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目的：探讨支气管肺炎合并心力衰竭（心衰）发病机制和地高辛的治疗机制。方法：对１７例正常对照小儿（Ａ组）、１７例肺炎患儿（Ｂ组）和１３例肺炎合并心衰患儿（Ｃ组）应用超声心动图检查，测定左室收缩末室壁应力、射血分数（ＥＦ）、缩短分数（ＦＳ）和心率矫正之左室周径平均缩短速度（ｍＶｃｆｃ），测定血管紧张素Ⅱ（ＡｎｇⅡ）和红细胞内游离钙水平。结果：Ｃ组左室收缩末室壁应力ＡｎｇⅡ较Ｂ组和Ａ组增加；Ｃ组和Ｂ组红细胞内游离钙较Ａ组增加，３组ＥＦ、ＦＳ和ｍＶｃｆｃ差异无显著性。Ｃ组应用地高辛治疗后左室收缩末室壁应力下降，ＡｎｇⅡ下降，红细胞内游离钙增加，ＥＦ、ＦＳ和ｍＶｃｆｃ无明显改变。结论：支气管肺炎合并心衰并无心肌收缩力下降；ＡｎｇⅡ增加和心脏后负荷增加在发病中起到重要作用。地高辛的治疗机制不是通过增加细胞内游离钙而增加心肌收缩力，而可能是对ＡｎｇⅡ的抑制及由此导致心脏后负荷下降
Objective: To investigate the pathogenesis of bronchial pneumonia complicated with heart failure (CHF) and the therapeutic mechanism of digoxin. Methods: Echocardiography was used in 17 children with normal control (group A), 17 children with pneumonia (group B) and 13 children with pneumonia complicated with heart failure (group C). The left ventricular end-systolic wall stress, (EF), fractional shortening (FS) and heart rate corrected left ventricular diameter average shortening velocity (mVcfc) were measured. Angiotensin Ⅱ (AngⅡ) and intracellular free calcium levels were measured. Results: Compared with group B and group A, the Ang Ⅱ of left ventricular end-systolic wall increased in group C and that of group C and B increased more than that of group A, while there was no significant difference in EF, FS and mVcfc in group C. After treatment with digoxin, the stress in left ventricular end-systolic wall decreased, AngⅡ decreased, intracellular free calcium increased, while EF, FS and mVcfc did not change in group C after digoxin treatment. CONCLUSION: There is no decrease of myocardial contractility in patients with bronchopneumonia complicated with heart failure. Increased Ang Ⅱ and post-cardiac load play an important role in the pathogenesis. The mechanism of action of digoxin is not to increase myocardial contractility by increasing intracellular free calcium, but may be the inhibition of Ang ¢ ò and the consequent decrease of post-cardiac load