Characterization of arterial pressure and carotid blood flow responses to pulsatile perfusion therapy in a rat model of hemorrhage




Bhuiyan, Nasrul
Farmer, George
Anderson, Garen K.
Davis, Kenneth
Cunningham, Joseph
Rickards, Caroline


0000-0002-1013-3478 (Anderson, Garen K.)
0000-0002-1277-6266 (Davis, Kenneth)

Journal Title

Journal ISSN

Volume Title



Introduction: In a human model of simulated blood loss, oscillatory patterns of arterial pressure and blood flow, or "pulsatile perfusion", can protect cerebral and peripheral tissue oxygenation, and prolong tolerance to this stress. In this pilot study, we investigate whether pulsatile perfusion therapy can protect arterial pressure and cerebral blood flow in a rat model of actual blood loss. We hypothesized that pulsatile perfusion therapy (PPT), applied via repeated thigh cuff inflations, would attenuate the reduction in arterial pressure and cerebral blood flow following hemorrhage. Methods: Sprague Dawley rats underwent the following protocols: hemorrhage alone (control: N=4; 2 male, 2 female), or hemorrhage plus PPT (N=3; 1 male, 2 female). PPT was applied via rapid 1 s inflations and deflations of a thigh cuff (0.5 Hz). A catheter was inserted in the femoral artery for continuous measurement of arterial pressure, and a perivascular flow probe was placed around the common carotid artery (CCA) for measurement of blood flow. Following instrumentation, each animal completed a baseline period (15 min), followed by a ~55% hemorrhage (25 min), PPT or control (30 min), and a recovery period (155 min or until death). Results: Decreases in mean arterial pressure (MAP) and CCA blood flow were observed in response to hemorrhage (P≤0.002). At the end of the PPT period, no differences were observed between the PPT and control groups for MAP (PPT: 46.7±27.3 mmHg vs. control: 30.2±13.5 mmHg; P=0.44) or CCA peak blood flow (PPT: 2.7±1.5 ml/min vs. control: 1.9±1.3 ml/min; P=0.92). Similarly, no differences were observed in the relative change from baseline to the end of the PPT period for MAP (PPT: -45±38% vs. control: -55±14%; P=0.65) or CCA peak blood flow (PPT: -65±21% vs. control: -66±12%; P=0.70). Conclusion: These results suggest that following a 55% hemorrhage in rats, PPT did not protect arterial pressure or carotid blood flow. However, the sample size was low in this pilot study, resulting in high variability in the observed responses. Accordingly, additional experiments are needed with an increased sample size to accurately determine the potential beneficial effects of PPT following hemorrhage.