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

• Published in: American journal of physiology. Heart and circulatory physiology 1998-01, Vol.274 (1), p.H187-H192
• Main Authors: Vanteeffelen, Jurgen W. G. E, Merkus, Daphne, Bos, Luc J, Vergroesen, Isabelle, Spaan, Jos A. E
• Format: Article
• Language: English
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.1998.274.1.h187

Department of Medical Physics, Academic Medical Center, University of Amsterdam, 1100 DE Amsterdam, The Netherlands 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 /d t 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 /d t 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 /d t 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. lidocaine; contractility; left ventricular pressure transmission; myocardial edema