(Stroke. 1998;29:2396-2403.)
© 1998 American Heart Association, Inc.
Original Contributions |
Angiographic and Histological Evaluation of Porcine Retinal Vascular Damage and Protection With Perfluorocarbons After Massive Air Embolism
From the Center for Bioengineering (J.I.H.); the Division of Cardiothoracic Surgery, Department of Surgery (K.S.K., C.V., R.P.C.); and the Division of Cardiothoracic Anesthesiology, Department of Anesthesiology (B.D.S.), University of Washington, Seattle, Washington.
Correspondence to Janelle I. Herren, MSE, Mail Stop RLT-04, Rt 120 and Wilson Rd, Round Lake, IL 60073. E-mail herrenj{at}baxter.com
Background and Purpose—We have previously shown that perfluorocarbon emulsions (PFEs) reduce the severity of cerebral injury (indicated by infarct, reduced blood flow, and depressed EEG) induced by air embolism during cardiopulmonary bypass (CPB). This study used retinal fluorescein angiography to define the mechanisms of cerebral injury and to determine the efficacy of PFEs in cerebral protection. These angiographic findings were correlated to previously reported histologic findings.
Methods—Twenty domestic pigs underwent CPB with a prime of standard crystalloid or PFE (5 mg/kg) and crystalloid. After 10 minutes on CPB, a single (5 mL/kg) or double (2x2.5 mL/kg) bolus of room air or saline (control) was delivered via the right carotid artery. Retinal fluorescein angiograms were captured at 4 time points: baseline, air insult, postbypass, and postreperfusion. Following euthanasia, both eyes were removed and the retinas isolated for histological analysis with horseradish peroxidase (HRP), as previously reported.
Results—In control pigs, postreperfusion angiograms showed small nonperfused areas, and retinal whole mounts demonstrated vascular damage as previously reported. In 5 PFE-primed animals, postreperfusion angiograms showed hyperfluorescence, but angiograms and HRP mounts were otherwise not significantly different from baseline. Severely hyperfluorescent vessels observed angiographically also showed a correlation with HRP extravasation but were not consistently indicative of severe vascular damage.
Conclusions—Retinal fluorescein angiography and retinal staining with HRP indicate that mechanisms of cerebral air embolism include nonperfusion, vascular leakage and spasm, red blood cell sludging, and hemorrhage. Priming with PFE prevented many of the sequelae associated with air embolism.
Editorial Comment
Department of Internal Medicine, Cardiovascular Division, University of Iowa College of Medicine, Iowa City, Iowa
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