Impairment of contraction increases sensitivity of epicardial lymph pressure for left ventricular pressure.

In the present study, cardiac contraction was regionally impaired to investigate the relationship between contractility [maximum first time derivative of left ventricular pressure (dPLV/d t max)] and PLV on epicardial lymph pressure (Plymph) generation. Measurements were performed in open-chest anesthetized dogs under control conditions and while local contraction was abolished by intracoronary administration of lidocaine. Lidocaine significantly lowered dPLV/d t maxand PLV pulse to 77 ± 9 (SD; n = 5) and 82 ± 5% of control, respectively, whereas Plymph pulse increased to 186 ± 101%. The relative increase of maximum Plymph to PLV related inversely to the change in dPLV/d t maxafter lidocaine administration. Additional data were obtained when PLV was transiently increased by constriction of the descending aorta. The ratio of pulse Plymph to PLV during aortic clamping increased after lidocaine administration, from 0.063 ± 0.03 to 0.15 ± 0.09. The results suggest that transmission of PLV to the cardiac lymphatic vasculature is enhanced when regional contraction is impaired. These findings imply that during normal, unimpaired contraction lymph vessels are shielded from high systolic PLV by the myocardium itself.