Miyamoto M, McClure D E, Schertel E R, Andrews P J, Jones G A, Pratt J W, Ross P, Myerowitz P D
Department of Surgery, Ohio State University, Columbus 43210, USA.
Am J Physiol. 1998 Mar;274(3):H937-44. doi: 10.1152/ajpheart.1998.274.3.H937.
In previous studies, we observed left ventricular (LV) systolic and diastolic dysfunction in association with interstitial myocardial edema (IME) induced by either coronary venous hypertension (CVH) or lymphatic obstruction. In the present study, we examined the effects of myocardial edema induced by acute hypoproteinemia (HP) on LV systolic and diastolic function. We also combined the methods of HP and CVH (HP-CVH) to determine their combined effects on LV function and myocardial water content (MWC). We used a cell-saving device to lower plasma protein concentration in HP and HP-CVH groups. CVH was induced by inflating the balloon in the coronary sinus. Six control dogs were treated to sham HP. Conductance and micromanometer catheters were used to assess LV function. Contractility, as measured by preload recruitable stroke work, did not change in control or HP groups but declined significantly (14.5%) in the HP-CVH group. The time constant of isovolumic LV pressure decline (tau) increased significantly from baseline by 3 h in the HP (24.8%) and HP-CVH (27.1%) groups. The end-diastolic pressure-volume relationship (stiffness) also increased significantly from baseline by 3 h in the HP (78.6%) and HP-CVH (42.6%) groups. Total plasma protein concentration decreased from 5.2 +/- 0.2 g/dl at baseline to 2.5 +/- 0.0 g/dl by 3 h in the HP and HP-CVH groups. MWC of the HP (79.8 +/- 0.25%) and HP-CVH groups (79.8 +/- 0.2%) were significantly greater than that of the control group (77.8 +/- 0.3%) but not different from one another. In conclusion, hypoproteinemia-induced myocardial edema was associated with diastolic LV dysfunction but not systolic dysfunction. The edema caused by hypoproteinemia was more than twice that produced by our previous models, yet it was not associated with systolic dysfunction. CVH had a negative inotropic effect and no significant influence on MWC. IME may not have the inverse causal relationship with LV contractility that has been previously postulated but appears to have a direct causal association with diastolic stiffness as has been previously demonstrated.
在先前的研究中，我们观察到左心室（LV）收缩和舒张功能障碍与冠状动脉静脉高压（CVH）或淋巴管阻塞所诱发的心肌间质水肿（IME）有关。在本研究中，我们研究了急性低蛋白血症（HP）诱发的心肌水肿对左心室收缩和舒张功能的影响。我们还将HP和CVH的方法相结合（HP-CVH），以确定它们对左心室功能和心肌含水量（MWC）的联合作用。我们使用细胞保存装置降低HP组和HP-CVH组的血浆蛋白浓度。通过向冠状窦内充气气球诱发CVH。六只对照犬接受假HP处理。使用电导和微测压导管评估左心室功能。通过预负荷可募集搏功测量的收缩性在对照组或HP组中未发生变化，但在HP-CVH组中显著下降（14.5%）。HP组（24.8%）和HP-CVH组（27.1%）中，左心室等容压力下降时间常数（tau）在3小时时较基线显著增加。舒张末期压力-容积关系（僵硬度）在HP组（78.6%）和HP-CVH组（42.6%）中在3小时时也较基线显著增加。HP组和HP-CVH组的总血浆蛋白浓度从基线时的5.2±0.2 g/dl在3小时时降至2.5±0.0 g/dl。HP组（79.8±0.25%）和HP-CVH组（79.8±0.2%）的MWC显著高于对照组（77.8±0.3%），但两组之间无差异。总之，低蛋白血症诱发的心肌水肿与左心室舒张功能障碍有关，但与收缩功能障碍无关。低蛋白血症引起的水肿是我们先前模型所产生水肿的两倍多，但它与收缩功能障碍无关。CVH具有负性肌力作用，对MWC无显著影响。IME可能与先前假设的左心室收缩性不存在反向因果关系，但似乎与先前已证明的舒张僵硬度存在直接因果关联。
