PTL treatment could effectively down-regulate α receptor activity and block its downstream signaling pathway, and relieve pulmonary artery spasm, especially in the non-embolization area, pulmonary blood flow recovery in the non-embolization area could then effectively break the pathophysiological vicious cycle of APE combined with shock, and reverse pulmonary and systemic circulatory failure in this rabbit model of APE combined with shock. The gene discussed is PNLIP; the disease is apparent mineralocorticoid excess.