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

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. To first...

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Bibliographic Details
Published in:Stroke (1970) 1996-02, Vol.27 (2), p.303-310
Main Authors: Ryu, K H, Hindman, B J, Reasoner, D K, Dexter, F
Format: Article
Language:English
Subjects:
Animals
Anticoagulants - therapeutic use
Behavior, Animal - drug effects
Blood Pressure
Consciousness - drug effects
Cranial Nerves - drug effects
Cranial Nerves - physiopathology
Embolism, Air - drug therapy
Embolism, Air - physiopathology
Gait - drug effects
Heparin - therapeutic use
Intracranial Embolism and Thrombosis - drug therapy
Intracranial Embolism and Thrombosis - physiopathology
Motor Activity - drug effects
Rabbits
Respiration - drug effects
Space life sciences
Time Factors
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Summary: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. 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. 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). When given prophylactically, heparin decreases neurological impairment caused by severe cerebral arterial air embolism.
ISSN:0039-2499
1524-4628
DOI:10.1161/01.STR.27.2.303