Malpartida F, Muguerza I, Caro D M
Arch Inst Cardiol Mex. 1975 Sep-Oct;45(5):523-36.
An experimental study of the production of cardiogenic shock together with the results of its treatment by means of the intraaortic balloon was carried out. Cardiogenic shock was produced in dogs with closed thorax and spontaneous respiration. In 13 of the 21 dogs studied, the production of acute myocardial infarction by means of selective embolism of the left circumflex artery permitted the reproduction of a model of cardiogenic shock. Embolism was produced by injecting metalic mercury through a double catheter. Six of the 8 remaining dogs died due to accidental introduction of mercury in the anterior descending coronary artery which produced irreversible ventricular fibrillation. The other 2 died due to rupture of the ascending aorta during the maneuveres to place the coronarygraphy catheter. The 13 dogs with cardiogenic shock were treated with intraaortic balloon pumping during 3-4 hours. The left ventricular systolic pressure fell from 128 +/- 12.07 to 124 +/- 4.65 mm. Hg. The cardiac index increased by 42%. These findings confirm the fact that intraaortic balloon pumping lessens the after load. The fall of the telediastolic pressure by 20% was an index of the lessening or the preload. The aortic telediastolic pressure rose by a mean value of 32.21 mm. Hg. This raises the coronary perfusion pressure thus limiting the extension or reducing the size of the infarction. A frank reduction of the electrographic subepicardiac lesion was observed after using intraaortic balloon pumping. The mean aortic pressure only rose by 8%, the central venous pressure remained unchanged and the increase in diuresis was not estimable. The maximum dP/dt was unaltered and the Vmax. rose 17%. Two dogs were left alive after the experiment and lived for 3 and 12 days respectively. To conclude the results obtained permit us to indicate that intraaortic balloon pumping when used in dogs with this standard type of cardiogenic shock produces an important reduction of the after load, a discrete reduction of the preload and a significative increase in coronary blood flow. There were no changes in cardiac frequency and although the results of myocardial contractility were not definite, they seem to indicate a moderate improvement.
进行了一项关于心源性休克的产生及其通过主动脉内球囊治疗结果的实验研究。心源性休克是在开胸并自主呼吸的狗身上诱发的。在研究的21只狗中,有13只通过左旋支动脉选择性栓塞产生急性心肌梗死,从而复制了心源性休克模型。栓塞是通过双导管注入金属汞产生的。其余8只狗中有6只因意外将汞注入前降支冠状动脉导致不可逆的心室颤动而死亡。另外2只因放置冠状动脉造影导管操作过程中升主动脉破裂而死亡。对13只心源性休克的狗进行了3至4小时的主动脉内球囊反搏治疗。左心室收缩压从128±12.07降至124±4.65毫米汞柱。心脏指数增加了42%。这些发现证实了主动脉内球囊反搏可减轻后负荷这一事实。舒张末期压力下降20%是前负荷减轻的指标。主动脉舒张末期压力平均升高32.21毫米汞柱。这提高了冠状动脉灌注压力,从而限制梗死范围的扩大或减小梗死面积。使用主动脉内球囊反搏后,心外膜下电图显示的病变明显减轻。平均主动脉压仅升高8%,中心静脉压保持不变,尿量增加情况无法评估。最大dp/dt未改变,Vmax升高17%。实验后有2只狗存活,分别存活了3天和12天。总之,所得结果表明,在患有这种标准类型心源性休克的狗中使用主动脉内球囊反搏可显著降低后负荷,轻微降低前负荷,并显著增加冠状动脉血流量。心率没有变化,虽然心肌收缩力的结果不明确,但似乎表明有适度改善。