ORIGINS OF THE EXERCISE REFLEX

运动反射的起源

• 批准号: 3448991
• 负责人: CHARLES L STEBBINS
• 金额: $ 4.8万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 1985
• 资助国家: 美国
• 起止时间: 1985-07-10 至 1988-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3448991
• 关键词: adenosine; blood pressure; bradykinin; carbon dioxide tension; cardiovascular function; chemical stimulation; electrostimulus; exercise; heart contraction; heart rate; high performance liquid chromatography; histamine; lactates; microelectrodes; muscle contraction; oxygen tension; prostaglandin E; radioimmunoassay; reflex; respiratory gas analyzer; scintillation counter; striated muscles; vascular resistance; vasodilation

The objective of this proposed research is to address specific deficiencies in our understanding of the chemical factors within contracting muscle that contribute to the reflex cardiovascular response to exercise. A better understanding of these factors may allow physicians to modify these responses where they may be harmful, for instance in patients with ischemic heart disease. The specific aims and methodologies are: 1) determination of the reflex potential of chemical stimuli released during muscular contraction. This will be accomplished by stimulating the cat's skeletal muscle with intra-arterial injections of each chemical to evoke a cardiovascular response. The reflex nature of the response will be confirmed by denervation of the gracilis. 2) Evaluation of the contribution of those chemical stimuli with reflex potential to the reflex cardiovascular response evoked by static muscular contraction. To evaluate the potential contribution of each chemical, the cardiovascular response to ventral root stimulated static contraction will be attenuated by inhibiting the production or action of the substance pharmacologically or by enhancing its degradation by infusing the appropriate enzyme responsible for catabolism. Alternatively, the degradation of a given chemical will be inhibited pharmacologically to demonstrate an augmented contraction-induced cardiovascular response. 3) Evaluation of the relationship between changes in interstitial PO2, PCO2 and pH to the onset and magnitude of the cardiovascular response to electrically stimulated contraction. To study this effect, skeletal muscle interstitial PO2, PCO2 and pH will be measured with mini-electrodes during contraction and contraction accompanied with ischemia. The time course and magnitude of changes in these variables will be compared to the onset and magnitude of the cardiovascular responses to contraction and contraction with ischemia. The cardiovascular response to pharmacological stimulation and hindlimb contraction will be evaluated by assessing changes in arterial blood pressure, heart rate and contractility. In some animals changes in preload, aortic flow and systemic vascular resistance also will be assessed.

这项拟议的研究的目的是解决特定的缺陷 在我们对收缩肌肉中化学因素的理解中 有助于反射心血管对运动的反应。 更好 了解这些因素可能会使医生可以修改这些因素 例如，缺血患者的反应可能有害 心脏病。 具体目的和方法是：1）确定 在肌肉期间释放的化学刺激的反射潜力 收缩。 这将通过刺激猫的骨骼来实现 动脉内注射每种化学物质的肌肉以唤起A 心血管反应。 响应的反射性将是 通过对gracilis的神经的看法确认。 2）评估 这些具有反射潜力的化学刺激对反射的贡献 静态肌肉收缩引起的心血管反应。 评估 每种化学物质的潜在贡献，心血管对 腹侧根刺激的静态收缩将通过抑制减弱 该物质在药理学上的生产或作用或通过增强 通过注入适当的酶来降解 分解代谢。 或者，给定化学化学物质的降解将是 抑制药理学以证明收缩诱导的 心血管反应。 3）评估变化之间的关系 在间质PO2中，PCO2和pH发作和大小 对电刺激收缩的心血管反应。 学习 将测量此效果，骨骼肌间质PO2，PCO2和pH将测量 收缩期间和收缩期间的迷你电极 缺血。 这些变量的时间过程和变化的幅度将 将其与心血管反应的开始和大小 缺血的收缩和收缩。 对心血管的反应 药理学刺激和后肢收缩将通过 评估动脉血压的变化，心率和 收缩力。 在某些动物中，预紧力，主动脉流动和 还将评估全身性血管抗性。