Publications by authors named "Katarina Lakovic"
Bilirubin and its oxidation products damage brain white matter.
J Cereb Blood Flow Metab
November 2014
Article Synopsis
- Brain injury from intracerebral hemorrhage (ICH) affects both the cortex and white matter, potentially caused by the breakdown of blood products like bilirubin and its oxidation products.
- Research showed that bilirubin significantly damages myelinated axons in brain slices, but unmyelinated axons are more susceptible to damage in live experiments.
- The study suggests that preventing the toxic effects of bilirubin and its compounds, possibly using dimethyl sulfoxide, could be a therapeutic strategy to protect against axonal damage post-hemorrhagic stroke.
Animal models have been developed to simulate angiographic vasospasm secondary to subarachnoid hemorrhage (SAH) and to test pharmacologic treatments. Our aim was to evaluate the effect of pharmacologic treatments that have been tested in humans and in preclinical studies to determine if animal models inform results reported in humans. A systematic review and meta-analysis of SAH studies was performed.
View Article and Find Full Text PDFMicrocirculatory dysfunction may contribute to delayed cerebral ischemia after subarachnoid hemorrhage (SAH). This study investigated structural changes in microvessels and their relationship to brain injury after SAH. We used 15 mice (n = 5 for each group) to create sham, saline-injected (100 μl 0.
View Article and Find Full Text PDFAnimal models have been developed to simulate angiographic vasospasm secondary to subarachnoid hemorrhage (SAH) and to test pharmacologic treatments. Our aim was to evaluate the effect of pharmacologic treatments that have been tested in humans and in preclinical studies to determine if animal models inform results reported in humans. A systematic review and meta-analysis of SAH studies was performed.
View Article and Find Full Text PDFOne of the major complications after subarachnoid hemorrhage (SAH) is angiographic vasospasm in the large arteries at the base of the brain. However, a clinical trial of clazosentan demonstrated a 65% relative risk reduction in angiographic vasospasm but no effect on mortality or clinical outcome, raising questions about the role of angiographic vasospasm played in outcome after SAH. The purpose of this study was to determine if reducing or reversing angiographic vasospasm with clazosentan reduced other secondary complications such as microthromboembolism, loss of long-term potentiation (LTP) and neuronal cell death in a rat model of SAH.
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