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J Thorac Cardiovasc Surg 1995;109:1173-1181
© 1995 Mosby, Inc.


CARDIOPULMONARY BYPASS,
MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Pharmacologic intervention for ischemic brain edema after retrograde cerebral perfusion

Naoki Yoshimura, MD, Masayoshi Okada, MD, Toshiaki Ota, MD, Hideaki Nohara, MD


Kobe, Japan

From the Department of Surgery, Division II, Kobe University, School of Medicine, Kobe, Japan.

Received for publication April 21, 1994. Accepted for publication Sept. 19, 1994. Address for reprints: Naoki Yoshimura, MD, Department of Surgery, Division II, Kobe University, School of Medicine, 7-5-2, Kusunoki-cho, Chuo-ku, Kobe 650, Japan.

Abstract

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. Therefore cerebral protection via pharmacologic agents is recommended to prevent neurologic complications during aortic arch operations with the use of retrograde cerebral perfusion. (J THORAC CARDIOVASC SURG 1995;109:1173-81)




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