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大鼠全身性低氧诱导的呼吸与心血管变化的相互依存关系:腺苷的作用。

Interdependence of respiratory and cardiovascular changes induced by systemic hypoxia in the rat: the roles of adenosine.

作者信息

Thomas T, Marshall J M

机构信息

Department of Physiology, Medical School, Birmingham, UK.

出版信息

J Physiol. 1994 Nov 1;480 ( Pt 3)(Pt 3):627-36. doi: 10.1113/jphysiol.1994.sp020389.

Abstract
  1. In ten spontaneously breathing, Saffan-anaesthetized rats (group I), respiratory and cardiovascular responses evoked by 10 min periods of hypoxia (arterial partial pressure of O2, Pa,O2, 33 mmHg) were recorded before and after the administration of the adenosine receptor antagonist 8-phenyltheophylline (8-PT, 10 mg kg-1 i.v.). Similar experiments were performed on nine constantly ventilated rats (group II; Pa,O2, 29 mmHg) with arterial partial pressure of CO2 (Pa,CO2) held constant. 2. In group I, hypoxia induced an initial increase and a secondary fall in ventilation (VE) with an accompanying secondary fall in heart rate (HR), arterial pressure (ABP) fell and cerebral vascular conductance (CVC) increased progressively. Cerebral blood flow (CBF) tended to fall with time during hypoxia. 8-PT abolished the secondary falls in VE and HR and reduced the fall in ABP and increase in CVC, while CBF was better maintained. 3. In group II, hypoxia induced a similar cardiovascular response to that in group I, but at the 1st minute of hypoxia, the HR was lower and the increase in CVC was greater. 8-PT did not affect the hypoxia-induced changes in HR, ABP, CVC or CBF. 4. These results indicate specific ways in which the ventilatory and cardiovascular responses induced by hypoxia in the spontaneously breathing rat are interdependent. They also indicate that the influences of 8-PT on the cardiovascular changes induced by hypoxia during spontaneous ventilation are mainly a consequence of its ability to block the centrally mediated contribution of adenosine to the secondary fall in ventilation.
摘要
  1. 在十只自主呼吸、用沙芬麻醉的大鼠(第一组)中,在静脉注射腺苷受体拮抗剂8-苯基茶碱(8-PT,10毫克/千克)之前和之后,记录了10分钟缺氧期(动脉血氧分压,Pa,O2,33毫米汞柱)诱发的呼吸和心血管反应。对九只持续通气的大鼠(第二组;Pa,O2,29毫米汞柱)进行了类似实验,同时使动脉血二氧化碳分压(Pa,CO2)保持恒定。2. 在第一组中,缺氧导致通气量(VE)先增加后下降,同时心率(HR)继发性下降,动脉压(ABP)下降,脑血管传导性(CVC)逐渐增加。缺氧期间脑血流量(CBF)随时间有下降趋势。8-PT消除了VE和HR的继发性下降,并减轻了ABP的下降和CVC的增加,同时CBF得到了更好的维持。3. 在第二组中,缺氧诱发的心血管反应与第一组相似,但在缺氧第1分钟时,HR较低,CVC增加幅度更大。8-PT不影响缺氧诱发的HR、ABP、CVC或CBF的变化。4. 这些结果表明了缺氧在自主呼吸大鼠中诱发的通气和心血管反应相互依存的具体方式。它们还表明,8-PT对自主通气期间缺氧诱发的心血管变化的影响主要是由于其能够阻断腺苷对通气继发性下降的中枢介导作用。

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