ArticleBritish journal of pharmacology2005
Pharmacological neutropenia prevents endothelial dysfunction but not smooth muscle functions impairment induced by middle cerebral artery occlusion.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Integrative imaging and transcriptomics implicate neutrophils in microvascular no-reflow after stroke.Journal of neuroinflammation · 2026Article
- Article
- Leukocyte indicators and variations predict worse outcomes after intravenous thrombolysis in patients with acute ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- High neutrophil counts before endovascular treatment for acute basilar artery occlusion predict worse outcomes.Frontiers in aging neuroscience · 2022Article
- Neutrophil to Lymphocyte Ratio Is a Therapeutic Biomarker for Spontaneous Hemorrhagic Transformation.Neurotoxicity research · 2020Article
- Mechanisms of I/R-Induced Endothelium-Dependent Vasodilator Dysfunction.Advances in pharmacology (San Diego, Calif.) · 2018Review
- Neutrophil-To-Lymphocyte Ratio Predicts 3-Month Outcome of Acute Ischemic Stroke.Neurotoxicity research · 2017Article
- Cerebral Vascular Disease and Neurovascular Injury in Ischemic Stroke.Circulation research · 2017Review
- Early treatment with atorvastatin exerts parenchymal and vascular protective effects in experimental cerebral ischaemia.British journal of pharmacology · 2015Article
- Higher neutrophil counts before thrombolysis for cerebral ischemia predict worse outcomes.Neurology · 2015Article
- Targeting neutrophils in ischemic stroke: translational insights from experimental studies.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Review
- Impact of the neutrophil response to granulocyte colony-stimulating factor on the risk of hemorrhage when used in combination with tissue plasminogen activator during the acute phase of experimental stroke.Journal of neuroinflammation · 2014Article
- Effects of the PPAR-α agonist fenofibrate on acute and short-term consequences of brain ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Article
- Hemorrhagic transformation after ischemic stroke in animals and humans.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Review
- Peripheral polymorphonuclear leukocyte activation as a systemic inflammatory response in ischemic stroke.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2013Review
- Effects of reactive oxygen species and neutrophils on endothelium-dependent relaxation of rat thoracic aorta.Interdisciplinary toxicology · 2011Article
- Neutrophils contribute to intracerebral haemorrhages after treatment with recombinant tissue plasminogen activator following cerebral ischaemia.British journal of pharmacology · 2009Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The polymorphonuclear neutrophils (PMN) activation and mobilization observed in acute cerebral infarction contribute to the brain tissue damage, but PMN could also be involved in postischemic functional injury of ischemied blood vessel. 2. This study was undertaken to investigate whether pharmacological neutropenia could modify the postischemic endothelial dysfunction in comparison to smooth muscle whose impairment is likely more related to reperfusion and oxidative stress. 3. A cerebral ischemia-reperfusion by endoluminal occlusion of right middle cerebral artery (MCA) was performed 4 days after intravenous administration of vinblastine or 12 h after RP-3 anti-rat neutrophils monoclonal antibody (mAb RP-3) injection into the peritoneal cavity, on male Wistar rats with 1-h ischemia then followed by 24-h reperfusion period. Brain infarct volume was measured by histomorphometric analysis and vascular endothelial and smooth muscle reactivity of MCA was analysed using Halpern myograph. 4. Neutropenia induced a neuroprotective effect as demonstrated by a significant decrease of brain infarct size. In parallel to neuroprotection, neutropenia prevented postischemic impairment of endothelium-dependent relaxing response to acetylcholine. In contrast, smooth muscle functional alterations were not prevented by neutropenia. Ischemia-reperfusion-induced myogenic tone impairment remained unchanged in vinblastine and mAb RP-3-treated rats. Postischemic Kir2.x-dependent relaxation impairment was not prevented in neutropenic conditions. The fully relaxation of smooth muscle response to sodium nitroprusside was similar in all groups. 5. Our results evidenced the dissociate prevention of pharmacologically induced neutropenia on postischemic vascular endothelial and smooth muscle impairment. The selective endothelial protection by neutropenia is parallel to a neuroprotective effect suggesting a possible relationship between the two phenomena.
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