加压素引起麻醉犬心输出量显著下降的机制研究

THE RESPONSIBLE MECHANISM OF AVP FOR CARDIAC OUTPUT DECREASE IN ANAESTHETIZED DOGS

研究加压素引起麻醉犬ＣＯ显著下降的机制。应用传导（容量）导管技术测定左心室容量和收缩末期压力容量关系及相关的左室收缩功能指标（Ｅｅｓ），并通过心房起博固定心率，以消除心率影响，比较ＡＶＰ和ＡⅡ在自主神经反射完整和阻断组犬中引起的血流动力学改变。数据经ｔ检验。结果：在自主神经反射完整犬，当ＡＶＰ和ＡⅡ引起相似水平的平均血管阻力增加（５０％）时，ＡＶＰ显著减少ＣＯ，减少值为（２９．６２±９．０８）％；轻度增加平均动脉血压（ＭＢＰ）和左室舒张末期容量（ＥＤＶ），增加值分别为（５．５３±４．７４）％和（１１．１１±３．７５）％。ＡⅡ显著增加ＭＢＰ和ＥＤＶ，增加值分别为（２２．２４±４．４２）％和（３０．９１±１４．０８）％；轻度减少ＣＯ，减少值为（１８．７５±１２．７１）％。在自主神经反射阻断犬，这种反应的不一致性完全消失。在上述两种实验状态下，ＡＶＰ和ＡⅡ均未引起Ｅｅｓ显著改变。结论：ＡＶＰ导致ＣＯ显著下降是由于它引起较大的静脉充盈，以致舒张末期的ＣＯ增加比ＡⅡ较少。此作用是通过自主神经反射调节。

PURPOSE Previous studies have shown that for equipressor doses of Arginine vasopressin(AVP) and angiotesion Ⅱ(AⅡ),AVP decreased cardiac output(CO) almost twice as much as A Ⅱ,In this work,the possible responsible mechanism of AVP for CO decrease in dogs were investigated.METHODS By using conductance catheter technique to measure left ventricular pres sure- volume relations,CO was measured by thermodilution.Heart rate was constant by fixed rate atrial pacing.Hemodynamic effects of AVP and A Ⅱ were studied in intact and arefiexic dogs.Data were analyzed by t test.RESULTS When mean arterial resistance(R=MBP/CO) rose by about 50% with AVP and A Ⅱ,CO fell more and Mean Blood Pressure(MBP),End-Diastolic Volume(EDV)increased less with AVP than A Ⅱ.the decreases of CO were(29.62±9.08)% for AVP and(18.75±12.71)%for A Ⅱ respectively.However,the increases of MBP,EDV were(5.53±4.74)%,(11.11±3.75)%for AVP and(22.24±4.42)%,30.91±14.08)% for A Ⅱ respectively.Ganglionic blockade eliminated the disparaties mostly via a greater rise in EDV with AVP,LV contractility,indexed by the end- systolic elastance(Ees) was not siglificantly altered.CONCLUSIONS Under our experimental conditions,the AVP-induced obvious decrease of CO responded to equipressor dose of AVP and A Ⅱ is due to greater venous pooling with AVP,an effect modulated by autonomic refiex.