ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2009
Endothelin rather than 20-HETE contributes to loss of pial arteriolar dilation during focal cerebral ischemia with and without polymeric hemoglobin transfusion.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Sex-dependent role of 20-HETE synthesis in outcome from ischemic stroke in rats.Physiological reports · 2026Article
- The contribution of TRPV1 channel to 20-HETE-Aggravated ischemic neuronal injury.Prostaglandins & other lipid mediators · 2018Review
- P450 Eicosanoids and Reactive Oxygen Species Interplay in Brain Injury and Neuroprotection.Antioxidants & redox signaling · 2018Article
- Upregulation of 20-HETE Synthetic Cytochrome P450 Isoforms by Oxygen-Glucose Deprivation in Cortical Neurons.Cellular and molecular neurobiology · 2017Article
- Transfusion of Polynitroxylated Pegylated Hemoglobin Stabilizes Pial Arterial Dilation and Decreases Infarct Volume After Transient Middle Cerebral Artery Occlusion.Journal of the American Heart Association · 2017Article
- Cyclooxygenase- and cytochrome P450-derived eicosanoids in stroke.Prostaglandins & other lipid mediators · 2016Review
- Additive Neuroprotection of a 20-HETE Inhibitor with Delayed Therapeutic Hypothermia after Hypoxia-Ischemia in Neonatal Piglets.Developmental neuroscience · 2015Article
- Transfusion of hemoglobin-based oxygen carriers in the carboxy state is beneficial during transient focal cerebral ischemia.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor.Journal of neurochemistry · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Partial exchange transfusion with a cell-free hemoglobin (Hb) polymer during transient middle cerebral artery occlusion (MCAO) reduces infarct volume but fails to increase blood flow, as might be expected with the induced decrease in hematocrit. In ischemic brain, endothelin antagonists are known to produce vasodilation. In nonischemic brain, pial arterioles constrict after Hb exchange transfusion, and the constriction is blocked by an inhibitor of 20-HETE synthesis. We tested the hypothesis that a 20-HETE synthesis inhibitor and an endothelin A receptor antagonist increase pial arteriolar dilation after Hb exchange transfusion during MCAO. Pial arteriolar diameter was measured in the ischemic border region of the distal MCA border region through closed cranial windows in anesthetized rats subjected to the filament model of MCAO. During 2 h of MCAO, pial arteriolar dilation gradually subsided from 37 +/- 3 to 7 +/- 5% (+/-SE). Compared with residual dilation at 2 h of MCAO with vehicle superfusion (14 +/- 3%), loss of dilation was not prevented by superfusion of a 20-HETE synthesis inhibitor (21 +/- 5%), partial Hb exchange transfusion (7 +/- 5%) that decreased hematocrit to 23%, or a combination of the two (5 +/- 5%). However, loss of dilation was prevented by superfusion of an endothelin A receptor antagonist with (35 +/- 4%) or without (32 +/- 5%) Hb transfusion. Pial artery constriction during reperfusion was attenuated by HET0016 alone and by BQ610 with or without Hb transfusion. Systemic administration of the endothelin antagonist during prolonged MCAO increased blood flow in the border region. Thus loss of pial arteriolar dilation in the ischemic border region during prolonged MCAO depends on endothelin A receptor activation, and this effect was independent of the presence of cell-free Hb polymers in the plasma. In contrast to previous work in nonischemic brain, inhibition of oxygen-dependent 20-HETE synthesis does not significantly influence the pial arteriolar response to polymeric Hb exchange transfusion during focal ischemia.
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