Panel A shows a line graph of sarcomere length (SL) over time with four different traces: solid black line for LVCM control, black dotted line for LVCM with SMTC, solid gray line for RVCM control, and gray dotted line for RVCM with SMTC. The x-axis represents time in milliseconds, and the y-axis represents sarcomere length in micrometers. Panel B shows the same data normalized to the amplitude of sarcomere shortening to compare the time course of shortening and relaxation across conditions. Panel C is a bar graph showing diastolic sarcomere length in LVCMs and RVCMs under control and SMTC-treated conditions, with individual cardiomyocytes represented by gray dots and mean values for each animal by black dots. The x-axis labels the conditions, and the y-axis represents diastolic sarcomere length in micrometers. Panel D is a bar graph showing absolute sarcomere shortening in LVCMs and RVCMs under control and SMTC-treated conditions, with the x-axis labeling the conditions and the y-axis representing the change in sarcomere length in micrometers. Panel E is a bar graph showing sarcomere shortening normalized to diastolic sarcomere length, with the x-axis labeling the conditions and the y-axis representing the percentage. Panels F, G, and H are bar graphs showing the time to 10 percent, 50 percent, and 90 percent relengthening following peak sarcomere shortening in LVCMs and RVCMs under control and SMTC-treated conditions, respectively. The x-axis labels the conditions, and the y-axis represents time in milliseconds. Each panel includes statistical significance indicators for the comparisons made.
nNOS inhibition enhances sarcomere shortening and delays relaxation more prominently in RVCMs. (A) Representative SL traces from LVCMs and RVCMs under control conditions and following nNOS inhibition with SMTC. The timing of electrical stimulation and peak shortening are indicated. Solid black line, LVCM control; black dotted line, LVCM + SMTC; solid gray line, RVCM control; gray dotted line, RVCM + SMTC. The timing of electrical stimulation and peak shortening are indicated. (B) SL traces from panel A normalized to the amplitude of sarcomere shortening (ΔSL) to compare the time course of shortening and relaxation across conditions. (C) Diastolic SL measured in LVCMs and RVCMs under control (C) and SMTC-treated (S) conditions. (D) Absolute sarcomere shortening (ΔSL) in LVCMs and RVCMs under control and SMTC-treated conditions. (E) Sarcomere shortening normalized to diastolic SL (ΔSL/diastolic SL). (F–H) Time to 10% (F), 50% (G), and 90% (H) relengthening following peak sarcomere shortening in LVCMs and RVCMs under control and SMTC-treated conditions. In panels C–H, gray dots represent individual cardiomyocytes, whereas black dots represent the mean value for each animal. Sample sizes were as follows (N = 10 animals per group): LVCM, n = 92; LVCM + SMTC, n = 152; RVCM, n = 165; RVCM + SMTC, n = 209. n.s., not significant.