Pump perfusion abolishes autoregulation possibly via prostaglandin release.

The influence of pump perfusion on autoregulation was studied in the hindleg of the halothane- and chloralose-anesthetized cat. Flow was measured with an electromagnetic flow probe in a tube between aorta and the vascularly isolated, denervated leg and varied with a calibrated occluder. Perfusion pressure was measured via a T-piece distal to the occluder. The steady-state pressure-flow relations could be fit with a sigmoidal curve. The mean closed-loop gain (0 less than Gc less than 1) for autoregulation in six cats was 0.46 +/- 0.11 (SD). When in these cats a roller pump was used, an almost linear pressure-flow relation was found (Gc = 0.01 +/- 0.09), while the resistance at control flow was decreased by 15 +/- 4%. Administration of indomethacin (5 mg/kg iv), a cyclooxygenase inhibitor, partly restored autoregulation during pumping (Gc = 0.34 +/- 0.09) and slowly increased the resistance to above its original value (20 +/- 13%). In six other cats, pump perfusion had no influence on autoregulation when started after indomethacin administration but resistance increased. This increase could not be prevented with ketanserin, a specific serotonin 2 receptor blocker. We conclude that pump perfusion abolishes autoregulation and decreases resistance via a process that involves prostaglandins. Blockade of the prostaglandin synthesis unmasks a slow vasoconstrictor influence in the bed.