Inhaled Nitric Oxide Treatment for Aneurysmal SAH Patients With Delayed Cerebral Ischemia.

Background: We demonstrated experimentally that inhaled nitric oxide (iNO) dilates hypoperfused arterioles, increases tissue perfusion, and improves neurological outcome following subarachnoid hemorrhage (SAH) in mice. We performed a prospective pilot study to evaluate iNO in patients with delayed cerebral ischemia after SAH.

Methods: SAH patients with delayed cerebral ischemia and hypoperfusion despite conservative treatment were included.

The Contractile Apparatus Is Essential for the Integrity of the Blood-Brain Barrier After Experimental Subarachnoid Hemorrhage.

Development of vasogenic brain edema is a key event contributing to mortality after subarachnoid hemorrhage (SAH). The precise underlying mechanisms at the neurovascular level that lead to disruption of the blood-brain barrier (BBB) are still unknown. Activation of myosin light chain kinases (MLCK) may result in change of endothelial cell shape and opening of the intercellular gap with subsequent vascular leakage.

Nitric oxide inhalation reduces brain damage, prevents mortality, and improves neurological outcome after subarachnoid hemorrhage by resolving early pial microvasospasms.

Subarachnoid hemorrhage is a stroke subtype with particularly bad outcome. Recent findings suggest that constrictions of pial arterioles occurring early after hemorrhage may be responsible for cerebral ischemia and - subsequently - unfavorable outcome after subarachnoid hemorrhage. Since we recently hypothesized that the lack of nitric oxide may cause post-hemorrhagic microvasospasms, our aim was to investigate whether inhaled nitric oxide, a treatment paradigm selectively delivering nitric oxide to ischemic microvessels, is able to dilate post-hemorrhagic microvasospasms; thereby improving outcome after experimental subarachnoid hemorrhage.

Experimental subarachnoid hemorrhage causes early and long-lasting microarterial constriction and microthrombosis: an in-vivo microscopy study.

Early brain injury (EBI) after subarachnoid hemorrhage (SAH) is characterized by a severe, cerebral perfusion pressure (CPP)-independent reduction in cerebral blood flow suggesting alterations on the level of cerebral microvessels. Therefore, we aimed to use in-vivo imaging to investigate the cerebral microcirculation after experimental SAH. Subarachnoid hemorrhage was induced in C57/BL6 mice by endovascular perforation.

Contribution of matrix metalloproteinase-9 to cerebral edema and functional outcome following experimental subarachnoid hemorrhage.

Background: Cerebral edema is an important risk factor for death and poor outcome following subarachnoid hemorrhage (SAH). However, underlying mechanisms are still poorly understood. Matrix metalloproteinase (MMP)-9 is held responsible for the degradation of microvascular basal lamina proteins leading to blood-brain barrier dysfunction and, thus, formation of vasogenic cerebral edema.

Contribution of bradykinin receptors to the development of secondary brain damage after experimental subarachnoid hemorrhage.

Background: Subarachnoid hemorrhage (SAH) is the stroke subtype with the highest mortality and morbidity. Which molecular events mediate brain damage after SAH is not well understood.

Objective: To investigate the role of proinflammatory bradykinin B(1) and B(2) receptors for the pathophysiology of SAH.

Standardized induction of subarachnoid hemorrhage in mice by intracranial pressure monitoring.

Background And Purpose: Subarachnoid hemorrhage (SAH) is the subtype of stroke with the most unfavorable outcome but the least well investigated molecular pathophysiology. Among others, not sufficiently well standardized in vivo models suitable for the use with transgenic animals may be responsible for this situation. Therefore the aim of the current study was to detect suitable intra-operative parameters for the controlled and standardized induction of SAH in mice and to characterize the long-term functional and histopathological outcome of mice subjected to this procedure.

The intrinsic renal compartment syndrome: new perspectives in kidney transplantation.

Purpose: Inflammatory edema after ischemia-reperfusion may impair renal allograft function after kidney transplantation. This study examines the effect of edema-related pressure elevation on renal function and describes a simple method to relieve pressure within the renal compartment.

Methods: Subcapsular pressure at 6, 12, 24, 48 hr, and 18 days after a 45 min warm ischemia was determined in a murine model of renal ischemia-reperfusion injury.