PHARMACOLOGICAL INTERVENTION FOR ISCHEMIC BRAIN EDEMA AFTER RETROGRADE CEREBRAL PERFUSION

Retrograde cerebral perfusion has recently been the focus of interest as a simple new technique of brain protection during aortic arch opera tions, We undertook the experimental protocol of 120 minutes of retrog rade cerebral perfusion followed by antegrade reperfusion. Eighteen mo ngrel dogs were used. Retrograde cerebral perfusion was maintained at a flow rate of 150 to 250 ml/min to keep the perfusion pressure from 1 5 to 25 mm Hg. Animals were divided into three groups as follows: in g roup I, no treatment was received during and after retrograde cerebral perfusion; in group II, mannitol (2 gm/kg) was administered before ca rdiopulmonary bypass was restarted; and in group III, antivasospastic substance (1,2-bis[nicotinamido]-propane) was continuously injected du ring and after retrograde cerebral perfusion (1 mg/kg per minute). Cer ebral blood flow decreased during retrograde cerebral perfusion in all three groups, Cerebrovascular resistance showed marked increases 30 a nd 60 minutes after cardiopulmonary bypass was restarted in group I co mpared with the values in groups II and III (group I: 3.35 +/- 0.73 an d 5.00 +/- 1.57 mm Hg/ml per 100 gm per minute; group II: 1.30 +/- 0.3 3 and 1.03 +/- 0.17 mm Hg/ml per 100 gm per minute; group III: 1.24 +/ - 0.41 and 0.98 +/- 0.24 mm Hg/ml per 100 gm per minute). The oxygen e xtraction level was reduced by cooling, but it rose to a higher level as a result of significant desaturation of returned blood even in deep hypothermia during retrograde cerebral perfusion. Both cerebral metab olic rate of oxygen and cerebral metabolic rate of glucose remained at low levels during retrograde cerebral perfusion. Ratios of cerebral b lood flow to cerebral metabolic rate of oxygen and cerebral blood flow to cerebral metabolic rate of glucose were markedly reduced during re trograde cerebral perfusion. Intracranial pressure showed significant increases 30 and 60 minutes after cardiopulmonary bypass was restarted in group I compared with values in group IT or group III (group I: 22 .7 +/- 2.8 and 20.6 +/- 5.1 mm Hg; group II: 6.3 +/- 1.8 and 5.3 +/- 1 .3 mm Hg; group III: 4.2 +/- 1.7 and 7.7 +/- 2.8 mm Hg). Water content of the brain tissue in group I (77.54% +/- 0.29%) was significantly h igher than that in group IT (74.71% +/- 0.76%) or group III (74.14% +/ - 0.48%). These data suggest that the supply of oxygen or glucose by r etrograde cerebral perfusion is not enough to maintain sufficient cere bral metabolism, which may cause brain edema during antegrade reperfus ion. Therefore cerebral protection via pharmacologic agents is recomme nded to prevent neurologic complications during aortic arch operations with the use of retrograde cerebral perfusion.