Edaravone, a free radical scavenger, attenuates cerebral infarction and hemorrhagic infarction in rats with hyperglycemia.

Background: Thrombolysis due to acute ischemic stroke is associated with the risk of hemorrhagic infarction, especially after reperfusion. Recent experimental studies suggest that the main mechanism contributing to hemorrhagic infarction is oxidative stress caused by disruption of the blood-brain barrier. Edaravone, a free radical scavenger, decreases oxidative stress, thereby preventing hemorrhagic infarction during ischemia and reperfusion.

Hyperglycemia and hemorrhagic transformation of cerebral infarction: a macroscopic hemorrhagic transformation rat model.

The recombinant tissue plasminogen activator (t-PA) is a useful therapy for acute ischemic stroke patients, but there is a major risk factor of hemorrhagic transformation. Hyperglycemic patients are not able to admit t-PA because hyperglycemia exaggerates ischemic brain and vascular damage following transient focal cerebral ischemia and frequently induces hemorrhagic transformation of the infarct during reperfusion. However, the mechanisms underlying hemorrhagic transformation induced by hyperglycemia are still unknown.

Mechanisms of statin treatment in cerebral vasospasm.

3-Hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, commonly known as statins, are widely used clinically for their lipid lowering properties. Recent experimental evidence shows that statins are also effective in ameliorating cerebral vasospasm, which occurs as sequelae of subarachnoid hemorrhage. This literature review focuses on the literature-based putative mechanisms involved in statin mediated attenuation of cerebral vasospasm, such as eNOS, vascular inflammation, apoptosis, especially the phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway from our experimental study.

Granulocyte colony-stimulating factor protects the brain against experimental stroke via inhibition of apoptosis and inflammation.

Objectives: The molecular mechanisms of the anti-apoptotic and anti-inflammatory properties of granulocyte-colony stimulating factor (G-CSF) following focal cerebral ischemia in rats were examined in this study.

Methods: Sprague-Dawley rats were randomly divided into three groups: sham, middle cerebral artery occlusion (MCAO) non-treatment and MCAO with G-CSF treatment. Focal ischemia was induced with the suture occlusion method for 90 minutes, and treatment was given at the onset of reperfusion.

Simvastatin attenuation of cerebral vasospasm after subarachnoid hemorrhage in rats via increased phosphorylation of Akt and endothelial nitric oxide synthase.

The mechanisms involved in simvastatin-mediated attenuation of cerebral vasospasm after subarachnoid hemorrhage (SAH) are unclear. We investigated the role of the phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway and endothelial nitric oxide synthase (eNOS) in the cerebral vasculature in statin-mediated attenuation of cerebral vasospasm using wortmannin, an irreversible pharmacological PI3K inhibitor, and a rat SAH endovascular perforation model. Simvastatin was administered intraperitoneally in two dosages (1 mg/kg and 20 mg/kg) at 0.

Role of c-Jun N-terminal kinase in early brain injury after subarachnoid hemorrhage.

The c-Jun N-terminal kinase (JNK) is induced by cerebral ischemia and injurious blood components acutely after subarachnoid hemorrhage (SAH). We hypothesized that inhibition of JNK will prevent damage to the neurovascular unit in the early brain injury period after SAH. Ninety-nine male SD rats (300-350 g) were randomly assigned to sham, SAH, and SAH treated with JNK inhibitor groups.

Granulocyte-colony stimulating factor inhibits apoptotic neuron loss after neonatal hypoxia-ischemia in rats.

Neonatal hypoxia-ischemia (HI) is an important clinical problem with few effective treatments. Granulocyte-colony stimulating factor (G-CSF) is an endogenous peptide hormone of the hematopoietic system that has been shown to be neuroprotective in focal ischemia in vivo and is currently in phase I/II clinical trials for ischemic stroke in humans. We tested G-CSF in a rat model of neonatal hypoxia-ischemia in postnatal day 7 unsexed rat pups.

Lecithinized superoxide dismutase improves outcomes and attenuates focal cerebral ischemic injury via antiapoptotic mechanisms in rats.

Background And Purpose: Recent studies have shown the antiapoptotic neuroprotective effects of lecithinized superoxide dismutase (PC-SOD) in different forms of brain injury. We tested the effects of PC-SOD in focal cerebral ischemia in the rat middle cerebral artery occlusion model (MCAO).

Methods: Adult male Sprague-Dawley rats were treated with PC-SOD (0.

Inhibition of integrin alphavbeta3 reduces blood-brain barrier breakdown in focal ischemia in rats.

Ischemic stroke is a major cause of morbidity and mortality in industrialized nations. We tested the effect of postischemic treatment of cyclo-RGDfV (cRGDfV), a selective inhibitor of integrin alphavbeta3, in the middle cerebral artery occlusion (MCAO) model of ischemic stroke in rats. Rats were randomly divided into three groups: sham operation (n = 13), MCAO with no treatment (n = 18), and MCAO with cRGDfV treatment (n = 28).

Neurovascular and neuronal protection by E64d after focal cerebral ischemia in rats.

Calpains and cathepsins are two families of proteases that play an important role in ischemic cell death. In this study, we investigated the effect of E64d, a mu-calpain and cathepsin B inhibitor, in the prevention of neuronal and endothelial apoptotic cell death after focal cerebral ischemia in rats. Rats underwent 2 hr of transient focal ischemia from middle cerebral artery occlusion (MCAO) and were sacrificed 24 hr later.

Cathepsin and calpain inhibitor E64d attenuates matrix metalloproteinase-9 activity after focal cerebral ischemia in rats.

Background And Purpose: Matrix metalloproteinases (MMPs) and cysteine proteases (calpain and cathepsin B) play an important role in cell death and are upregulated after focal cerebral ischemia. Because there is a significant interaction between MMP-9 with calpain and cathepsin B, we investigated the role of E64d (a calpain and cathepsin B inhibitor) on MMP-9 activation in the rat focal ischemia model.

Methods: Male Sprague-Dawley rats were subjected to 2 hours of middle cerebral artery occlusion by using the suture insertion method followed by 22 hours of reperfusion.

Comparison of silicon-coated nylon suture to plain nylon suture in the rat middle cerebral artery occlusion model.

Unlabelled: A variety of intraluminal sutures have been used in the middle cerebral artery occlusion model (MCAO) of focal ischemia. In the present study we tested commercially available silicon-coated nylon suture in the MCAO model and compared the results to traditional monofilament nylon suture occlusion. Twelve Sprague-Dawley male rats were randomly divided two groups, MCAO with 4-0 nylon suture (Group N, n=6) and MCAO with silicone-coated 4-0 nylon suture (Group S, n=6).

[Our current technique for basic pterional craniotomy].

Pterional cnaniotomy is frequently used in neurosurgical practice, but still poses significant cosmetic and functional drawbacks. Here, we describe our modified technique to overcome such problems as the sterilization of the scalp without brush and razor, preemptive analgesia, preservation of the periostium for reconstruction, retrograde dissection of the temporal muscle, and complete sphenoidotomy using chisel or drills. The tips of our pterional craniotomy offer suitable size and depth of working field around the paraclinoidal regions, maintaining cosmetic satisfaction of the patients.

High plasma concentration of brain natriuretic peptide in patients with ruptured anterior communicating artery aneurysm.

The purpose of this study is to investigate the mechanism of increased atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in patients with subarachnoid hemorrhage due to ruptured aneurysms. ANP and BNP plasma concentrations were measured by immunoradiometoric assay in 53 patients at the day of onset of ruptured aneurysm, the correlation between values of increased ANP or BNP, and sex, age, location of ruptured aneurysm, degree of SAH, and severity of WFNS were statistically studied. The concentration of BNP in ruptured anterior communicating artery aneurysm (A-com) shows a significant elevation compared with other site aneurysms (p = 0.

[Clinical significance of natriuretic peptides in patients with aneurysmal subarachnoid hemorrhage].

Hyponatremia and hypovolemia following aneurysmal subarachnoid hemorrhage (SAH) might be speculated by exaggerated secretion of natriuretic peptides and resulted ischemic sequela caused by cerebral vasospasm. We measured serum concentration of natriuretic peptides and investigated their influence on post-SAH hyponatremia. Among 49 patients of SAH, their plasma concentration of the natriuretic peptides (atrial natriuretic peptide: ANP and brain natriuretic peptide: BNP) were measured at the day of ictus and 7th day of SAH.