HORSERADISH-PEROXIDASE AS A HISTOLOGICAL INDICATOR OF MECHANISMS OF PORCINE RETINAL VASCULAR DAMAGE AND PROTECTION WITH PERFLUOROCARBONS AFTER MASSIVE AIR-EMBOLISM
Ji. Herren et al., HORSERADISH-PEROXIDASE AS A HISTOLOGICAL INDICATOR OF MECHANISMS OF PORCINE RETINAL VASCULAR DAMAGE AND PROTECTION WITH PERFLUOROCARBONS AFTER MASSIVE AIR-EMBOLISM, Stroke, 28(10), 1997, pp. 2025-2030
Background and Purpose This laboratory has previously shown that a sec
ond-generation perfluorocarbon emulsion (PFE) reduces the severity of
cerebral injury induced by air embolism during cardiopulmonary bypass
(CPB). Horseradish peroxidase examines vascular permeability and was u
sed in this study of the mechanisms of cellular protection afforded by
the PFE. Methods Twenty domestic pigs underwent CPB with a prime of s
tandard crystalloid or PFE (5 mg/kg) and crystalloid. After 10 minutes
on CPB, a 5-mL/kg bolus of room air or saline (control) was delivered
via the right carotid artery. The air insult was delivered as either
a single bolus or double bolus. After 1 hour of CPB and 1 hour of spon
taneous reperfusion, horseradish peroxidase was injected intravenously
and circulated for 15 minutes. After euthanasia, both eyes were remov
ed, and the retinas were isolated for histological analysis. Results T
otal length of retinal vessels exhibiting horseradish peroxidase extra
vasation was significantly less in PFE pigs (P<.05). Vascular spasm an
d red blood cell hemorrhages were unaffected by PFE. PFE pigs exhibite
d mild to moderate vascular nonperfusion and red blood cell sludging;
crystalloid groups demonstrated severe nonperfusion and sludging. Conc
lusions Histological staining with horseradish peroxidase indicated th
at mechanisms of cerebral air embolism include vascular endothelial le
akage, vascular nonperfusion, and red blood cell sludging and hemorrha
ge. Pretreatment with PFE prevented some sequelae associated with mass
ive air embolism and CPB.