Characterization of Rat Cardiovascular System by Anacrotic/Dicrotic Notches in the Condition of Increase/Decrease of NO Bioavailability

Figures

• 

  Figure 1. The left common carotid artery pulse waveform (APW) in the anesthetized rat. Anacrotic (AnN) notch (d) and dicrotic (DiN) notch (h) marked at control APW (red) and after i.v. administration of 32 nmol·kg−1 NO-donor S-nitrosoglutathione (GSNO) (blue) or 25 mg·kg−1 l-NAME (green). For the definition of time interval (DiN-AnN in ms) and the difference of blood pressure (BP) (DiN-AnN in mmHg) of dicrotic and anacrotic nothes, see Supplementary Materials Figure S1.

• 

  Figure 2. Time-dependent changes of hemodynamic parameters (HPs) of anesthetized rat after i.v. bolus administration of 32 nmol·kg–1 S-nitrosoglutathione (GSNO) (marked by dash lines). The red line starts 3 s before GSNO administration. Time period corresponding to the decrease of systolic BP (red), increase of systolic BP to the control value (blue), further increase of systolic BP to maximum (green), and decrease of systolic BP to the control value (black). Units in plots (gg), (hh), (pp), and (qq) are informative only.

• 

  Figure 3. Two-dimensional relationships of HPs to the pressure interval between dicrotic (DiN) and anacrotic (AnN) notches after the administration of 32 nmol·kg–1 GSNO. The colors and time-dependent data correspond to Figure 2. Time period corresponding to the decrease of systolic BP (red), increase of systolic BP to the control value (blue), further increase of systolic BP to maximum (green), and decrease of systolic BP to the control value (black). The hysteresis was arbitrary defined as HPs-(DiN-AnN in mmHg) loop > 5 mmHg of DiN-AnN. The non-hysteresis was arbitrary defined as HPs-(DiN-AnN in mmHg) loop ≤ 5 mmHg of DiN-AnN.

• 

  Figure 4. Non-hysteresis/hysteresis patterns of the two-dimensional relationships of HPs to pressure differences of DiN-AnN in mmHg. Data were taken from Figure 3 and Figure S2 (red and blue lines, which represent the time interval of decrease and increase of BP after administration of 32 nmol·kg–1 GSNO). Number of rats in which non-hysteresis (blue) or hysteresis (red) patterns were observed (n = 7). The hysteresis was arbitrarily defined as HPs-(DiN-AnN in mmHg) loop > 5 mmHg of DiN-AnN (in mmHg).

• 

  Figure 5. Relationships of HPs to the time interval between dicrotic (DiN) and anacrotic (AnN) notches after the administration of 32 nmol·kg–1 GSNO. The colors and time-dependent data correspond to Figure 2. Time period corresponding to the decrease of systolic BP (red), increase of systolic BP to the control value (blue), further increase of systolic BP to maximum (green), and decrease of systolic BP to the control value (black). The hysteresis was arbitrary defined as HPs-(DiN-AnN in ms) loop > 3 ms of DiN-AnN.

• 

  Figure 6. Two-dimensional cross-relationships of DiN-AnN pressure difference (in mmHg) to 34 rat HPs for conditions of increased/decreased NO bioavailability. The increase of NO bioavailability was caused by i.v. administration of 32 nmol·kg−1 GSNO (red line; average from 10 experiments; data calculated from Figure 6 published in [22]). Red line was calculated from the time segment during which BP decreased after GSNO administration. The decrease of NO bioavailability after i.v. administration of 25 mg·kg−1 l-NAME (blue line; average from six experiments; data calculated from Figure 3 published in [23]) is shown. Blue line was calculated from the time segment during which BP increased after l-NAME administration. Arrows indicate the time direction after GSNO and l-NAME administration.

• 

  Figure 7. Two-dimensional cross-relationships of DiN-AnN time interval difference (in ms) to 34 rat HPs for conditions of increased/decreased NO bioavailability. The increase of NO bioavailability was caused by i.v. administration of 32 nmol·kg−1 GSNO (red line; average from 10 experiments; data calculated from Figure 6 published in [22]). Red line was calculated from the time segment during which BP decreased after GSNO administration. The decrease of NO bioavailability was caused by i.v. administration of 25 mg·kg−1 l-NAME (blue line; average from 6 experiments; data calculated from Figure 3 published in [23]). Blue line was calculated from the time segment during which BP increased after l-NAME administration. Arrow indicates the time direction after l-NAME administration.