HYPOTHESIS:To measure and evaluate clinical scores and various inflammation parameters for providing a better outcome assessment of patients with secondary peritonitis.DESIGN:Prospective study.SETTING:ICU of a university and a university affiliated hospital.PATIENTS:Fifty-six patients with severe secondary peritonitis were enrolled in this study executed within 4 years.MEASUREMENTS AND MAIN RESULTS:Blood samples were taken preoperatively and 2, 6, 8, 12, 18, 24, 30, 36, 42 and 48 hours post operation, thereafter every 12th hour until day 5 respectively once daily until day 14. Etiology of peritonitis, clinical score systems (APACHE II, MOF and SOFA), and 27 mainly with activity tests or enzyme-immunoassays measurable inflammation parameters were simultaneously analyzed and stratified into lethal outcome (n = 11) or survival (n = 45), respectively. The etiological distribution of peritonitis was identical among both groups. Proportion of intraperitoneal fungi, E. coli, and bacteroids was substantially higher during the primary operation in the group with lethal outcome. With increasing significance initial and follow-up APACHE II, MOF and SOFA scores provided higher values in this group. Various plasma/serum parameters of hemostasis, leukocyte proteolytic system, acute phase reaction, cytokine system, cell adhesion, opsonization, and main organ functions showed significantly different values between both groups at the preoperative stage and/or during observation period I (day 0-4). Logistic regression analysis revealed the SOFA score and neopterin concentration as the combination with the best sensitivity (63.6%) and specificity (93.2%) for predicting the patients' survival even at the preoperative stage. For the observation period I, the combination of SOFA score and TNF receptor II showed the highest predictive sensitivity (72.7%) and specificity (95.6%).CONCLUSION:Evaluation of the severity of secondary peritonitis using a scoring system with high prognostic relevance could conceivably result in an earlier and adequate application of intensive care such as hemofiltration, administration of immunoglobulins and serial abdominal lavage to improve successful outcome.

Objectives: This study was designed to apply the rapid Elecsys (R) S 100 irnrnunoassay for real-time measurement of S100 protein serum levels indicating acute brain damage in patients undergoing carotid artery stenting (CAS) or endarterectomy (CEA).Design and methods: Data of 14 CAS patients were compared to those of 43 CEA and 14 control patients undergoing coronary angiography (CA). S100 serum levels were measured by the full-automatic Elecsys (R) S100 immunoassay and compared to those obtained by the well-established LIA-mat (R) S100 system.Results: In contrast to CAS and CA patients, median S100 serum levels of CEA patients significantly increased to 0.24 ng/mL before declamping, but subsequently returned to baseline. Three CEA patients with neurological deficits showed sustained elevated S 100 levels 6 h after extubation. Absolute S100 values were not significantly different between the two methods. Bland-Altman plot analyses displayed a good agreement, mostly indicating slightly smaller Values applying the Elecsys (R) S100 system.Conclusions: The Elecsys (R) S100 system appears to be suitable for rapid real-time detection of neurological deficits in patients undergoing CAS and CEA. Persistent elevations of Elecsys (R) S100 levels during CEA were associated with prolonged neurological disorders, whereas transient increases seem to represent impaired blood-brain barrier integrity without neurological deficits. (c) 2006 The Canadian Society of Clinical Chemists. All rights reserved.

Background: The neuroprotein S100 released into the circulation has been suggested as a reliable marker for primary brain damage. However, safe identification of relevant traumatic brain injury (TBI) may possibly be hampered by S100 release from peripheral tissue. The objective of this study was to measure early S100 levels using the Elecsys((R)) S100 immunoassay for real-time assessment of severe TBI in multiple trauma.Methods: Consecutively admitted multiple trauma patients (injury severity score >= 16 points) were stratified according to the results of the initial cerebral computed tomography (CCT) examination. S100 serum levels were determined at admission and at 6, 12, 24, 48 and 72 h after trauma. Data were correlated to creatine phosphokinase (CK) and lactate dehydrogenase (LDH) serum levels. Using receiver operating characteristic (ROC) analysis, the discriminating power of S100 measurement was calculated for the detection of CCT+ findings.Results: Median S100 levels of CCT+ patients (n=9; 37 years) decreased from 3.30 mu g/L at admission to 0.41 mu g/L 72 h after trauma. They revealed no significant differences to CCT- patients (n=18; 44 years), but remained elevated compared to controls. Median CK and LDH levels correlated with the corresponding S100 levels during the first 24 h after trauma. ROC analysis displayed a maximum area under the curve of only 0.653 at 12 h after trauma. No significant difference was calculated for the differentiation between CCT+ and CCT- patients.Conclusions: Measurements of S100 serum levels using the Elecsys((R)) S100 immunoassay are not reliable for the real-time detection of severe TBI in multiple trauma patients. Due to soft tissue trauma or bone fractures, S100 is mainly released from peripheral sources such as adipocytes or skeletal muscle cells.

Objective: This study evaluates the effects of bronchoalveolar lavage with diluted surfactant on unilateral lung contusion-induced lung dysfunction. Design: Randomized prospective animal study. Setting: An animal laboratory. Subjects: Twenty adult pigs, weighing 25–35 kg. Interventions: Animals were randomly assigned to controls and surfactant treatment. Bilateral lavage with surfactant treatment began 30 mins after unilateral lung contusion. Then 25 mg/kg of body weight diluted Curosurf (5 mg/mL) was applied in a volume of 5 mL/kg of body weight. Observation time was 8 hrs postinjury. Measurements and Main Results: The Pao2/Fio2 ratio fell from 500 to 250 and then recovered gradually in controls and surfactant-treated pigs. After another 4 hrs, the Pao2/Fio2 ratio deteriorated again in controls, but not in surfactant-treated animals. Total compliance fell by 50% after injury but was completely restored by surfactant treatment. Lung contusion increased the median number of neutrophils in bronchoalveolar lavage fluid from 2% to 30% of total cells and peaked >60% at 480 mins in the contused lungs of control pigs. Surfactant-treated pigs had 40% neutrophils at 480 mins without reaching significant difference to controls. The leukocyte neutral proteinase inhibitor increased to 500 ng/mL at 30 mins postinjury in the contused lungs and increased to 2000 ng/mL after surfactant treatment. Conclusions: Bilateral bronchoalveolar lavage with diluted surfactant can effectively improve lung function after experimental unilateral lung contusion in pigs.

The human lysosomal cysteine-type carboxypeptidase cathepsin X is mainly present in monocytes and macrophages and may be released into the circulation due to constitutive and/or regulated secretion by (activated) immune cells. To define its potential diagnostic value as an inflammatory marker, we have developed a highly sensitive and specific sandwich-type immunoassay (ELISA) for cathepsin X permitting both intra- and extracellular detection and quantification.The dynamic range of the cathepsin X ELISA was determined to be 100 (detection limit) to 8000 pg/ml. Reproducibility of both within and between runs yielded coefficients of variation (CVs) of 2.7-3.5% and 6.3-7.3%, respectively. Cross-reactivity with other members (cathepsin B, L) of the thiol-dependent cathepsin family was not observed. The ELISA was used to quantify cathepsin X in leukocytes as well as in plasma of healthy volunteers and patients with multiple trauma. During the first 72 h after trauma, plasma levels of cathepsin X increased significantly, particularly in patients who died during the posttraumatic period. In comparison to the well-known inflammation marker neutrophil elastase, cathepsin X levels predicted survival with a higher significance in the later posttraumatic phase.In conclusion, this report provides the first evidence of cathepsin X immunoreactivity not only in cell lysates but also in plasma samples. We suggest that the newly developed highly reproducible ELISA will be of great value for further evaluation of this protease as a diagnostic and/or prognostic marker in inflammatory diseases. (c) 2005 Elsevier B.V. All rights reserved.

A variety of serine proteases, including urokinase-type plasminogen activator (uPA), plasmin,and polymorphonuclear leukocyte elastase (PMN-E), have been implicated in the processes of tumor cell invasion and metastasis. Besides degrading of matrix proteins, PMN-E has been shown to be able to cleave and inactivate plasminogen activator inhibitor-1 (PAI-1), the main inhibitor of uPA, and alpha2-antiplasmin, the natural inhibitor of plasmin, thus enabling an uncontrolled matrix degradation by the fibrinolytic enzymes. Because only limited data are available on a relationship between the tumor level of PMN-E and prognosis in primary breast cancer patients, in the present study we have measured with an ELISA the levels of PMN-E (in complex with alpha1-proteinase inhibitor) in cytosolic extracts of 1143 primary breast tumors. Levels of complexed PMN-E have been correlated with the lengths of metastasis-free survival (MFS), relapse-free survival, and overall survival, and a comparison was made with data previously obtained for uPA and PAI-1. Our results show that patients with a high PMN-E level in their primary tumor had a rapid relapse and an early death compared with patients with a low tumor level of PMN-E. This held true for node-negative and node-positive subgroups of patients as well. The relationship of PMN-E with a poor prognosis was especially obvious during short-term follow-up (0-60 months). In Cox multivariate regression analysis, corrected for the traditional prognostic factors, PMN-E was an independent prognostic factor, and high levels of PMN-E were associated with a poor MFS [hazard ratio (HR), 1.63; 95% confidence interval (CI), 1.23-2.16; P < 0.001], relapse-free survival (HR, 1.45; 95% CI, 1.10-1.89; P = 0.01), and overall survival (HR, 1.64; 95% CI, 1.20-2.23; P = 0.003). Furthermore, in all three multivariate models, PMN-E still added significantly to the model after the additional inclusion of the uPA. PMN-E was an independent prognostic factor for MFS even in the multivariate analysis including the traditional clinical prognostic factors and the strong established biochemical prognostic factors uPA and PAI-1. Our present study suggests that PMN-E is associated with breast cancer metastasis, and knowledge of the tumor PMN-E status might be helpful in selecting the appropriate individualized (adjuvant) treatment for patients with breast cancer.

Besides a variety of other proteases, polymorphonuclear leukocyte elastase (PMN-E) is also suggested to play a role in the processes of tumour cell invasion and metastasis. Yet, there is only limited data available on the relation between the tumour level of PMN-E and prognosis in patients with primary breast cancer, and no published information exists on its relation with the efficacy of response to systemic therapy in patients with advanced breast cancer. In the present study, we have measured with enzyme-linked immunosorbent assay the levels of total PMN-E in cytosolic extracts of 463 primary breast tumours, and have correlated their levels with the rate and duration of response on first-line tamoxifen therapy (387 patients) or chemotherapy (76 patients) in patients with locally advanced and/or distant metastatic breast cancer. Furthermore, the probabilities of progression-free survival and postrelapse survival were studied in relation to the tumour levels of PMN-E. Our results show that in logistic regression analysis for response to tamoxifen treatment in patients with advanced disease, high PMN-E tumour levels were associated with a poor rate of response compared with those with low PMN-E levels (odds ratio: OR, 0.40; 95% CI, 0.22–0.73; P =0.003). After correction for the contribution of the traditional predictive factors in multivariate analysis, the tumour PMN-E status was an independent predictor of response ( P =0.01). Furthermore, a high tumour PMN-E level was related with a poor progression-free survival ( P <0.001) and postrelapse survival ( P =0.002) in a time-dependent analysis. In contrast, the tumour level of PMN-E was not significantly related with the efficacy of response to first-line chemotherapy in patients with advanced breast cancer. Our present results suggest that PMN-E is an independent predictive marker for the efficacy of tamoxifen treatment in patients with advanced breast cancer.

The release of the neuronal proteinS-100B into the circulation has been suggested as an early indicationof cellular brain damage. The objective of this prospective pilot studywas to determine S-100B serum levels in patients undergoingcross-clamping during carotid endarterectomy (CEA) and to correlate theresults with the monitoring of somatosensory evoked potentials (SSEP)and the neurological short-term outcome. Arterial blood samples of 21patients were drawn before oral intubation, cross-clamping, andunclamping, as well as before extubation and 6 hours later. Recordingof SSEP was obtained during carotid occlusion and reperfusion. If lossof SSEP appeared, cerebral ischemia was assumed and an intraluminalshunt was placed. During cross-clamping, S-100B serum levels of 14patients increased significantly from 0.05 ng/ml to 0.21 ng/ml, butreturned to baseline levels after unclamping. In 5 cases, loss of SSEPamplitudes occurred but was reversed by the shunt insertion. Nosignificant differences of S-100B serum values, neurologicalexamination, and carotid duplex surveillance became obvious in thisgroup when compared to the patients with undisturbed SSEP. However, 2patients with complete disappearance of postcentral SSEP componentssuffered from neurological deficits in the postoperative period. S-100Bserum levels remained highly elevated 6 hours after extubation (0.78ng/ml and 0.41 ng/ml) compared to the baseline values (0.15 ng/ml and0.07 ng/ml). During CEA a transitory increase of the S-100B serumlevels appears to present an impairment of the blood–brain barrierintegrity without any neurological deficits. In contrast, persistentlyelevated S-100B serum levels seem to be associated with transient lossof SSEP and development of neurological deficits.

Mussack, T.*; Biberthaler, P.*; Gippner-Steppert, C.+; Mutschler, W.*; Jochum, M.+ Author Information

BACKGROUNDElevated blood S-100B levels were described by several authors for reliable identification of patients with intracerebral complications after minor head trauma (MHT). Yet, test systems used so far require more than 3 hours processing period which is too long to enable immediate further diagnostic or therapeutic consequences. Therefore we validate a new rapid test version for S-100B measurements and established an effective cut-off level to identify high risk patients.METHODS104 patients suffering from MHT were enrolled. After taking blood samples S-100B values were achieved by the long-term and rapid (40 min processing time) test system, respectively, and compared using linear regression analysis. For determination of an effective cut-off level receiver operating characteristics curves were calculated in accordance with cranial computed tomography findings.RESULTSS-100B concentrations correlated significantly using both test systems. A cut-off level of 0.18ng/ml was calculated in plasma samples.CONCLUSIONSS-100B concentrations above the cut-off level measured within 40 min after blood sampling allows safe identification and immediate treatment of intracerebral lesions (e.g. epidural and subdural hematoma, subarachnoid hemorrhage, diffuse brain edema etc.) in MHT patients.

OBJECTIVE:To compare S-100B and interleukin-8 serum values on scene/at admission and 12 hrs later with respect to neurologic long-term outcome 12 months after cardiac arrest and return of spontaneous circulation, as well as after severe traumatic brain injury. DESIGN:Prospective comparative cohort study. SETTING:On scene; intensive care units of a university hospital. PATIENTS:Twenty patients with out-of-hospital cardiac arrest. Twenty patients with severe traumatic brain injury. INTERVENTIONS:Therapy was adjusted to the standards of modern prehospital and intensive care management by physicians who were not involved in the study. MEASUREMENTS AND MAIN RESULTS:First median S-100B values of the cardiac arrest group (4.42 ng/mL) mounted as high as those of the traumatic brain injury group (4.11 ng/mL). Within 12 hrs, S-100B levels significantly decreased to 0.75 ng/mL in cardiac arrest patients and to 0.68 ng/mL in traumatic brain injury patients but remained significantly elevated compared with the controls (0.04 ng/mL). Interleukin-8 levels of the cardiac arrest patients on scene (30.33 pg/mL) were clearly elevated above normal (12.60 pg/mL) and increased significantly to 101.40 pg/mL after 12 hrs. They showed no significant difference compared with those of the traumatic brain injury patients (78.75 pg/mL and 96.00 pg/mL, respectively). Multivariate Cox regression analysis in cardiac arrest patients identified only the S-100B level measured 12 hrs after study entry as an independent predictor for unfavorable neurologic outcome according to the Glasgow Outcome Scale score. In contrast, S-100B as well as interleukin-8 levels quantified 12 hrs after admission significantly predicted an unfavorable neurologic course in the traumatic brain injury group. CONCLUSIONS:Significantly elevated S-100B and interleukin-8 serum levels 12 hrs after cardiac arrest suggest that primary brain damage and systemic inflammatory response are comparably serious with that of traumatic brain injury. In both collectives, increased S-100B values measured 12 hrs after insult correlated well with an unfavorable neurologic outcome after 12 months.

BACKGROUND:This study describes a modified catheterization technique with subcutaneously implanted port catheters to be inserted in a retrograde manner across the aortic valve into the left heart ventricle through the right carotid artery to measure organ perfusion.MATERIALS AND METHODS:The specially designed arterial port catheters were implanted in New Zealand rabbits (n = 11, 3.7 +/- 0.1 kg [mean +/- SEM]) under iv anesthesia (medetomidine/ketamine) and single-shot perioperative antibiotic therapy. Hemodynamics were registered continuously during the operation via an ear artery catheter.RESULTS:Implantation of ports was performed in all animals (11/11) without major complications (mean operation time: 70 +/- 3 min). We did not observe catheter-associated arrhythmia, fall in mean arterial pressure (MAP before and post OP: 70 +/- 2 and 68 +/- 2 Torr, respectively), or change in arterial oxygen saturation (SaO2 before and post OP: 89 +/- 3 and 95 +/- 2%, respectively). With a specifically modified microsurgical insertion technique, cerebral blood supply was effectively preserved as evidenced from postmortem histological examinations, cerebral blood flow determination with fluorescent microspheres, and measurement of S-100b protein serum concentrations, a specific marker of neuronal damage. The positioning of the catheter tip in the left ventricle was found to be correct in 10/11 animals.CONCLUSIONS:Repeated and atraumatic microsphere injections into the left ventricle have become feasible by transcutaneous puncture of subcutaneous port systems over several weeks under light sedation. Hence, this new approach (i) avoids the necessity of repeated intracardiac injections and port insertions via thoracotomy, thus reducing the perioperative stress for the animals, and (ii) allows for the first time minimally invasive repetitive and chronic measurements of regional organ blood flow under various experimental settings.

HYPOTHESIS Planned relaparotomy (PRL) has been suggested to have detrimental effects on the systemic activation of inflammation mediators, thereby enhancing organ dysfunctions as assessed by clinical scores in secondary peritonitis. DESIGN Prospective, nonrandomized control trial. SETTING Intensive care units of an urban and a university teaching hospital. PATIENTS Twenty-nine patients with secondary peritonitis. INTERVENTIONS Of the 29 patients with comparable initial peritonitis conditions, 11 underwent PRL and 18 obtained primary abdominal closure. Blood samples were obtained preoperatively and at 2, 6, 8, 12, 18, 24, 30, 36, 42, and 48 hours after the primary operation, then every 12th hour until day 5 and once daily until day 8. MAIN OUTCOME MEASURES Quantification of circulating inflammation parameters (coagulation, acute-phase proteins, cytokine system, cell adhesion, opsonization) in correlation with Acute Physiology and Chronic Health Evaluation II, multiple organ failure, and Sepsis-Related Organ Failure Assessment scores. RESULTS Preoperatively, the patient groups did not differ in mean age, cause of peritonitis, or clinical scores. On average, 5.1 (SEM, +/- 0.7; range, 3-11) lavage treatments were performed in the PRL group, with 90% of the procedures executed during the first 6 days. The PRL treatment resulted in a significantly higher need of blood components and an increased inflammation mediator response, especially concerning coagulation factors, proinflammatory cytokines, adhesion molecules, and opsonic parameters. During PRL, clinical score systems showed higher values and a delayed decline compared with primary abdominal closure treatment. Incidence of multiorgan failure, mortality, and the mean intensive care unit hospitalization period were clearly more pronounced in the PRL group. CONCLUSION In our pilot study, additional lavage treatment of secondary peritonitis resulted in an enhancement of systemic inflammatory mediator response (in particular interleukin 8), which may contribute to a further impairment of organ function.

Elevated systemic levels of S-100B are proposed as a potential indicator of brain damage In identifying high-risk patients after mild head trauma (MHT), Although incidence of alcohol intoxication is high in these patients, the influence of alcohol intoxication on S-100B levels is unclear. Therefore, the aim of our study was to investigate serum concentrations of S-100B. in intoxicated (group 1) and sober (group 2) patients after MHT in comparison with those of mild (group 3) or severely Intoxicated (group 4) individuals without trauma. S-100B was significantly increased in MHT patients exhibiting posttraumatic lesions in initial cranial computed tomography scan. Alcohol intoxication did not elevate S-100B levels in group 3 or 4 subjects. Our data indicate for the first time that alcohol intoxication does not influence the diagnostic value of S-100B measurements in patients after MHT.

Cortisol is known to be an immunomodulatory hormone that exerts suppressive and permissive effects on the immune response. Little is known regarding the evolution of the cytokine response in human septic shock in the presence of hypercortisolemia induced by infusion of stress doses of hydrocortisone. Twenty-four consecutive patients with high-out-put circulatory failure (cardiac index, >4 liters/min per m(2)) who met the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee criteria for septic shock were enrolled in a prospective, double-blind study. The severity of illness at the time of enrollment was graded using the Acute Physiology and Chronic Health Evaluation II system, and the evolution of sepsis-induced organ dysfunction syndrome was assessed using Sepsis-Related Organ Failure Assessment scores. After randomization, hyper-cortisolemia was induced in 12 patients by infusion of 100 mg of hydrocortisone, followed by continuous infusion of 0.18 mg/kg per h. Levels of the circulating cytokines tumor necrosis factor alpha (TNF), interleukin 6 (IL-6), IL-8, and IL-10 were serially measured at prospectively defined time points during the first 5 d after randomization. The infusion of hydrocortisone was associated with significant reductions in serum IL-6 and IL-8 levels and with earlier resolution of the sepsis-induced organ dysfunction syndrome. IL-6 levels started to differ between the groups on day 5. The TNF and IL-10 responses were not altered by hydrocortisone infusion. Hydrocortisone infusion in septic shock differentially regulated the cytokine responses. IL-6 and IL-8 levels decreased significantly and IL-6 levels differed between the groups, whereas TNF and IL-10 levels were not affected by hydrocortisone. Stress doses of hydrocortisone may be a valuable immunomodulatory therapy for septic shock.

We compared a functional (amidolytic) and an enzyme-linked immunosorbent assay (ELISA) method for determining aprotinin concentration in 82 plasma samples obtained from patients undergoing cardiac surgery with aprotinin therapy. There was good correlation between methods (r= 0.87); however, aprotinin measurements by chromogenic assay were significantly higher than by ELISA [234 ± 104 kallikrein inhibitory units (KIU)/ml versus 155 ± 88 KIU/ml;P= 0.0001]. This appeared to be attributable to differences in the potency of the material used to standardize the assays. When results were corrected to allow for potency of the standard, there was no significant difference between chromogenic and ELISA methods (234 ± 104 KIU/ml versus 240 ± 137 KIU/ml), although the ELISA results tended to be higher in some samples. These data suggest that aprotinin concentrations measured by these methods cannot be used interchangeably, and care must be taken when interpreting data from studies measuring aprotinin.

To determine whether a weight-related dose had advantages over a fixed, large-dose regimen, we measured plasma concentrations of aprotinin by using an enzyme-linked immunosorbent assay method at set time points in 30 patients having heart surgery with cardiopulmonary bypass. A weight-related dose comprising a preincision bolus injection of 40,000 kallikrein-inhibiting units (KIU)/kg (5.6 mg/kg) with the same amount given in the oxygenator prime was compared with a large-dose regimen of 2 × 106 KIU (280 mg) preincision bolus and addition to prime, together with an infusion of 500,000 KIU/h (70 mg/h). Peak plasma concentration in the Weight-Related group was less variable than with the fixed-dose regimen. Forty percent of patients allocated to the fixed-dose regimen had an aprotinin concentration of more than 400 KIU/mL, compared with none in the Weight-Related group; this suggests a relative overdosing in the early surgical period in the Fixed-Dose group. There was great individual variability between patients in the time-concentration curves for aprotinin, with no difference between the two regimens. The weight-related dose regimen benefited by not requiring an intraoperative infusion while achieving the same plasma concentrations of aprotinin.

. S-100b is thought to be a screening marker of hypoxic brain damage in patients with cardiac arrest. However, the time-dependent occurrence and relevance of increased S-100b serum levels in out-of-hospital patients with cardiopulmonary resuscitation (CPR) is still discussed. The purpose of our study was to evaluate the diagnostic utility of S-100b measurements in comparison to that of adhesion molecules sE-selectin and sP-selectin in patients with CPR. Sixteen out-of-hospital patients (median age 69.6 years; range 59.2–82.2 years) suffering from cardiac arrest due to ventricular fibrillation, asystole, or electromechanical dissociation were recruited prospectively. Blood samples were drawn on scene after the return of spontaneous circulation (ROSC) and 12 hours after successful CPR. The reference group consisted of 10 patients with isolated severe head trauma (SHT) (Glasgow Coma Score ≤ 8), and the control group comprised 20 healthy volunteers. Serum concentrations of S-100b, determined by immunoluminometric assay, were compared with serum levels of sE-selectin and sP-selectin measured by an enzyme-linked immunosorbent assay and correlated with the patients' survival. In the CPR group, S-100b serum levels (2.37 ng/ml; 1.37–4.09 ng/ml) at study entry (11.6 minutes after arriving on scene) did not significantly differ from those of SHT patients (2.88 ng/ml; 1.78–8.81 ng/ml). Both groups showed significant differences from the healthy controls (0.04 ng/ml; 0.01–0.82 ng/ml). At 12 hours after CPR the serum levels had decreased to 0.41 ng/ml (0.24–0.51 ng/ml) but continued to be significantly elevated compared to that of the control group. sE-selectin values in serum increased from 56.00 ng/ml (38.50–85.50 ng/ml) on scene to 79.00 ng/ml (52.00–127.00 ng/ml) after 12 hours ( p < 0.05). The first measurements differed significantly from serum levels of the control group (22.50 ng/ml; 14.00–34.00 ng/ml) and from those of the SHT group (45.00 ng/ml; 39.00–63.75 ng/ml). At 12 hours after study entry the sE-selectin values were not significantly different from those of the SHT group (51.50 ng/ml; 39.00–95.88 ng/ml). sP-selectin serum levels increased slightly from 199.50 ng/ml (184.25–227.25 ng/ml) to 247.00 ng/ml (206.50–354.75 ng/ml). First and second measurements did not reveal any significant differences in either the SHT group or the healthy controls. When correlated with survival, S-100b measurements exhibited constantly high serum levels for patients, decreasing within the first 24 hours, whereas they decreased significantly in patients with longer survival. sP-selectin values on scene slightly increased in cases of survivals less than 24 hours after CPR. sE-selectin serum levels always remained within normal levels and revealed no significance later on. In contrast to the endothelium-derived adhesion molecules sE-selectin and sP-selectin, comparison of measurements of specific neuroprotein S-100b early after cardiac arrest and 12 hours later seem to provide an indication of the severity of hypoxic brain damage and the prognosis after CPR. Further investigations are required to better understand the CPR-related mechanisms of blood-brain barrier damage.