PULSATILE VERSUS NONPULSATILE FLOW - NO DIFFERENCE IN CEREBRAL BLOOD-FLOW OR METABOLISM DURING NORMOTHERMIC CARDIOPULMONARY BYPASS IN RABBITS

Background: Although pulsatile and nonpulsatile cardiopulmonary bypass (CPB) do not differentially affect cerebral blood now (CBF) or metabo lism during hypothermia, studies suggest pulsatile CPB may result in g reater CBF than nonpulsatile CPB under normothermic conditions. Conseq uently, nonpulsatile flow may contribute to poorer neurologic outcome observed in some studies of normothermic CPB. This study compared CBF and cerebral metabolic rate for oxygen (CMR(O2)) between pulsatile and nonpulsatile CPB at 37 degrees C. Methods: In experiment A, 16 anesth etized New Zealand white rabbits were randomized to one of two pulsati le CPB groups based on pump systolic ejection period (100 and 140 ms, respectively). Each animal was perfused at 37 degrees C for 30 min at each of two pulse rates (150 and 250 pulse/min, respectively). This sc heme created four different arterial pressure waveforms. At the end of each perfusion period, arterial pressure waveform, arterial and cereb ral venous oxygen content, CBF (microspheres), and CMR(O2) (Fick) were measured. In experiment B, 22 rabbits were randomized to pulsatile (1 00-ms ejection period, 250 pulse/min) or nonpulsatile CPB at 37 degree s C. At 30 and 60 min of CPB, physiologic measurements were made as be fore. Results: In experiment A, CBF and CMR(O2), were independent of e jection period and pulse rate. Thus, all four waveforms were physiolog ically equivalent. In experiment B, CBF did not differ between pulsati le and nonpulsatile CPB (72 +/- 6 vs. 77 +/- 9 ml.100 g(-1).min(-1), r espectively (median +/- quartile deviation)), CMR(O2), did not differ between pulsatile and nonpulsatile CPB (4.7 +/- 0.5 vs. 4.1 +/- 0.6 ml O-2.100 g(-1).min(-1), respectively) and decreased slightly (0.4 +/- 0.4 ml.O-2 100 g(-1).min(-1)) between measurements, Conclusions: Durin g CPB in rabbits at 37 degrees C, neither CBF nor CMR(O2) is affected by arterial pulsation. The absence of pulsation per se is not responsi ble for the small decreases in CMR(O2) observed during CPB.