EFFECTS OF HYPOPROTEINEMIA-INDUCED MYOCARDIAL EDEMA ON LEFT-VENTRICULAR FUNCTION

In previous studies, we observed left ventricular (LV) systolic and di astolic dysfunction in association with interstitial myocardial edema (IME) induced by either coronary venous hypertension (CVH) or lymphati c obstruction. In the present study, we examined the effects of myocar dial edema induced by acute hypoproteinemia (KP) on LV systolic and di astolic function. We also combined the methods of HP and CVH (HP-CVH) to determine their combined effects on LV function and myocardial wate r content (MWC). We used a cell-saving device to lower plasma protein concentration in HP and HP-CVH groups. CVH was induced by inflating th e balloon in the coronary sinus. Six control dogs were treated to sham HP. Conductance and micromanometer catheters were used to assess LV f unction. Contractility, as measured by preload recruitable stroke work , did not change in control or HP groups but declined significantly (1 4.5%) 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 r elationship (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 +/- 0.256) were significantly greater tha n 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 dysfu nction. CVH had a negative inotropic effect and no significant influen ce on MWC. IME may not have the inverse causal relationship with LV co ntractility that has been previously postulated but appears to have a direct causal association with diastolic stiffness as has been previou sly demonstrated.