DOXYCYCLINE REDUCES EARLY NEUROLOGIC IMPAIRMENT AFTER CEREBRAL ARTERIAL AIR-EMBOLISM IN THE RABBIT

Citation
Dk. Reasoner et al., DOXYCYCLINE REDUCES EARLY NEUROLOGIC IMPAIRMENT AFTER CEREBRAL ARTERIAL AIR-EMBOLISM IN THE RABBIT, Anesthesiology, 87(3), 1997, pp. 569-576
Citations number
55
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00033022
Volume
87
Issue
3
Year of publication
1997
Pages
569 - 576
Database
ISI
SICI code
0003-3022(1997)87:3<569:DRENIA>2.0.ZU;2-N
Abstract
Background: Previous studies indicate leukocytes play a role in the pa thogenesis of cerebral arterial air embolism. Because doxycycline inhi bits numerous leukocyte activities, the authors hypothesized doxycycli ne would decrease neurologic impairment after cerebral arterial air em bolism. Methods: New Zealand White rabbits anaesthetized with methohex ital received either intravenous saline (n = 7) or 10 mg/kg doxycyclin e (n = 7) 1 h before administration of 100 mu l/kg of air into the int ernal carotid artery. Somatosensory-evoked potentials (SSEPs) were rec orded at 30-min intervals for the next 2 h. After the final recording, the anesthetic was discontinued, and animals recovered. Animals were neurologically evaluated 4 h after air embolism on a scale of 0 (norma l) to 99 (coma) points. Results: At 4 h, doxycycline animals had lesse r neurologic impairment (46 +/- 23; median, 41) than animals that rece ived saline (77 +/- 20; median, 81); P = 0.007. SSEP amplitude was gre ater in the doxycycline group at 60, 90, and 120 min after air embolis m; P = 0.001, 0.006, 0.026, respectively. SSEP amplitudes at 30, 60, 9 0, and 120 min inversely correlated with 4 h neurologic impairment; pi = -0.43, -0.75, -0.85, -0.79, respectively. Conclusions: Doxycycline decreased electrophysiologic and neurologic abnormalities after cerebr al air embolism. Because groups could be distinguished electrophysiolo gically as soon as 1 h after air embolism and because SSEP amplitude i nversely correlated with neurologic impairment, doxycycline appears to inhibit a key early (similar to 1 h) process in the pathophysiology o f cerebral air embolism.