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Impairment of left ventricular function by acute cardiac lymphatic obstruction

L.L Ludwig, E.R Schertel, J.W Pratt, D.E McClure, A.J Ying, C.F Heck, P.D Myerowitz
DOI: http://dx.doi.org/10.1016/S0008-6363(96)00177-0 164-171 First published online: 1 January 1997


Objectives: We performed the following study to define the effects of acute cardiac lymphatic obstruction on left ventricular (LV) systolic and diastolic function. Methods: Cardiac lymphatic obstruction was created in 8 pentobarbital-anesthetized dogs by identifying (Evans blue) and ligating the right and left epicardial lymphatics, the afferent and efferent lymphatics associated with the pretrachael and cardiac lymph nodes, and the thoracic duct. Left ventricular function was assessed by analysis of micromanometer-conductance catheter-derived LV pressure-volume relationships. Contractility was assessed by preload recruitable stroke work (PRSW). The active and passive phases of LV relaxation were assessed by the time constant of isovolumic relaxation (τ) and the end-diastolic pressure-volume relationship (stiffness), respectively. Results: PRSW decreased significantly and τ increased significantly from baseline at 1, 2, and 3 h after cardiac lymphatic obstruction (n = 8), but stiffness did not change. Cardiac lymphatic obstruction had similar effects on LV function in a group of autonomically blocked dogs (n = 5). Left ventricular function did not change in sham treated controls (n = 8). Cardiac lymphatic obstruction induced a significant increase in LV wet/dry weight ratios (3.58 ± 0.01) when compared to the control group (3.53 ± 0.02). Histophatology of the myocardium in the lymphatic obstruction groups revealed significant lymphangiectasis and increased interstitial spacing when compared to controls. Conclusions: Acute cardiac lymphatic obstruction depresses contractility and active relaxation and causes mild LV myocardial edema, but does not alter diastolic stiffness.

  • Ventricular function
  • Lymph flow
  • Edema
  • Dog
  • anesthetized
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