ULFS-49 Causes Bradycardia Without Decreasing Right Ventricular Systolic and Diastolic Performance

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Abstract
Summary: The effects of ULFS-49, a new calcium channel blocker, on right ventricular (RV) systolic and diastolic performance were evaluated in nine anesthetized, closed-chest dogs by load-insensitive indexes. ULFS-49 (0.3 mg/kg) decreased heart rate (HR) from 76 × 25 to 47 × 11 beats/min (p < 0.01) and cardiac output (CO) from 1.89 × 0.62 to 1.42 × 0.72 L/min (p < 0.01), as RV free wall end-diastolic area increased from 486 × 126 to 581 × 45 mm2 (p < 0.01) and RV end-diastolic volume increased from 66.6 × 26.4 to 85.3 × 28.5 ml (p < 0.05). Pacing at 100 beats/min ablated these hemodynamic and dimensional changes. RV free wall contractility was assessed by the slope and midrange intercept values of the relation between RV end-systolic pressure (Pes) and end-systolic free wall area (Aes) and between RV free wall segmental work (SW) and end-diastolic area (Aed). RV free wall stiffness was measured by exponential fit of the RV endiastolic pressure (Ped)-Aed points during caval occlusion. With pacing at 100 beats/min, the slope of the Pes—Aes relationship was unchanged by ULFS-49 (0.52 × 0.29 vs. 0.60 × 0.35 mm Hg/mm2), as was the midrange intercept (382.3 × 114.7 vs. 387.1 × 121.5 mm2). After administration of ULFS-49, the slope of the SW-Aed relation increased from 31.8 × 14.4 to 37.3 × 17.7 mm Hg × mm2 (p < 0.05) without changing the midrange intercept (410.5 × 108.1 mm2 vs. 413.0 × 107.0 mm2). Similarly, neither the position nor curvature of the Ped–Aed relation was changed by ULFS-49. These data demonstrate that ULFS-49 causes significant bradycardia and increases the size of the right ventricle without directly depressing RV free wall systolic or diastolic performance.

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