Plasma volume expansion with 5% albumin compared to Ringer's acetate during normal and increased microvascular permeability in the rat.

Background: It is believed that the effectiveness of colloids as plasma volume expanders is dependent on the endothelial permeability for macromolecules. The objective of this study was to test the hypothesis that the plasma volume expanding effect of 5% albumin relative to that of a crystalloid solution is reduced if microvascular permeability is increased.

Methods: A control group was resuscitated with either 5% albumin (8 ml/kg) or Ringer's acetate (36 ml/kg) immediately after a hemorrhage of 8 ml/kg (n = 29).

Hemodynamic and histological effects of traumatic brain injury in eNOS-deficient mice.

Microvascular dysfunction in the brain, characterized by vasoconstriction, vascular occlusion, and disruption of the blood brain barrier, may adversely affect outcome following traumatic brain injury (TBI). Because of its vasodilating and antiaggregative properties, nitric oxide (NO) produced by nitric oxide synthase in the endothelium (eNOS) is a key regulator of vascular homeostasis. The objective of the present study was to evaluate the role of eNOS in vascular disturbances and histological outcome in the brain following TBI.

Increased cortical cell loss and prolonged hemodynamic depression after traumatic brain injury in mice lacking the IP receptor for prostacyclin.

Prostacyclin is the major arachidonic acid metabolite of the vascular endothelium and is produced mainly via the cyclooxygenase-2 pathway. By acting on the prostacyclin (IP) receptor on platelets and vascular smooth muscle cells, prostacyclin exerts vasodilatory and antiaggregative/antiadhesive effects. Previous studies have shown that prostacyclin production increases after brain trauma, but the importance of prostacyclin for posttraumatic hemodynamic alterations and neuron survival has not been investigated.

Effects of L-arginine on cerebral blood flow, microvascular permeability, number of perfused capillaries, and brain water content in the traumatized mouse brain.

It is has been suggested that decreased production of the vasodilatory and anti-aggregative substance NO (nitric oxide) may result in lower cerebral blood flow (CBF) in injured areas of the traumatized brain. The NO-precursor L-arginine has been shown to counteract CBF decreases early after trauma, but microcirculatory and more long-term effects on CBF of L-arginine have not been investigated. In an attempt to analyze effects of L-arginine on the microcirculation in the traumatized brain, the present study was designed to evaluate the effects of L-arginine compared to vehicle (0.

A mouse model for evaluation of capillary perfusion, microvascular permeability, cortical blood flow, and cortical edema in the traumatized brain.

Genetically engineered mice have successfully been used to investigate molecular and cellular mechanisms associated with cell dysfunction following brain trauma. Such animals may also offer a possibility to investigate mechanisms involved in posttraumatic hemodynamic alterations. The objective of the study was to establish a mouse model in which important hemodynamic alterations following trauma could be analyzed.

Low-dose prostacyclin improves cortical perfusion following experimental brain injury in the rat.

It was recently shown that prostacyclin at a low dose reduces cortical cell death following brain trauma in the rat. Conceivably, prostacyclin with its vasodilatory, anti-aggregatory, anti-adhesive and permeability-reducing properties improved a compromised perfusion caused by post-traumatic vasoconstriction, microthrombosis and increased microvascular permeability. The objective of the present study was therefore to investigate the hemodynamic effects of low-dose prostacyclin in the traumatized rat cortex.