title: Comparative experimental study between retrograde cerebral perfusion and circulatory arrest.
abstract: To evaluate the efficacy of retrograde cerebral perfusion in protecting the brain, we comparatively studied retrograde cerebral perfusion and total circulatory arrest in 18 hypothermic (20 degrees C) mongrel dogs (retrograde cerebral perfusion, n = 10; total circulatory arrest, n = 8). Retrograde cerebral perfusion was performed, maintaining an external jugular venous pressure of 25 mm Hg for 60 minutes. Retrograde cerebral perfusion provided half the cerebral blood flow and a third of the oxygen that was supplied during hypothermic cardiopulmonary bypass, which had a flow rate of 100 ml/min per kilogram. Oxygen consumption and carbon dioxide exudation did not increase on resuming cardiopulmonary bypass after retrograde cerebral perfusion, whereas they increased after total circulatory arrest (oxygen consumption 10.7 +/- 5.3 versus 19.1 +/- 8.6 ml/min, p < 0.05; carbon dioxide exudation, 0.92 +/- 0.54 versus 1.64 +/- 0.78 mmol/min, p < 0.05). Therefore, oxygen debt during retrograde cerebral perfusion was smaller than during total circulatory arrest. Retrograde cerebral perfusion also cooled the brain better than did total circulatory arrest (20.4 degrees +/- 1.5 degrees C versus 22.7 degrees +/- 0.7 degrees C, p < 0.01). Cerebral tissue oxygen tension decreased slightly (27.5 +/- 7.7 versus 12.3 +/- 3.0 mm Hg, p < 0.01), and cerebral tissue carbon dioxide tension increased slowly during retrograde cerebral perfusion (95 +/- 34 versus 147 +/- 44 mm Hg, p < 0.05). These changes were smaller than those seen in total circulatory arrest. Tissue concentrations of adenosine triphosphate in the brain remained relatively high during retrograde cerebral perfusion but decreased rapidly during total circulatory arrest (0.49 +/- 0.16 versus 0.21 +/- 0.05 mmol/gm, p < 0.01, just before resuming cardiopulmonary bypass). Retrograde cerebral perfusion cannot maintain aerobic metabolism but may reduce ischemic damage of the brain and may safely extend the cerebral circulation interruption time.
authors.affiliation: Nagoya University School of Medicine, Department of Thoracic Surgery, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Usui
authors.forename: K
authors.initials: K
authors.lastname: Oohara
authors.forename: T L
authors.initials: TL
authors.lastname: Liu
authors.forename: M
authors.initials: M
authors.lastname: Murase
authors.forename: M
authors.initials: M
authors.lastname: Tanaka
authors.forename: E
authors.initials: E
authors.lastname: Takeuchi
authors.forename: T
authors.initials: T
authors.lastname: Abe
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism; D002545:Brain Ischemia / Q000517:prevention & control*; D002315:Cardiopulmonary Bypass; D002405:Catheterization, Central Venous; D002560:Cerebrovascular Circulation; D004285:Dogs; D006324:Heart Arrest, Induced; D010101:Oxygen Consumption / Q000502:physiology; D010477:Perfusion / Q000379:methods; D013997:Time Factors; D014683:Vena Cava, Superior
chemical_list: D000255:Adenosine Triphosphate