Fig. 2

Representative data of LV end-systolic pressure–volume relation (ESPVR), LV end-diastolic pressure–volume relation (EDPVR), and myocardial oxygen consumption per beat (VO₂)-systolic pressure–volume area (PVA) relation in the presence of CPZ (1.59 µg/mL in blood) during 42 °C (a and b, dotted lines) and in the presence of capsaicin (Cap) (0–461 ng/mL in blood) at 37 °C (c and d, dotted lines), respectively. The arrows in panel A indicate that the decrease in LV ESP at mLVV at 42 °C (solid triangle) was partially inhibited by CPZ (open square). The fine line indicates the estimated LV ESPVR at 42 °C. Thus, the VO₂–PVA data point at mLVV in CPZ-treated heart at 42 °C (solid square) shifted right-downward from that in hyperthermia-heart (solid triangle), which left-downward shifted data point from it at 37 °C (solid circle) (b). On the other hand, the LV ESPVRs in Cap-treated heart shifted downward (c) and each PVA and VO₂ values (open triangles) at each LVV during Cap infusion (230 ng/mL in blood) was smaller than each control value (solid circles), and the VO₂–PVA linear relations during Cap infusion shifted downward; VO₂-intercept values decreased without changes in the slope (d). The open circles indicate that Cap dose-dependently decreased the LV ESP and thus shifted in parallel estimated VO₂–PVA relation according to stepwise elevation of the Cap infusion rate (0, 1, 2, 4, 6, 8, 10, 20 µL/mL) with infusion pump (c and d). The fine lines indicate the estimated LV ESPVRs and VO₂–PVA linear relations at various Cap infusion rates c and d)