Bradykinin-induced leukocyte- and platelet-endothelium interactions in the cerebral microcirculation.

Bradykinin is known for its pathophysiological role as mediator of inflammation. Following cerebral ischemia, bradykinin promotes the secondary brain damage through an increase of vascular permeability and brain edema formation, again hallmarks of inflammation. It is not clear, whether bradykinin also activates inflammatory cells and regulates microcirculatory blood flow in the brain.

Inflammatory response to nitrous oxide in the central nervous system.

Nitrous oxide is a widely used anesthetic gas. The aim of this study was to investigate the effect of this agent on inflammatory side effects in the brain. The cerebral microcirculation of Mongolian gerbils was investigated by fluorescent intravital microscopy for up to 7 h after induction of anesthesia.

Arteriovenous transit time as a measure for microvascular perfusion in cerebral ischemia and reperfusion.

Objective: The aim of this study was to measure microvascular perfusion (MVP) on the brain surface in global ischemia and reperfusion by means of intravital fluorescence microscopy.

Methods: Global ischemia was induced in gerbils for 15 minutes with 3 hours of reperfusion. The passage of a rhodamine bolus (25 mul intravenously) from an arteriole to a venule was analyzed by intravital fluorescence microscopy through a cranial window.

Activation of leukocyte-endothelial interactions and reduction of selective neuronal death after global cerebral ischemia.

The role of leukocyte-endothelial interactions (LEI) as part of the inflammatory response after global cerebral ischemia (GCI) is hardly understood and may be detrimental as well as beneficial. Objective of the current study was to investigate the cause-effect relationship of activated leukocytes for the development of ischemic brain damage. Mongolian gerbils were subjected to 15 min of global cerebral ischemia.

Effect of oxidative stress on glial cell volume.

Cytotoxic brain edema is a major contributor of tissue damage following cerebral ischemia and traumatic brain injury. The pathophysiology of cytotoxic edema formation is still not well understood. Although it is widely believed that oxidative stress causes cytotoxic brain edema, experimental proof is lacking.