Effects of hypoproteinemia-induced myocardial edema on left ventricular function.

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 (τ) 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.

[1]  P. Myerowitz,et al.  Acute transient coronary sinus hypertension impairs left ventricular function and induces myocardial edema. , 1996, The American journal of physiology.

[2]  L. Navar,et al.  Relationship between colloid osmotic pressure and plasma protein concentration in the dog. , 1977, The American journal of physiology.

[3]  S. Allen,et al.  Myocardial edema, left ventricular function, and pulmonary hypertension. , 1995, Journal of applied physiology.

[4]  P. Salisbury,et al.  Influence of coronary perfusion and myocardial edema on pressure-volume diagram of left ventricle. , 1961, The American journal of physiology.

[5]  Gloria R. Gogola,et al.  Normothermic continuous antegrade blood cardioplegia does not prevent myocardial edema and cardiac dysfunction. , 1995, Circulation.

[6]  P. Sobotka,et al.  Effect of acute edema on left ventricular function and coronary vascular resistance in the isolated rat heart. , 1994, The American journal of physiology.

[7]  R. Schlant,et al.  Pathologic and functional effects on the heart following interruption of the cardiac lymph drainage. , 1969, The Journal of thoracic and cardiovascular surgery.

[8]  G. Buckberg,et al.  Iatrogenic Myocardial Edema with Crystalloid Primes , 1986 .

[9]  G. Kouraklis,et al.  The influence of hemodilution on left ventricular function. , 1990, International Angiology.

[10]  S. Hagl,et al.  Cardiac performance during limited hemodilution. , 1975, Bibliotheca haematologica.

[11]  A. Nicolosi,et al.  Effects of perfusion-induced edema on diastolic stress-strain relations in intact swine papillary muscle. , 1994, The Journal of thoracic and cardiovascular surgery.

[12]  S J Allen,et al.  Left ventricular myocardial edema. Lymph flow, interstitial fibrosis, and cardiac function. , 1991, Circulation research.

[13]  L. Michael,et al.  Elevated coronary sinus pressure does not alter myocardial blood flow or left ventricular contractile function in mature sheep. Implications after the Fontan operation. , 1988, The Journal of thoracic and cardiovascular surgery.

[14]  G. Laine,et al.  Change in (dP/dt)max as an index of myocardial microvascular permeability. , 1987, Circulation research.

[15]  P. Myerowitz,et al.  Effects of acid aspiration-induced lung injury on left ventricular function. , 1996, Surgery.

[16]  H. Grigoriew,et al.  STUDY OF THE MECHANICAL NANOCRYSTALLIZATION PROCESS OF AMORPHOUS FE78B13SI9 ALLOY USING THE PAIR FUNCTION METHOD , 1995 .

[17]  M. Ilbawi,et al.  Effects of elevated coronary sinus pressure on left ventricular function after the Fontan operation. An experimental and clinical correlation. , 1986, The Journal of thoracic and cardiovascular surgery.

[18]  J. Weiss,et al.  Quantification of incomplete left ventricular relaxation: relationship to the time constant for isovolumic pressure fall. , 1980, European heart journal.

[19]  M. Sunamori,et al.  Correlation among water content, left ventricular function, coronary blood flow, and myocardial metabolism after hypothermic ischemic cardiac arrest. , 1983, Advances in myocardiology.

[20]  P. Myerowitz,et al.  Impairment of left ventricular function by acute cardiac lymphatic obstruction. , 1997, Cardiovascular research.

[21]  B Buis,et al.  Continuous measurement of left ventricular volume in animals and humans by conductance catheter. , 1984, Circulation.

[22]  W. J. Powell,et al.  Ventricular performance and myocardial water content during hemodilution in dogs. , 1978, The American journal of physiology.

[23]  S. Allen,et al.  Impact of cardiopulmonary bypass and cardioplegic arrest on myocardial lymphatic function. , 1995, American Journal of Physiology.

[24]  P. Ashmore,et al.  Myocardial oedema and ventricular function after cardioplegia with added mannitol , 1991, Canadian journal of anaesthesia = Journal canadien d'anesthesie.

[25]  P. Salisbury,et al.  Distensibility and Water Content of Heart Muscle Before and After Injury , 1960, Circulation research.