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Arrhythmogenic effects induced by coronary conversion of pulmonary big endothelin to endothelin

Aggravation of this phenomenon in heritable hyperlipidemia

^a Medizinische Klinik und Poliklinik I, Charité, Humboldt-Universität zu Berlin, D-10098 Berlin, Germany

View larger version (43K): [in a new window]   Figure 1 Incidence of VES during 40 min of separate perfusion and an additional 40 min of serial perfusion in NZW (n = 12) and WHHL (n = 8) rabbits. During serial perfusion, isolated hearts are perfused with the effluent of the same animal’s isolated lung. To exclude flow-dependency of arrhythmias, mechanical flow reduction (i.e., volume-controlled perfusion) comparable to the effects seen during serial perfusion was performed in isolated NZW and WHHL hearts (M-NZW, New Zealand mechanical flow reduction group; M-WHHL, Watanabe mechanical flow reduction group, n = 6 for both groups). ##, p < 0.01 vs. separate perfusion.

View larger version (42K): [in a new window]   Figure 2 Incidence of VES in NZW and Watanabe hearts when serial perfusion (40 min) was conducted in the presence of PD-145065 (nonselective ET antagonist, 10 µmol/liter), A-127722 (ETA antagonist, 20 µmol/liter), BQ-123 (ETA antagonist, 2 µmol/liter) and phosphoramidon (Phrd, ECE inhibitor, 50 µmol/liter) (n = 6 per group). #, p < 0.05; ##, p < 0.01 vs. separate perfusion; *, p < 0.05; **, p < 0.01 vs. serial perfusion without intervention.