Figure 2
CXCR4/ACKR3 ligands modulate hemodynamics during the cardiovascular stress response to hemorrhagic shock and resuscitation. Rats were hemorrhaged to a MAP of 30 mmHg for 30 min, followed by crystalloid resuscitation to maintain MAP of 70 mmHg. *: p < 0.05 versus vehicle. (A–C) CXCR4/ACKR3 ligands (350 nmol/kg) were injected 5 min before hemorrhage. Open circles: vehicle (n = 5); Red circles: ubiquitin (n = 5); Yellow squares: AMD3100 (n = 7). Blue squares: CXCL12 (n = 3). (A) Blood volume hemorrhaged (mL/kg). (B) MAP (mmHg). (C) Cumulative fluid requirements to maintain MAP at 70 mmHg (mL/kg). (D–F) CXCR4/ACKR3 ligands (350 nmol/kg) were injected at the end of the shock period (t = 30 min), prior to fluid resuscitation. Open circles: vehicle (n = 7); Red circles: ubiquitin (n = 7); Yellow squares: AMD3100 (n = 7). Blue squares: CXCL12 (n = 9). Green diamonds: ubiquitin plus AMD3100 (350 nmol/kg each; n = 6). (D) Blood volume hemorrhaged (mL/kg). (E) MAP (mmHg). (F) Cumulative fluid requirements to maintain MAP at 70 mmHg (mL/kg). (G) Representative left ventricular pressure-volume loops at baseline, during the shock period and 30 min after drug injection and fluid resuscitation. (H) Left ventricular contractility (dP/dtmax/Pmax, n = 3 to 5/group). (I) Isovolumic relaxation constants (τ(Mirsky), n = 3 to 5/group).