Tucker C E, James W E, Berry M A, Johnstone C J, Grover R F
J Appl Physiol. 1976 Sep;41(3):356-61. doi: 10.1152/jappl.1976.41.3.356.
To determine if depressed myocardial function contributes to the reported decrease in cardiac performance at high altitude, six chronically instrumented, unsedated goats were studied before, during, and after 2-wk exposure to hypobaric hypoxia (PaO2 44 mmHg). Undistorted ventricular pressure wave form was obtained from a miniature transducer implanted in the left ventricular cavity. The relationship between (dP/dt)/28P and P was extrapolated to obtain Vmax as an index of myocardial function. With beta sympathetic blockade (practolol) and pacing to reproduce heart rates, Vmax was uniformly and significantly depressed (P less than 0.01) during chronic hypoxia, and returned to control values following descent to low altitude. Likewise, stroke volume following saline infusion was decreased at high altitude and returned to control values following descent. Acute relief of hypoxia at high altitude by administration of 100% oxygen by mask did not reverse the depressed Vmax. These findings indicate that chronic hypobaric hypoxia produces a depression of myocardial function which is reversible by chronic but not acute relief of hypoxia.
为了确定心肌功能减退是否导致了所报道的高海拔地区心脏功能下降，对6只长期植入仪器且未使用镇静剂的山羊在暴露于低压缺氧环境（动脉血氧分压44 mmHg）2周之前、期间及之后进行了研究。通过植入左心室腔的微型传感器获得未失真的心室压力波形。将(dP/dt)/28P与P之间的关系进行外推，以获得Vmax作为心肌功能指标。在使用β-交感神经阻滞剂（心得宁）并通过起搏使心率恢复后，慢性缺氧期间Vmax持续且显著降低（P<0.01），降至低海拔后恢复至对照值。同样，输注生理盐水后的每搏输出量在高海拔时降低，降至低海拔后恢复至对照值。在高海拔通过面罩给予100%氧气急性缓解缺氧并未逆转降低的Vmax。这些发现表明，慢性低压缺氧会导致心肌功能减退，这种减退可通过慢性但非急性缓解缺氧来逆转。
