Biomedical subjects

Peter Biberthaler

Publications and source records attributed to Peter Biberthaler.

24 records · Page 2Linked to original sources

PubMed2002

Assessment of early brain damage in carotid endarterectomy: evaluation of S-100B serum levels and somatosensory evoked potentials in a pilot study.

The release of the neuronal protein S-100B into the circulation has been suggested as an early indication of cellular brain damage. The objective of this prospective pilot study was to determine S-100B serum levels in patients undergoing cross-clamping during carotid endarterectomy (CEA) and to correlate the results with the monitoring of somatosensory evoked potentials (SSEP) and the neurological short-term outcome. Arterial blood samples of 21 patients were drawn before oral intubation, cross-clamping, and unclamping, as well as before extubation and 6 hours later. Recording of SSEP was obtained during carotid occlusion and reperfusion. If loss of SSEP appeared, cerebral ischemia was assumed and an intraluminal shunt was placed. During cross-clamping, S-100B serum levels of 14 patients increased significantly from 0.05 ng/ml to 0.21 ng/ml, but returned to baseline levels after unclamping. In 5 cases, loss of SSEP amplitudes occurred but was reversed by the shunt insertion. No significant differences of S-100B serum values, neurological examination, and carotid duplex surveillance became obvious in this group when compared to the patients with undisturbed SSEP. However, 2 patients with complete disappearance of postcentral SSEP components suffered from neurological deficits in the postoperative period. S-100B serum levels remained highly elevated 6 hours after extubation (0.78 ng/ml and 0.41 ng/ml) compared to the baseline values (0.15 ng/ml and 0.07 ng/ml). During CEA a transitory increase of the S-100B serum levels appears to present an impairment of the blood-brain barrier integrity without any neurological deficits. In contrast, persistently elevated S-100B serum levels seem to be associated with transient loss of SSEP and development of neurological deficits.

Aged↗

PubMed2002

Revascularization of transplanted adipose tissue: a study in the dorsal skinfold chamber of hamsters.

Adipose tissue seems to be an ideal material for use as a permanent soft-tissue substitute in reconstructive surgery. However, knowledge of the behavior of the graft--in particular, its revascularization--is scarce. Therefore, the aim of the current study was to establish a novel model that allows for long-term in vivo quantitative analysis of revascularization of adipose tissue after transplantation. Hamsters (n = 8) were fitted with transparent titanium dorsal skinfold chambers. Immediately after en bloc harvest of adipose tissue from the left inguinal area, the graft was placed gently into the chamber. At days 1, 3, 12, and 21, red blood cell-perfused vessels were assessed in surrounding host tissue, in the border of the graft, and in its center (n = 6 areas each) using intravital fluorescent microscopy. The model allowed for permanent observations of adipose tissue and quantitative analysis of functional vessel density (FVD). At the border zone of the graft, an FVD of 2 +/- 1 cm per cm(2) was measured at day 1. In this region FVD increased constantly and finally reached values (184 +/- 10 cm per cm(2); day 21) that were comparable with those of the surrounding host tissue. Revascularization in the center of the graft started at day 3 after transplantation (14 +/- 3 cm per cm(2)). Here, FVD increased constantly, but lower values compared with the grafts' border zone were measured (139 +/- 10 cm per cm(2); day 21). FVD data obtained from transplanted adipose tissue may contribute to understanding fundamental mechanisms of graft failure.

Adipose Tissue↗

PubMed2002

Serum S-100B and interleukin-8 as predictive markers for comparative neurologic outcome analysis of patients after cardiac arrest and severe traumatic brain injury.

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.

Adult↗

PubMed2002

Immediate S-100B and neuron-specific enolase plasma measurements for rapid evaluation of primary brain damage in alcohol-intoxicated, minor head-injured patients.

The neuroproteins S-100B and neuron-specific enolase (NSE) released into the circulation are suggested to be reliable markers for primary brain damage. However, safe identification of relevant post-traumatic complications after minor head injury (MHI) is often hampered by acute intoxication of the patients. The objective of this study was to determine the diagnostic validity of immediate plasma measurements of S-100B and NSE in comparison with neurological examinations and cerebral computed tomography (CCT) findings in alcohol-intoxicated MHI patients. One hundered thrity-nine MHI individuals were enrolled in this prospective study during Munich's Oktoberfest 2000. Plasma levels of S-100B and NSE as well as serum alcohol and glucose values were determined by fully automated assays immediately after admission. The results were compared with Glasgow Coma Scale score, a brief neurological examination, and the CCT findings. Without being influenced by alcohol, median S-100B levels of the CCT+ group were significantly increased compared with those of the CCT- group (P < 0.001). NSE, alcohol, and glucose levels showed no significant group differences. As calculated by the ROC analysis, a cutoff value of 0.21 ng/mL with an area under the curve of 0.864 clearly differentiates between CCT+ and CCT- patients at a sensitivity of 100%, a specificity of 50.0%, and a positive likelihood ratio of 2.0. Although acute alcohol intoxication did not confound plasma measurements of S-100B and NSE, only S-100B levels below the cutoff level of 0.21 ng/mL seem to indicate absence of primary brain damage. Thus, in addition to routine neurological examinations, S-100B measurements immediately after admission might help to reduce CCT scans in alcohol-intoxicated patients early after MHI.

Adult↗

PubMed2002

P-selectin mediates platelet-endothelial cell interactions and reperfusion injury in the mouse liver in vivo.

Platelets are suggested to participate in the pathogenesis of hepatic ischemia-reperfusion (I/R) injury. This study was designed to analyze platelet-endothelial cell interactions in the postischemic mouse liver in vivo and to define the role of endothelial versus platelet P-selectin for these interactions. Platelet-endothelial cell interactions were quantitatively analyzed using intravital fluorescence microscopy after lobar hepatic I/R in C57BL/6 wild-type and P-selectin-deficient mice after infusion of ex vivo rhodamine-6G-labeled wild-type and P-selectin-deficient platelets. Reperfusion injury and apoptosis were assessed by established methods. In wild-type animals, hepatic I/R caused significantly enhanced platelet-endothelial cell interactions in terminal arterioles and postsinusoidal venules as well as platelet stagnation in sinusoids. Concomitantly, transaminase and caspase-3 activities were elevated and sinusoidal perfusion was impaired. In contrast, platelet-endothelial cell interactions were nearly absent in arterioles and venules of mice lacking endothelial P-selectin, irrespective of the presence of P-selectin on infused platelets, but still significantly elevated in sinusoids. Simultaneously, sinusoidal perfusion failure was ameliorated, and transaminase- and caspase-3 activities were significantly reduced in P-selectin-deficient mice as compared with wild-type animals. The present intravital microscopic study provides, for the first time, quantitative analyses of platelet-endothelial cell interactions in the postischemic hepatic microcirculation. Our in vivo data show that endothelial P-selectin is critical for postischemic platelet-endothelial cell interactions within hepatic presinusoidal arterioles and postsinusoidal venules. P-selectin deficiency prevents microvascular injury and apoptosis after warm hepatic I/R.

Animals↗

PubMed2002

Poly(ADP-ribose) polymerase triggers the microvascular mechanisms of hepatic ischemia-reperfusion injury.

Activation of poly(ADP-ribose) polymerase (PARP) mediates oxidative stress-induced cell injury. We tested the hypothesis that PARP contributes to ischemia-reperfusion (I/R) damage of the liver by triggering the mechanisms of microcirculatory failure. Leukocyte- and platelet-endothelial cell interactions as well as sinusoidal perfusion were analyzed by intravital fluorescence microscopy after lobar hepatic I/R (90 min/30 min) in C57BL/6 x 129/Sv wild-type (PARP+/+) and PARP-deficient (PARP-/-) mice. Hepatic I/R induced leukocyte/platelet-endothelial cell interactions and tissue injury in PARP+/+ mice, as indicated by impaired sinusoidal perfusion and increased alanine aminotransferase (ALT)/aspartate aminotransferase (AST) serum activities. In PARP-/- mice, however, the postischemic increase in the numbers of rolling/adherent leukocytes and platelets was significantly lower. In addition, I/R-induced translocation of CD62P as well as mRNA expression of CD62E, CD54, and CD106 were attenuated. The degree of perfusion failure was reduced and the increase in the ALT/AST activities was lower in PARP-/- mice compared with PARP+/+ mice. We conclude that PARP contributes to hepatic microvascular injury by triggering the expression/translocation of adhesion molecules and modulating leukocyte/platelet-endothelial cell interactions.

Alanine Transaminase↗