PATHOPHYSIOLOGIC STUDIES OF Ill GULF WAR VETERANS & CONTROLS

生病的海湾战争退伍军人的病理生理学研究

• 批准号: 6265024
• 负责人: ROBERT W HALEY
• 金额: $ 3.48万
• 依托单位: UT SOUTHWESTERN MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-12-01 至 1999-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6265024
• 关键词: brain injury; brain stem; clinical research; cortisol; disease /disorder etiology; environmental toxicology; human subject; interleukin 6; microglia; neurogenic hypertension; neurotoxins; norepinephrine; organophosphorus insecticide; pathologic process; sign /symptom; sleep apnea; sympathetic nervous system; syndrome; veterans; war /peace

The hypotheses to be tested are as follows: The Gulf War syndrome is due to exposure to combinations of organophosphates in the war that caused brainstem injury. Malfunction of the brainstem regulatory processes are causing central sleep apnea, which is producing sympathetic nerve hyperactivity through peripheral or central chemoreflex sensitization, resulting in a form of neurogenic hypertension. Alternatively, it is possible that injured microglia in the area of brainstem injury are overproducing interleukin-6, which in turn is stimulating overproduction of cortisol, norepinephrine and sympathetic nervous system activity, as has recently been found in patients after CVA's. Pharmacologically interrupting the metabolic consequences of the brainstem dysfunction may provide substantial relief from many of the symptoms of Gulf War syndrome.

需要检验的假设如下：海湾战争综合症是由于在战争中接触到有机磷化合物而导致脑干损伤。脑干调节过程的故障导致中枢性睡眠呼吸暂停，后者通过外周或中枢性化学反射敏化产生交感神经过度活动，导致一种形式的神经源性高血压。另一种可能是，脑干损伤区域受损的小胶质细胞过度产生白介素6，进而刺激皮质醇、去甲肾上腺素和交感神经系统活动的过度产生，就像最近在CVA患者中发现的那样。从药物上阻断脑干功能障碍的代谢后果可能会大大缓解海湾战争综合征的许多症状。