Vascular Regulatory Mechanisms of Palmitic Acid Methyl Ester

棕榈酸甲酯的血管调节机制

基本信息

批准号：
9912874
负责人：
Hung Wen (Kevin) Lin
金额：
$ 31.72万
依托单位：
LOUISIANA STATE UNIV HSC SHREVEPORT
依托单位国家：
美国
项目类别：
财政年份：
2017
资助国家：
美国
起止时间：
2017-07-15 至 2022-04-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9912874
关键词：
Acute Affect Aftercare Arginine Arteries Biological Blood Blood Vessels Brain Brain Injuries Cardiopulmonary Arrest Cause of Death Cell Nucleus Cerebral Ischemia Cerebrovascular Circulation Cerebrum Circle of Willis Cognition Cognitive Cytoplasm Disease Electric Countershock Electric Stimulation Emergency response Emergency treatment Endothelium Enzyme-Linked Immunosorbent Assay Esters Foundations Goals Heart Arrest Hippocampus (Brain)Home environment Homeostasis Hyperemia Intervention Ischemia Knockout Mice Laser Scanning Microscopy Laser-Doppler Flowmetry Lead Life Style Mass Fragmentography Measures Mediating Medical emergency Memory Metabolism Methylation Modeling N,N-dimethylarginine Nature Neurologic Deficit Neurons Neuroprotective Agents Nitric Oxide Donors Nitric Oxide Synthetase Inhibitor Oryctolagus cuniculus Outcome Palmitic Acids Patients Post-Translational Protein Processing Process Protein Inhibition Protein-Arginine N-Methyltransferase Rattus Reaction Recovery of Function Regulation Renal function Resuscitation Reverse Transcription Role Structure of superior cervical ganglion Survival Rate Sympathetic Nervous System Systemic blood pressure Techniques Thoracic aorta Time Vasodilation Vasodilator Agents behavioral outcome brain circulation cerebral artery cerebral microvasculature direct application disability electric field heart function hypoperfusion improved outcome innovation insight methyl group mouse model neuron loss neuroprotection novel platinum electrode two-photon

项目摘要

Project Summary Cardiopulmonary arrest (CA) is a major cause of death and disability in the US. CA affects up to 325,000 people each year with only a 10% survival rate. The whole-body ischemia following CA results in subsequent brain damage resulting in neurological deficits. Our long-term goal is to decrease brain damage by reviving cerebral blood flow and subsequent neurological deficits associated with CA. Therefore, it is important to understand the mechanism(s) underlying CA-induced brain injury. The importance of identifying regulatory factors that influence cerebral blood flow autoregulation and innovative neuroprotective agents in the context of CA is paramount to change the outcomes following CA and it is the main goal of this proposal. We propose to study a new vasotone regulatory mechanism, the release of palmitic acid methyl ester (a vasodilator and neuroprotectant) derived from the superior cervical ganglion innervating major cerebral arteries. Our central hypothesis is that protein arginine methyltransferases are the regulatory “switch” for the methylation of palmitic acid to form palmitic acid methyl ester responsible for vasodilation/neuroprotection during ischemia.

项目摘要心肺逮捕（CA）是美国死亡和残疾的主要原因。 CA最多影响325,000 每年只有10％的存活率的人。 CA之后的全身缺血导致随后脑损伤导致神经系统缺陷。我们的长期目标是通过复兴来减少大脑损伤脑血流和随后与大约相关的神经系统缺陷。因此，重要的是了解CA诱导的脑损伤的基本机制。确定监管的重要性影响脑血流自动调节和创新神经保护剂的因素 CA对于改变CA的结果至关重要，这是该提案的主要目标。我们建议研究一种新的血管酮调节机制，棕榈酸甲酯的释放（血管扩张剂和神经保护剂）源自宫颈上神经节的主要大脑动脉。我们的中心假设是蛋白精氨酸甲基转移酶是调节性的“转换” 棕榈酸形成棕榈酸甲酯，负责缺血期间血管舒张/神经保护作用。