barrier Disruption

“…In particular, we assessed the degree of BBB disruption by CT scan and measured levels of S100β increase in serum. S100β has been widely used as a surrogate serum marker of BBB integrity (Mussack et al, 2002; Jaranyi et al, 2003; Sendrowski et al, 2004; Vogelbaum et al, 2005). S100β increases sharply in blood immediately after a successful BBBD procedure (Kapural et al, 2002; Marchi et al, 2003a) and is now a recognized alternative to contrast enhanced radiological exams for BBB integrity (Vogelbaum et al, 2005).…”

Neurological Abnormalities in Full-Term Asphyxiated Newborns and Salivary S100B Testing: The “Cooperative Multitask against Brain Injury of Neonates” (CoMBINe) International Study

“…In the present study we report that soon after a severe hypoxic insult, salivary concentrations of S100B increase, in particular in asphyxiated infants with a poor short-term neonatal outcome. This results may be explained bearing in mind that: i) early and severe damage to the CNS is associated with the continuous release of S100B protein which is present and measurable in the bloodstream [ 33 , 34 ], and; ii) hypoxia/asphyxia triggers S100B release, so that raised protein’ concentrations have been interpreted as a direct indicator of active neuronal cell damage [ 14 , 16 – 19 , 35 – 37 ].…”

Biomarkers in traumatic brain injury (TBI): a review

“…It is not completely clear how these proteins leave the injured brain and enter the blood. BBB disruption 25 , 55 , 57 , 59 – 63 or release independent of BBB integrity, 64 , 65 as well as passage through the newly discovered glymphatic system, 66 has been suggested as possible routes for markers appearance in blood or other biological fluids. Presumably, these proteins are first released in the brain extracellular space, a component difficult to access for repeated sampling, before being transported to the cerebral spinal fluid (CSF) where a passive diffusion from CSF to blood occurs.…”