Unclamping the inferior vena cava during retrograde cerebral perfusion increases the safe range of retrograde perfusion pressures and improves brain perfusion.

Department of Biochemistry, University of Manitoba, Winnipeg, Man., Canada.
Interactive Cardiovascular and Thoracic Surgery (Impact Factor: 1.11). 07/2004; 3(2):265-9. DOI: 10.1016/j.icvts.2003.12.001
Source: PubMed

ABSTRACT We investigated the effect of different methods of management of the inferior vena cava (IVC) during retrograde cerebral perfusion (RCP) on the relationships between RCP pressure, regional cerebral blood flow, tissue oxygenation, and intracranial pressure (ICP). Fourteen pigs were subjected to hypothermic (15 degrees C) RCP at RCP pressures varying from 10 to 110 mmHg with clamping (closed group, n=7) or without clamping of the IVC (open group, n=7). Intracranial pressures increased more slowly in the open group than in the closed group and were significantly lower at any level of RCP pressure in the open group than in the closed group. In the closed group, RCP pressures of 20-30 mmHg resulted in an ICP of 25 mmHg. In contrast, in the open group, when RCP pressures were maintained below 70 mmHg, ICP never reached 25 mmHg. Brain tissue blood flow and CO2 production were relatively higher in the open group than in the closed group. The maximum brain tissue blood flow was achieved at an RCP pressure of 40 mmHg in the open group. We conclude that the maximum safe RCP pressure differs according to the type of management of the IVC. Opening the IVC during RCP not only improves brain tissue perfusion, but also significantly increases the safety margin of RCP pressures. In the pig model, when the IVC is not clamped, the optimal RCP pressure appears to be 40 mmHg.

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    ABSTRACT: OBJECTIVES: Retrograde cerebral perfusion (RCP) has been employed to protect the brain during cardiovascular surgery, requiring temporary hypothermic circulatory arrest (HCA). However, the protocol used for RCP remains to be modified if prolonged HCA is expected. The aim of this study was to determine the efficacy of a modified protocol for this purpose. METHODS: After establishment of HCA at 15°C, 14 pigs were subjected to 90-min RCP using either the conventional protocol (i.e. alpha-stat strategy, 25-mmHg perfusion pressure and occluded inferior vena cava, Group I, n = 7) or the new protocol (i.e. pH-stat strategy, 40-mmHg perfusion pressure and unoccluded inferior vena cava, Group II, n = 7). After being rewarmed to 37°C, pigs were perfused for another 60 min. Phosphorus-31 magnetic resonance spectroscopy was used to track the changes of brain high-energy phosphates [i.e. adenosine triphosphate and phosphocreatine (PCr)] and intracellular pH (pHi). At the end, brain water content was measured. RESULTS: During RCP, high-energy phosphates decreased in both groups, whereas adenosine triphosphate decreased much faster in Group I (10.4 ± 4.3 vs 30.4 ± 4.4% of the baseline, P = 0.007, 60-min RCP). After rewarming, the recovery of high-energy phosphates and pHi was much slower in Group I (PCr: 55.7 ± 9.1 vs 78.4 ± 5.1% of the baseline, P = 0.046; adenosine triphosphate: 26.6 ± 10.6 vs 64.8 ± 4.6% of the baseline, P = 0.007; pHi: 6.5 ± 0.4 vs 7.1 ± 0.1, P = 0.021 at 30-min normothermic perfusion after rewarming). Brain tissue water content was significantly higher in Group I (81.1 ± 0.4 vs 79.5 ± 0.4%, P = 0.016). CONCLUSIONS: Application of the modified RCP protocol significantly improved cerebral energy conservation during HCA and accelerated energy recovery after rewarming.
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    ABSTRACT: This study was carried out to determine if increased perfusion pressure during retrograde cerebral perfusion (RCP) provides better preservation of the brain Na+, K+-ATPase activity. Twenty pigs were subjected to anesthesia alone (control group, n=5), hypothermic circulatory arrest (HCA) (HCA group, n = 5), HCA+RCP at perfusion pressures of 24-29 mmHg (Low-pressure group, n=5), or HCA+RCP at perfusion pressures of 34-40 mmHg (High-pressure group, n = 5). The brain was harvested for the measurement of tissue Na+, K+-ATPase activity. Relative to the control pigs (67.2 +/- 2.1%), significant impairment of Na+, K+-ATPase activity was observed in all three experimental groups (29.8 +/- 7.4% in HCA group, 33.5 +/- 2.9% in the Low-pressure group, and 52.0 +/- 1.8% in the High-pressure group, p < 0.01). The best preservation of the enzyme, particularly in the cortex and cerebellum regions, was observed in the High-pressure group (p < 0.01). In conclusion, HCA causes severe impairment of Na+, K+-ATPase activity, and increasing perfusion pressures from 24-29 to 34-40 mmHg during RCP significantly improves preservation of Na+, K+-ATPase activity, and the improvement of the protection varies in different regions of the brain.
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