Vascular Protection in Brain Ischemia

Rodríguez‐Yáñez, Manuel; Blanco, Miguel; Mosquera, Esther; Castillo, José

doi:10.1159/000091700

Cited by 34 publications

(33 citation statements)

References 160 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to its effects on BBB integrity and vascular tone, oxidative damage is also responsible for delayed tissue damage, apoptosis, and inflammation after acute ischemic stroke. 41 Indeed, we found that A-tDCS applied during MCAO induced an increased number of cortical Caspase3 + cells compared with N-tDCS-MCAO mice (which did not preferentially affect neuronal or endothelial cell apoptosis), an increase of final ischemic volume, as well as a dramatic increase of blood-borne, central nervous system-infiltrating inflammatory CD45 + and MPO + cells. Consistently, we found that A-tDCS induced an increase of brain edema and hemorrhagic transformation, also when administered 4.5 hours after MCAO.…”

Section: Discussionmentioning

confidence: 70%

Safety and Efficacy of Transcranial Direct Current Stimulation in Acute Experimental Ischemic Stroke

Peruzzotti-Jametti

Cambiaghi

Bacigaluppi

et al. 2013

Stroke

124

151

View full text Add to dashboard Cite

Background and Purpose— Transcranial direct current stimulation is emerging as a promising tool for the treatment of several neurological conditions, including cerebral ischemia. The therapeutic role of this noninvasive treatment is, however, limited to chronic phases of stroke. We thus ought to investigate whether different stimulation protocols could also be beneficial in the acute phase of experimental brain ischemia. Methods— The influence of both cathodal and anodal transcranial direct current stimulation in modifying brain metabolism of healthy mice was first tested by nuclear magnetic resonance spectroscopy. Then, mice undergoing transient proximal middle cerebral artery occlusion were randomized and treated acutely with anodal, cathodal, or sham transcranial direct current stimulation. Brain metabolism, functional outcomes, and ischemic lesion volume, as well as the inflammatory reaction and blood brain barrier functionality, were analyzed. Results— Cathodal stimulation was able, if applied in the acute phase of stroke, to preserve cortical neurons from the ischemic damage, to reduce inflammation, and to promote a better clinical recovery compared with sham and anodal treatments. This finding was attributable to the significant decrease of cortical glutamate, as indicated by nuclear magnetic resonance spectroscopy. Conversely, anodal stimulation induced an increase in the postischemic lesion volume and augmented blood brain barrier derangement. Conclusions— Our data indicate that transcranial direct current stimulation exerts a measurable neuroprotective effect in the acute phase of stroke. However, its timing and polarity should be carefully identified on the base of the pathophysiological context to avoid potential harmful side effects.

show abstract

Section: Discussionmentioning

confidence: 70%

Safety and Efficacy of Transcranial Direct Current Stimulation in Acute Experimental Ischemic Stroke

Peruzzotti-Jametti

Cambiaghi

Bacigaluppi

et al. 2013

Stroke

124

151

View full text Add to dashboard Cite

show abstract

“…59 In addition to the detrimental vascular actions of O 2 Ϫ in decreasing blood-brain barrier integrity and increasing vascular tone as mentioned above, its reaction with endothelium-derived nitric oxide to form the highly toxic peroxynitrite radical would be expected to trigger apoptosis in vascular cells after ischemic stroke. 60 Evidence for vascular apoptosis has also been reported after subarachnoid hemorrhage in endothelial cells of basilar arteries, in which double fluorescence labeling demonstrated colocalisation of TUNEL, which detects DNA fragmentation, with either caspase-3, caspase-8 or TNFR1. 61 These observations suggest that the mechanism of apoptosis in cerebral endothelial cells after subarachnoid hemorrhage involves TNFR1 and the caspase-8 and caspase-3 pathways.…”

Section: Apoptosis In Nonneuronal Cellsmentioning

confidence: 87%

Apoptotic Mechanisms After Cerebral Ischemia

Broughton

Reutens²,

Sobey³

2009

Stroke

1,092

793

View full text Add to dashboard Cite

Background and Purpose-Traditionally, cell death after cerebral ischemia was considered to be exclusively necrotic in nature, but research over the past decade has revealed that after a stroke, many neurons in the ischemic penumbra will undergo apoptosis. Summary of Review-This brief review provides a general overview and update of various signaling pathways in the development of apoptosis in ischemic lesions. Cerebral ischemia triggers two general pathways of apoptosis: the intrinsic pathway, originating from mitochondrial release of cytochrome c and associated stimulation of caspase-3; and the extrinsic pathway, originating from the activation of cell surface death receptors, resulting in the stimulation of caspase-8. Although many of the key apoptotic proteins have been identified, our understanding of the complex underlying mechanisms remains poor and hence treatment of stroke patients by manipulating apoptotic pathways remains a daunting task. However, recent advances in the field have helped broaden our knowledge of apoptosis after cerebral ischemia. Further to the simplistic concept that stroke-induced apoptosis occurs predominantly in neurons and is caspase-dependent, accumulating evidence now indicates that apoptosis is prevalent in nonneuronal cells and that caspase-independent mechanisms also play a key role. Conclusions-Although the ischemic penumbra is under threat of infarction, it is potentially salvageable and thus represents an opportunity for therapeutic intervention. (Stroke. 2009;40:e331-e339.)

show abstract

“…The animals were placed in a heated chamber at an ambient temperature of 30-34 °C for 15 min and blood pressure values (1)(2)(3)(4)(5)(6)(7)(8)(9) were recorded for each animal. The lowest three readings were averaged to calculate the mean blood pressure.…”

Section: Blood Pressure Measurementsmentioning

confidence: 99%

“…Some conditions induced by hypertension such as oxidative stress, inflammation and endothelial dysfunction are important factors in pathogenetic background of brain damage [1,2]. Oxidative stress, which is characterized by increased bioavailability of reactive oxygen species, plays an important role in development and progression of cerebrovascular dysfunction associated with hypertensive disease [3]. Increased levels of reactive oxygen species such as superoxide anion, hydrogen peroxide and lipid peroxides are reported in patients with hypertension [3,4].…”

Section: Introductionmentioning

confidence: 99%

“…Oxidative stress, which is characterized by increased bioavailability of reactive oxygen species, plays an important role in development and progression of cerebrovascular dysfunction associated with hypertensive disease [3]. Increased levels of reactive oxygen species such as superoxide anion, hydrogen peroxide and lipid peroxides are reported in patients with hypertension [3,4]. Arterial hypertension is often associated with pathologies related with oxidative stress and may be considered as a result of systemic damage in different target organs or tissues induced by free radicals [5,6].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of lisinopril on oxidative stress in brain tissues of rats with L-NAME induced hypertension

Kırbaş¹,

Kutluhan²,

Kırbaş³

et al. 2013

Turk J Bioch

View full text Add to dashboard Cite

Objective: Arterial hypertension is often associated with pathologies related with oxidative stress. Angiotensin converting enzyme (ACE) inhibitors have been used as a safe and effective treatment of hypertension and coronary heart disease. However, the significance of ACE inhibitor usage in hypertension-induced cerebrovascular and neurodegenerative diseases is still unknown. In this study, we aimed to investigate the effects of lisinopril, an ACE inhibitor, on oxidative stress and antioxidant enzyme activities in brain tissues of rats with L-NAME (N ω -Nitro-L-Arginine Methyl Ester hydrochloride) induced hypertension. Methods: Thirty-two Sprague-Dawley rats were divided into four groups: Control, L-NAME, L-NAME plus lisinopril, and only lisinopril. Hypertension was induced by oral administration of the L-NAME (75 mg/kg/day) in drinking water for 6 weeks. Rats were treated with Lisinopril (10 mg/kg/day) for six weeks. Systolic blood pressures were measured at the first, third and sixth weeks by using tail cuff method. Malondialdehyde (MDA), Superoxide dismutase (SOD), Catalase (CAT) and Glutathione peroxidase (GSH-Px) activity were measured from the brain tissue. Nitric oxide (NO) levels were measured from plasma. Results: Our results showed that L-NAME leads to an increase in systolic blood pressure of animals. The antihypertensive effect of lisinopril was observed. MDA level was significantly increased, and antioxidant enzymes activities were decreased in L-NAME given group (p<0.05). However, there was no statistically significant differences between the lisinopril given and other groups according to antioxidant enzymes activities (p>0.05). Conclusion: In our study, hypertension led to oxidative damage in brain tissues. Although lisinopril prevents the hypertension induced oxidative damage, direct antioxidant effect was not observed. Further studies are needed in order to gain certainty effect of lisinopril in brain tissue.

show abstract

Vascular Protection in Brain Ischemia

Cited by 34 publications

References 160 publications

Safety and Efficacy of Transcranial Direct Current Stimulation in Acute Experimental Ischemic Stroke

Safety and Efficacy of Transcranial Direct Current Stimulation in Acute Experimental Ischemic Stroke

Apoptotic Mechanisms After Cerebral Ischemia

Effects of lisinopril on oxidative stress in brain tissues of rats with L-NAME induced hypertension

Contact Info

Product

Resources

About