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Journal ArticleDOI

Doxycycline Reduces Early Neurologic Impairment after Cerebral Arterial Air Embolism in the Rabbit

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TLDR
Doxycycline decreased electrophysiologic and neurologic abnormalities after cerebral air embolism and appears to inhibit a key early process in the pathophysiology of cerebral air Embolism.
Abstract
Background Previous studies indicate leukocytes play a role in the pathogenesis of cerebral arterial air embolism. Because doxycycline inhibits numerous leukocyte activities, the authors hypothesized doxycycline would decrease neurologic impairment after cerebral arterial air embolism. Methods New Zealand White rabbits anesthetized with methohexital received either intravenous saline (n = 7) or 10 mg/kg doxycycline (n = 7) 1 h before administration of 100 micro liter/kg of air into the internal carotid artery. Somatosensory-evoked potentials (SSEPs) were recorded 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 (normal) to 99 (coma) points. Results At 4 h, doxycycline animals had lesser neurologic impairment (46 +/- 23; median, 41) than animals that received saline (77 +/- 20; median, 81); P = 0.007. SSEP amplitude was greater in the doxycycline group at 60, 90, and 120 min after air embolism; P = 0.001, 0.006, 0.026, respectively. SSEP amplitudes at 30, 60, 90, and 120 min inversely correlated with 4 h neurologic impairment; tau = -0.43, -0.75, -0.85, -0.79, respectively. Conclusions Doxycycline decreased electrophysiologic and neurologic abnormalities after cerebral air embolism. Because groups could be distinguished electrophysiologically as soon as 1 h after air embolism and because SSEP amplitude inversely correlated with neurologic impairment, doxycycline appears to inhibit a key early ([approximately] 1 h) process in the pathophysiology of cerebral air embolism.

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Doxycycline Suppresses Microglial Activation by Inhibiting the p38 MAPK and NF-kB Signaling Pathways

TL;DR: The present results indicate that the effect of doxycycline on LPS-induced microglial activation probably occurs via the modulation of p38 MAP kinase and NF-kB signaling pathways, and support the idea that doxy cycline may be useful in preventing or slowing the progression of PD and other neurodegenerative diseases that exhibit altered glia function.
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Regional patterns of neuronal death after deep hypothermic circulatory arrest in newborn pigs

TL;DR: In neonates, neocortical and hippocampal neurons are selectively vulnerable to death after DHCA, suggesting the need for several neuroprotective strategies tailored to the region and death process, initiated during the operation and continued after the operation.
BookDOI

Tetracyclines in biology, chemistry, and medicine

TL;DR: Tetracyclines and CMTs modulate anti-inflammatory mediators such as IL-lO (mRNA level) and type II IL- l ~ decoy receptor (secretory enzyme level), which make them candidate drugs for complex multifactoral inflammatory diseases.
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Brain injury after adult cardiac surgery.

TL;DR: The incidence of brain injury may be reduced by modifying the surgical procedure according to carotid duplex scanning and epiaortic echocardiography, by using techniques to reduce microembolization during cardiopulmonary bypass and by optimizing patient temperature during and after surgery.
References
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TL;DR: Data suggest that endothelium-derived NO may be an important endogenous modulator of leukocyte adherence and that impairment of NO production results in a pattern ofLeukocyte adhesion and emigration that is characteristic of acute inflammation.
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The impact of microemboli during cardiopulmonary bypass on neuropsychological functioning

TL;DR: It is suggested that neuropsychological deficits after routine cardiopulmonary bypass are related to the number of microemboli delivered during surgery, and the numbers of microEmboli may be reduced by including a 40‐&mgr;m filter on the arterial line.
Journal ArticleDOI

Oxygen radicals induce human endothelial cells to express GMP-140 and bind neutrophils.

TL;DR: Exposure of endothelial cells to oxygen radicals induces the prolonged expression of GMP-140 on the cell surface, which results in enhanced PMN adherence, and the effect of oxidants on this process was examined by treating human endothelial Cells with H2O2, t-butylhydroperoxide, or menadione.
Journal ArticleDOI

Coexpression of GMP-140 and PAF by endothelium stimulated by histamine or thrombin: a juxtacrine system for adhesion and activation of neutrophils.

TL;DR: A complex cell recognition system in which tethering of PMNs by a selectin, GMP-140, facilitates juxtacrine activation of the leukocytes by a signaling molecule, PAF is defined.
Journal ArticleDOI

Correlation between myeloperoxidase-quantified neutrophil accumulation and ischemic brain injury in the rat. Effects of neutrophil depletion.

TL;DR: Depletion of neutrophils by RP3 treatment completely inhibited the increase in MPO activity in the ischemic brain after 24 hours of reperfusion and significantly attenuated the postischemic increase in brain water content at 24 hours after reperfusions.
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Does doxycycline affect platelets?

Doxycycline decreased electrophysiologic and neurologic abnormalities after cerebral air embolism.