Tucker A, Grover R F, Reeves J T
Am J Vet Res. 1984 Jan;45(1):104-8.
Cardiovascular responses to various degrees of acute isocapnic hypoxia were determined in spontaneously breathing anesthetized dogs. Cardiac output (CO), heart rate, stroke volume, systemic blood pressure, and systemic vascular resistance were measured at frequent intervals during 20-minute exposures to hypoxia (7% to 17% O2). Cardiac output increased during hypoxia, with the most severe degree of hypoxia producing the greatest increase in CO. Stroke volume increased significantly (P less than 0.05), whereas tachycardia was inconsistent. Systemic vascular resistance declined with hypoxia, with the greatest vasodilation observed with the most severe hypoxia. During the first 3 minutes of hypoxia, CO increased at all 3 degrees of hypoxia, whereas systemic vascular resistance remained relatively unchanged during this initial portion of the hypoxic exposures. Prevention of the hypoxia-induced increase in CO by partial caudal vena caval obstruction (reducing venous return) resulted in a maintenance of systemic vascular resistance at or above the base-line value before hypoxia. Seemingly, hypoxia can increase CO before systemic vasodilation is evident and systemic vasodilation depends, partly, on the increase in CO.
在自主呼吸的麻醉犬中测定了对不同程度急性等碳酸血症性缺氧的心血管反应。在20分钟的缺氧暴露（7%至17%氧气）期间，频繁测量心输出量（CO）、心率、每搏量、体循环血压和体循环血管阻力。缺氧期间心输出量增加，缺氧程度最严重时CO增加幅度最大。每搏量显著增加（P<0.05），而心动过速则不一致。缺氧时体循环血管阻力下降，缺氧最严重时观察到最大程度的血管舒张。在缺氧的最初3分钟内，所有3种缺氧程度下心输出量均增加，而在缺氧暴露的这一初始阶段，体循环血管阻力相对保持不变。通过部分尾腔静脉阻塞（减少静脉回流）预防缺氧诱导的心输出量增加，可使体循环血管阻力维持在缺氧前基线值或以上。似乎，在体循环血管舒张明显之前，缺氧可增加心输出量，且体循环血管舒张部分取决于心输出量的增加。
