ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2014
Protein kinase C delta modulates endothelial nitric oxide synthase after cardiac arrest.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2014. 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, 15 citations in OpenAlex.
- A Narrative Review of Drug Therapy in Adult and Pediatric Cardiac Arrest.Reviews in cardiovascular medicine · 2023Review
- Activation of Neuropeptide Y2 Receptor Can Inhibit Global Cerebral Ischemia-Induced Brain Injury.Neuromolecular medicine · 2022Article
- 20-HETE-promoted cerebral blood flow autoregulation is associated with enhanced pericyte contractility.Prostaglandins & other lipid mediators · 2021Article
- Reduced Apoptotic Injury by Phenothiazine in Ischemic Stroke through the NOX-Akt/PKC Pathway.Brain sciences · 2019Article
- Palmitic acid methyl ester is a novel neuroprotective agent against cardiac arrest.Prostaglandins, leukotrienes, and essential fatty acids · 2019Article
- Neurocardiology: Cardiovascular Changes and Specific Brain Region Infarcts.BioMed research international · 2017Review
- Acetylcholinesterase conformational states influence nitric oxide mobilization in the erythrocyte.The Journal of membrane biology · 2015Article
- Effect of cardiac arrest on cognitive impairment and hippocampal plasticity in middle-aged rats.PloS one · 2015Article
- Global and regional differences in cerebral blood flow after asphyxial versus ventricular fibrillation cardiac arrest in rats using ASL-MRI.Resuscitation · 2014Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We previously showed that inhibition of protein kinase C delta (PKCδ) improves brain perfusion 24 hours after asphyxial cardiac arrest (ACA) and confers neuroprotection in the cortex and CA1 region of the hippocampus 7 days after arrest. Therefore, in this study, we investigate the mechanism of action of PKCδ-mediated hypoperfusion after ACA in the rat by using the two-photon laser scanning microscopy (TPLSM) to observe cortical cerebral blood flow (CBF) and laser Doppler flowmetry (LDF) detecting regional CBF in the presence/absence of δV1-1 (specific PKCδ inhibitor), nitric oxide synthase (NOS) substrate (L-arginine, L-arg) and inhibitor (N(ω)-Nitro-L-arginine, NLA), and nitric oxide (NO) donor (sodium nitroprusside, SNP). There was an increase in regional LDF and local (TPLSM) CBF in the presence of δV1-1+L-arg, but only an increase in regional CBF under δV1-1+SNP treatments. Systemic blood nitrite levels were measured 15 minutes and 24 hours after ACA. Nitrite levels were enhanced by pretreatment with δV1-1 30 minutes before ACA possibly attributable to enhanced endothelial NOS protein levels. Our results suggest that PKCδ can modulate NO machinery in cerebral vasculature. Protein kinase C delta can depress endothelial NOS blunting CBF resulting in hypoperfusion, but can be reversed with δV1-1 improving brain perfusion, thus providing subsequent neuroprotection after ACA.
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