ORIGINS OF THE EXERCISE REFLEX

运动反射的起源

• 批准号: 3448994
• 负责人: CHARLES L STEBBINS
• 金额: $ 5.22万
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 财政年份: 1987
• 资助国家: 美国
• 起止时间: 1987-07-01 至 1989-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3448994
• 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.

这项拟议研究的目的是解决具体的不足之处 我们对肌肉收缩中的化学因素的理解， 有助于心血管对运动的反射反应。 更好的 对这些因素的理解可以使医生修改这些 可能有害的反应，例如缺血性心脏病患者 心脏病 具体目标和方法是：1）确定 化学刺激释放的反射电位 收缩。 这将通过刺激猫的骨骼来实现 肌肉与动脉内注射每种化学物质，以唤起 心血管反应 反应的反射性质将是 证实了股薄肌的神经切断 2)评价 具有反射电位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。 评价 每种化学物质的潜在作用， 前根刺激的静态收缩将通过抑制 物质的产生或作用，或通过增强 它的降解通过注入适当的酶负责 猫 或者，给定化学品的降解将是 抑制收缩，以显示增强的收缩诱导 心血管反应 3)评价变更之间的关系 在间隙PO2，PCO2和pH值的开始和大小， 心血管对电刺激收缩的反应。 研究 将测量这种效应、骨骼肌间质PO2、PCO2和pH 在收缩和伴随收缩的收缩期间使用微型电极 缺血 这些变量的时间进程和变化幅度将 与心血管反应的发作和幅度进行比较， 收缩和缺血性收缩。 心血管反应 药理学刺激和后肢收缩将通过 评估动脉血压、心率和 收缩性 在一些动物中，前负荷、主动脉流量和 还将评估全身血管阻力。