interleukin-8 and Brain-Edema

Many studies suggest that hyperbaric oxygen therapy (HBOT) can provide some clinically curative effects on blast-induced traumatic brain injury (bTBI). The specific mechanism by which this occurs still remains unknown, and no standardized time or course of hyperbaric oxygen treatment is currently used. In this study, bTBI was produced by paper detonators equivalent to 600 mg of TNT exploding at 6.5 cm vertical to the rabbit's head. HBO (100% O2 at 2.0 absolute atmospheres) was used once, 12 h after injury. Magnetic resonance spectroscopy was performed to investigate the impact of HBOT on the metabolism of local injured nerves in brain tissue. We also examined blood-brain barrier (BBB) integrity, brain water content, apoptotic factors, and some inflammatory mediators. Our results demonstrate that hyperbaric oxygen could confer neuroprotection and improve prognosis after explosive injury by promoting the metabolism of local neurons, inhibiting brain edema, protecting BBB integrity, decreasing cell apoptosis, and inhibiting the inflammatory response. Furthermore, timely intervention within 1 week after injury might be more conducive to improving the prognosis of patients with bTBI.

Topics: Animals; Blood-Brain Barrier; Brain; Brain Edema; Brain Injuries; Caspase 3; Encephalitis; Hyperbaric Oxygenation; Interleukin-8; Male; Rabbits; Tumor Necrosis Factor-alpha

Emboli and proinflammatory mediators are suspected of generating cerebral edema after coronary surgery. In contrast to cardiopulmonary bypass (CPB), off-pump coronary artery bypass surgery (OPCAB) reduces microemboli count and proinflammatory mediator release but carries the risk of hemodynamic instability. A microaxial blood pump can augment cardiac output.. Coronary bypasses were constructed in pigs with CPB and cardioplegia (n=9), OPCAB (n=9), or blood-pump support CAB (n=9). Nine animals underwent sham operation. Embolus count was monitored and regional cerebral blood flow was assessed with microspheres in 21 brain specimens per animal (n=189 per group). Interleukins 6 and 8 and tumor necrosis factor-alpha concentrations were determined. These variables were studied before, during, and for 4 hours after surgery. Finally, cerebral water content was determined.. During CPB and blood-pump CAB, a significant number of emboli were counted in contrast to OPCAB and controls (P<0.05). During CPB, regional cerebral blood flow was affected (32 of 189) and showed reactive hyperemia except in 10 specimens after aortic cross-clamp release. This impairment persisted in 20 specimens. During and after OPCAB, regional cerebral blood flow remained nearly unchanged but showed low flow during (58 of 189) and after (35 of 189) the blood-pump run. A significant increase in proinflammatory mediators was observed only in the CPB group. CPB and blood-pump CAB significantly increased cerebral water content (P<0.05). A strong correlation between embolic load and cerebral water content was observed in all groups. No correlation between proinflammatory mediator release and cerebral water content was detected.. Emboli formation rather than inflammatory mediators are responsible for increased cerebral water content after conventional and assisted beating-heart myocardial revascularization.

Topics: Animals; Brain; Brain Edema; Cardiopulmonary Bypass; Coronary Artery Bypass; Coronary Artery Bypass, Off-Pump; Disease Models, Animal; Female; Inflammation Mediators; Interleukin-6; Interleukin-8; Intracranial Embolism; Male; Myocardial Revascularization; Regional Blood Flow; Risk Factors; Swine; Tumor Necrosis Factor-alpha

To study the effects of a spin trap agent and a CD18 antibody administered after stroke induction on intracerebral hemorrhaging. The drugs can prevent leukocyte adhesion.. A rabbit embolic stroke model that produces intracerebral hemorrhage was used.. A time course study showed that hemorrhaging was grossly apparent in approximately 50% of the subjects at 5 hours and in 75% at 24 hours after embolization. MDL 101,002, a spin trap agent, administered IV 5 minutes after embolization, significantly decreased the volume of hemorrhage. It also improved the behavior score relative to vehicle-treated rabbits. The CD18 antibody tended to decrease hemorrhage volume.. The beneficial effect of MDL 101,002 may be caused by inhibition of free radical injury to brain tissue, thereby protecting brain microvessel integrity. Acute therapy for intracerebral hemorrhage may be feasible.

Topics: Animals; Antibodies, Monoclonal; Brain; Brain Edema; CD18 Antigens; Cerebral Hemorrhage; Cerebral Infarction; Disease Models, Animal; Extravasation of Diagnostic and Therapeutic Materials; Interleukin-8; Intracranial Embolism; Isoquinolines; Nitrogen Oxides; Rabbits; Spin Labels

Reperfusion after a transient ischemia is a frequently encountered clinical condition that often causes greater tissue damage than persistent ischemia itself. Reperfusion to rabbit brain, after a transient focal ischemia, induced neutrophil infiltration and aggregation--neither of which were observed in rabbit brain rendered ischemic alone for the same time interval--thereby leading to severe brain edema and infarct. Brain tissue levels of interleukin-8 (IL-8), a potent neutrophil chemotactic cytokine (chemokine), increased significantly at 6 hours after reperfusion, but without a noticeable elevation of plasma IL-8 levels. Moreover, we detected IL-8 protein immunohistologically in the vascular wall and, to a lesser degree, in infiltrated neutrophils, suggesting a local production of IL-8 in reperfused brain tissues. Furthermore, a neutralizing anti-IL-8 antibody significantly reduced brain edema and infarct size in comparison to rabbits receiving a control antibody. These results implicate locally produced IL-8 as a pivotal mediator of cerebral reperfusion and suggest that IL-8 is a novel target for the intervention of this injury.

Topics: Animals; Antibodies, Monoclonal; Blood-Brain Barrier; Brain Edema; Cerebral Infarction; Female; Interleukin-8; Mice; Neutrophils; Rabbits; Reperfusion Injury

Topics: Altitude Sickness; Angiogenesis Inducing Agents; Animals; Brain Edema; Cytokines; Endothelial Growth Factors; Endothelium, Vascular; Fibroblast Growth Factor 2; Humans; Interferon-alpha; Interleukin-2; Interleukin-8; Lignin; Lymphokines; Macrophage Activation; Neovascularization, Pathologic; Purpura; Retinal Hemorrhage; Transforming Growth Factor beta; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors