Müller-Strahl Gerhard, Hemker Jan, Zimmer Heinz-Gerd
Institut für Geschichte der Medizin, Ruhr-Universität Bochum, Germany; and.
Exp Clin Cardiol. 2002 Winter;7(4):180-7.
The afterload- (AL) and preload- (PL) dependent interactions between the left and right ventricle (LV, RV, respectively) of an isolated biventricular ejecting rat heart were measured in terms of left (L) and right (R) intraventricular peak pressure (LP(max) and RP(max), respectively) and aortic and pulmonary flow (AF, PF, respectively).
Starting with standardized loading conditions, LVPL was varied in six steps for each of five distinct LVALs (n=28) and then RVPL was varied in seven steps for each of five distinct RVALs (n=37). Thus, the entire range of loading conditions was covered.
Identification of AL-dependent systolic interactions revealed an important DeltaLP(max)-DeltaRP(max) gain of 0.25 (r(2)=0.78) and a still more dominant DeltaRP(max)-DeltaPF gain of 0.45 (r(2)=0.84). At least 26% of maximal PF were attributable to LV systolic function. In contrast, R-L systolic interaction impeded PF; there was no global crosstalk pressure gain and no ipsilateral pressure-flow gain. Reduction of RV activity augmented AF by at least 15%. PL-dependent L-R interactions were absent except for minimal LVAL. In contrast, the reverse interaction reflected an inverse correlation between RVPL and AF, which is coincidential with other studies (-11% AF for a doubling of the standard RVPL). For the minimal RVAL, there was a biphasic response of AF to RVPL. Unloading the maximally loaded RV revealed an overall inhibition of AF by 37% for the standardized LV. Unloading the standardized RV revealed a basal inhibition of AF by 6% for the standardized LV and a 4.5% augmentation for the highly loaded LV. Consequently, basal contribution of RV to LV performance depended on the conditions of LV loading.
The authors suggest a unidirectional transseptal R-L mechanism for diastolic interactions, and transseptal L-R and paraseptal R-L mechanisms for systolic interactions.
以左、右心室内峰值压力(分别为左心室峰值压力LP(max)和右心室峰值压力RP(max))以及主动脉和肺动脉血流(分别为AF和PF)为指标,测量离体双心室射血大鼠心脏左、右心室(分别为LV和RV)之间后负荷(AL)和前负荷(PL)依赖性相互作用。
从标准化负荷条件开始,对五个不同的左心室后负荷水平(LVALs,n = 28)中的每一个,将左心室前负荷(LVPL)分六个步骤进行变化,然后对五个不同的右心室后负荷水平(RVALs,n = 37)中的每一个,将右心室前负荷(RVPL)分七个步骤进行变化。从而涵盖了整个负荷条件范围。
对AL依赖性收缩期相互作用的识别显示,重要的ΔLP(max)-ΔRP(max)增益为0.25(r(2)=0.78),更显著的ΔRP(max)-ΔPF增益为0.45(r(2)=0.84)。至少26%的最大PF归因于左心室收缩功能。相反,右向左收缩期相互作用阻碍了PF;不存在整体串扰压力增益和同侧压力-血流增益。右心室活动的降低使主动脉血流增加至少15%。除了最小的左心室后负荷水平外,不存在PL依赖性的左-右相互作用。相反,反向相互作用反映了右心室前负荷(RVPL)与主动脉血流(AF)之间的负相关,这与其他研究一致(标准RVPL加倍时AF降低11%)。对于最小的右心室后负荷水平,主动脉血流(AF)对右心室前负荷(RVPL)有双相反应。对最大负荷的右心室进行卸载,对于标准化左心室,主动脉血流(AF)总体上受到37%的抑制。对标准化右心室进行卸载,对于标准化左心室,主动脉血流(AF)基础上受到6%的抑制,而对于高负荷左心室则增加4.5%。因此,右心室对左心室性能的基础贡献取决于左心室负荷条件。
作者提出舒张期相互作用存在单向经间隔右-左机制,收缩期相互作用存在经间隔左-右和旁间隔右-左机制。