Cardioplegic arrest (CPA) is associated with interstitial myocardial edema, which has been shown to impair myocardial function. The accumulation of interstitial myocardial edema may be enhanced by impaired myocardial lymph flow. The purpose of this study was to investigate the effects of CPA on myocardial lymphatic function. In nine anesthetized dogs, we cannulated a prenodal cardiac lymphatic and measured myocardial lymph flow rate (QL), myocardial lymph driving pressure (PL), and myocardial lymph hyaluronan (Hya) concentration. We determined left ventricular function using pressure-volume curves derived by sonomicrometry and micromanometry. The dogs were placed on cardiopulmonary bypass (CPB) (28 degrees C) and subjected to 60 min of hypothermic, crystalloid CPA. With the onset of asystole both QL and PL decreased significantly from 70.7 +/- 31.8 (SD) to 3.3 +/- 4.0 microliters/min and from 19.9 +/- 8.0 to 10.4 +/- 1.8 mmHg, respectively (P < 0.01). Following return of sinus rhythm after separation from CPB, QL and PL increased significantly to 135.4 +/- 28.0 microliters/min and 27.3 +/- 7.5 mmHg, respectively (P < 0.01). Post-CPA myocardial edema was demonstrated by gravimetric wet-to-dry weight determination of 3.67 +/- 0.20 (normal 2.90 +/- 0.20, P < 0.001) and was associated with significantly decreased left ventricular function. Myocardial Hya turnover rate was 1.3 +/- 1.0% per day under baseline conditions and increased significantly to 2.7 +/- 0.9% per day post-CPA (P < 0.01). We conclude that organized myocardial contraction is the major determinant of myocardial lymph flow. Myocardial lymph flow impairment during CPA may contribute to post-CPA myocardial edema and left ventricular dysfunction.
Cytokines are systemic effectors of lymphatic function in acute inflammation
