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Heparin reduces neurological impairment after cerebral arterial air embolism in the rabbit
Journal article   Open access   Peer reviewed

Heparin reduces neurological impairment after cerebral arterial air embolism in the rabbit

Keon Hee Ryu, Bradley J Hindman, Daniel K Reasoner and Franklin Dexter
Stroke, Vol.27(2), pp.303-310
1996
DOI: 10.1161/01.STR.27.2.303
PMID: 8571428
url
https://doi.org/10.1161/01.STR.27.2.303View
Published (Version of record) Open Access

Abstract

BACKGROUND AND PURPOSE: Neurological injury after cerebral air embolism may be due to thromboinflammatory responses at sites of air-injured endothelium. Because heparin inhibits multiple thromboinflammatory processes, we hypothesized that heparin would decrease neurological impairment after cerebral air embolism. METHODS: To first establish a dose of air that would cause unequivocal neurological injury, anesthetized New Zealand White rabbits received either 0, 50, 100, or 150 microL/kg of air into the internal carotid artery (n = 5 in each group). One hour later, anesthesia was discontinued. Animals were neurologically evaluated at 24 hours with the use of a scale ranging from 0 (normal) to 97 (coma) points. In a subsequent experiment, anesthetized rabbits received either heparin (n = 17) or saline (n = 15) 5 minutes before air injection (150 microL/kg). Heparin was given as a 200-IU/kg bolus and followed by a constant infusion of 75 IU.kg-1.h-1 for 2 hours. Equal volumes of saline were given to control rabbits. Two hours later, anesthesia was discontinued. Animals were neurologically evaluated 24 hours after air embolism. RESULTS: There was a monotonic relationship between dose of air and severity of neurological impairment at 24 hours (P = 1.1 x 10(-7)). Animals receiving 150 microL/kg of air were unequivocally injured (score, 60 +/- 16). In the second experiment, heparin animals had significantly less neurological impairment at 24 hours (34 +/- 14) than saline controls (52 +/- 8) (P = .0013). CONCLUSIONS: When given prophylactically, heparin decreases neurological impairment caused by severe cerebral arterial air embolism.

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