Yamashita H, Onodera S, Imamoto T, Obara A, Tanazawa S, Takashio T, Morimoto H, Inoue H
First Department of Internal Medicine, Asahikawa Medical College, Japan.
Jpn Circ J. 1989 Oct;53(10):1237-44. doi: 10.1253/jcj.53.1237.
To clarify the effects of right ventricular (RV) pressure overload on functional and geometrical interference and interdependency between the right and left ventricle, both ventricular internal diameters were measured by the microcrystal technique during lycopodium induced pulmonary embolization in the dog. By repeated embolization, RV systolic pressure was increased progressively until it reached a peak value of about 60-70 mmHg, then it began to fall. At the same time, the hemodynamics deteriorated progressively resulting in death. During the experiment, gradual leftward displacement of the interventricular septum (IVS) without any change in left ventricular (LV) free wall geometry was observed. In pulmonary embolic shock, which showed a fall in LV pressure to about 60 mmHg and cardiac output to about 40% of control, the leftward displacement of IVS became marked, and the cooperative movement of IVS to LV contraction disappeared. The IVS position during acute RV pressure overload was able to account for the transseptal pressure gradient. The importance of IVS position and motion in cardiac function during acute RV pressure overload was stressed. Furthermore, to establish the theoretical treatment in acute cardiopulmonary resuscitation, ligation of the descending aorta (AoL) or norepinephrine ("N") or isoproterenol ("I") administration were examined in a canine pulmonary embolic shock model. AoL or "N" improved the deteriorated hemodynamics with restoration of biventricular geometry. However, "I" did not restore the biventricular geometry despite the transiently improved hemodynamics, and the experimental animals were unable to survive. These results suggest the importance of the maintainance of systemic pressure for the restoration of failed RV function. Further integrated studies are required to understand biventricular interference and interdependency.
为阐明右心室(RV)压力过载对左右心室功能及几何形状的干扰和相互依存关系,在犬类因石松子诱导的肺栓塞过程中,采用微晶技术测量了两个心室的内径。通过反复栓塞,右心室收缩压逐渐升高,直至达到约60 - 70 mmHg的峰值,随后开始下降。与此同时,血流动力学逐渐恶化,最终导致死亡。实验过程中,观察到室间隔(IVS)逐渐向左移位,而左心室(LV)游离壁几何形状无任何变化。在肺栓塞性休克中,左心室压力降至约60 mmHg,心输出量降至对照组的约40%,此时室间隔的向左移位变得明显,室间隔与左心室收缩的协同运动消失。急性右心室压力过载时室间隔的位置能够解释跨间隔压力梯度。强调了急性右心室压力过载时室间隔位置和运动在心脏功能中的重要性。此外,为确立急性心肺复苏的理论治疗方法,在犬类肺栓塞性休克模型中研究了降主动脉结扎(AoL)或给予去甲肾上腺素(“N”)或异丙肾上腺素(“I”)的效果。AoL或“N”改善了恶化的血流动力学,恢复了双心室几何形状。然而,“I”尽管暂时改善了血流动力学,但并未恢复双心室几何形状,实验动物无法存活。这些结果表明维持体循环压力对恢复衰竭的右心室功能的重要性。需要进一步进行综合研究以了解双心室的干扰和相互依存关系。