O'Connor L R, Wheeler W S, Bethune J E
N Engl J Med. 1977 Oct 27;297(17):901-3. doi: 10.1056/NEJM197710272971702.
Severe hypophosphatemia is associated in man with low intracellular stores of ATP and a set of specific cellular dysfunctions. To investigate whether hypophosphatemia affects myocardial performance, we measured cardiac output by thermodilution and calculated stroke work in seven patients with severe hypophosphatemia before, during and after repletion with an intravenous potassium phosphate solution. Mean left ventricular stroke work for these patients increased from 49.57 to 71.71 g-m per beat (P less than 0.01) at the same or higher afterload whereas pulmonary-artery wedge pressure fell from a mean value of 10.1 to 6.7 torr (P less than 0.02). Return of serum phosphate to normal, therefore, improved myocardial stroke work independently of the Starling effect. The mechanism of this improvement in contractile force is unknown but may be related to intracellular availability of ATP.
严重低磷血症在人类中与细胞内ATP储备不足以及一系列特定的细胞功能障碍相关。为了研究低磷血症是否影响心肌功能,我们对7例严重低磷血症患者在静脉输注磷酸钾溶液补充磷之前、期间和之后,通过热稀释法测量心输出量并计算每搏功。这些患者的平均左心室每搏功在相同或更高后负荷情况下从每搏49.57克 - 米增加到71.71克 - 米(P小于0.01),而肺动脉楔压从平均值10.1托降至6.7托(P小于0.02)。因此,血清磷酸盐恢复正常独立于Starling效应改善了心肌每搏功。收缩力改善的机制尚不清楚,但可能与细胞内ATP的可利用性有关。