ORIGINS OF THE EXERCISE REFLEX

这项拟议的研究的目标是解决具体的缺陷。 在我们对收缩肌肉中的化学因素的理解中， 有助于运动对心血管的反射反应。更好的 对这些因素的了解可能会让医生修改这些因素 可能有害的反应，例如在缺血性心脏病患者中 心脏病。具体的目标和方法是：1)确定 肌肉过程中释放的化学刺激的反射电位 收缩。这将通过刺激猫的骨骼来实现 肌肉内动脉注射每种化学物质以唤起 心血管反应。反应的条件反射性质将是 确认为股薄肌的失神经。2)评估 具有反射潜力的化学刺激对反射的贡献 由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，心血管反应 腹根刺激的静态收缩将通过抑制减弱 药理作用物质的产生或作用或通过增强 通过注入适当的酶来降解它 分解代谢。或者，给定化学物质的降解将是 在药物上被抑制以显示增强的收缩诱导 心血管反应。3)变化之间关系的评估 在间质中的PO2、PCO2和pH对脑出血的发病和程度的影响 心血管对电刺激收缩的反应。学习 这种影响，骨骼肌间质的氧分压、二氧化碳分压和pH值将被测量 在收缩过程中带有微型电极，并伴随着 缺血症。这些变量的时间进程和变化幅度将 与心血管反应的发生和程度进行比较 收缩和伴有缺血的收缩。心血管反应 药理刺激和后肢收缩将通过 评估动脉血压、心率和 伸缩性。在一些动物中，前负荷、主动脉血流和 还将评估全身血管阻力。

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.