Pharmacologic 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 operations. We undertook the experimental protocol of 120 minutes of retrograde cerebral perfusion followed by antegrade reperfusion. Eighteen mongrel dogs were used. Retrograde cerebral perfusion was maintained at a flow rate of 150 to 250 ml/min to keep the perfusion pressure from 15 to 25 mm Hg. Animals were divided into three groups as follows: in group I, no treatment was received during and after retrograde cerebral perfusion; in group II, mannitol (2 gm/kg) was administered before cardiopulmonary bypass was restarted; and in group III, antivasospastic substance (1,2-bis nicotinamido]-propane) was continuously injected during and after retrograde cerebral perfusion (1 mg/kg per minute). Cerebral blood flow decreased during retrograde cerebral perfusion in all three groups. Cerebrovascular resistance showed marked increases 30 and 60 minutes after cardiopulmonary bypass was restarted in group I compared with the values in groups II and III (group I: 3.35 +/- 0.73 and 5.00 +/- 1.57 mm Hg/ml per 100 gm per minute; group II: 1.30 +/- 0.33 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 extraction 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 metabolic rate of oxygen and cerebral metabolic rate of glucose remained at low levels during retrograde cerebral perfusion. Ratios of cerebral blood flow to cerebral metabolic rate of oxygen and cerebral blood flow to cerebral metabolic rate of glucose were markedly reduced during retrograde cerebral perfusion. Intracranial pressure showed significant increases 30 and 60 minutes after cardiopulmonary bypass was restarted in group I compared with values in group II 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 higher than that in group II (74.71% +/- 0.76%) or group III (74.14% +/- 0.48%). These data suggest that the supply of oxygen or glucose by retrograde cerebral perfusion is not enough to maintain sufficient cerebral metabolism, which may cause brain edema during antegrade reperfusion.(ABSTRACT TRUNCATED AT 400 WORDS)
Yoshimura
N
N
Department of Surgery, Kobe University, School of Medicine, Japan.
Okada
M
M
Ota
T
T
Nohara
H
H
D000818:Animals; D001013:Aorta, Thoracic / Q000601:surgery; D017545:Aortic Aneurysm, Thoracic / Q000601:surgery; D001921:Brain / Q000378:metabolism; D001929:Brain Edema / Q000517:prevention & control*; D002545:Brain Ischemia / Q000517:prevention & control*; D002315:Cardiopulmonary Bypass; D002560:Cerebrovascular Circulation; D004285:Dogs; D016166:Free Radical Scavengers / Q000008:administration & dosage* / Q000627:therapeutic use; D008353:Mannitol / Q000008:administration & dosage* / Q000627:therapeutic use; D009536:Niacinamide / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use; D010477:Perfusion / Q000379:methods; D013997:Time Factors
D016166:Free Radical Scavengers; D009536:Niacinamide; D008353:Mannitol; C042625:nicaraven