In the present study, cardiac contraction was regionally impaired to investigate the relationship between contractility [maximum first time derivative of left ventricular pressure (dP_LV/dt_max)] and P_LV on epicardial lymph pressure (P_lymph) 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 dP_LV/dt_max and P_LV pulse to 77 ± 9 (SD; n = 5) and 82 ± 5% of control, respectively, whereas P_lymph pulse increased to 186 ± 101%. The relative increase of maximum P_lymph to P_LV related inversely to the change in dP_LV/dt_max after lidocaine administration. Additional data were obtained when P_LV was transiently increased by constriction of the descending aorta. The ratio of pulse P_lymph to P_LV during aortic clamping increased after lidocaine administration, from 0.063 ± 0.03 to 0.15 ± 0.09. The results suggest that transmission of P_LV 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 P_LV by the myocardium itself.