polyamine/edema

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Effects of MDL 72527, a specific inhibitor of polyamine oxidase, on brain edema, ischemic injury volume, and tissue polyamine levels in rats after temporary middle cerebral artery occlusion.

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The possible effects of the polyamine interconversion pathway on tissue polyamine levels, brain edema formation, and ischemic injury volume were studied by using a selective irreversible inhibitor, MDL 72527, of the interconversion pathway enzyme, polyamine oxidase. In an intraluminal suture

Suppression of polyamine biosynthesis prevents monocrotaline-induced pulmonary edema and arterial medial thickening.

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Previous work in our laboratory has shown that the continuous administration of alpha-difluoromethylornithine (DFMO), a highly specific irreversible inhibitor of ornithine decarboxylase (ODC), which is the rate-limiting enzyme in polyamine biosynthesis, prevented the development of pulmonary

Blood brain barrier breakdown in brain edema following cold injury is mediated by microvascular polyamines.

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A focal freeze injury to rat cerebral cortex induces an early (less than 5 min) increase in brain ornithine decarboxylase activity and an accumulation of polyamines involving cerebral microvessels. This polyamine synthesis correlates with the abnormal increase in microvascular permeability,

Attenuation of brain edema, blood-brain barrier breakdown, and injury volume by ifenprodil, a polyamine-site N-methyl-D-aspartate receptor antagonist, after experimental traumatic brain injury in rats.

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OBJECTIVE Traumatic brain injury (TBI) has been shown to induce a significant change in polyamine metabolism. Polyamines and polyamine-dependent calcium influx play an important role in mediating the effects of excitotoxic amino acids at the N-methyl-D-aspartate (NMDA) receptor site. We studied the

Polyamines induce blood-brain barrier disruption and edema formation in the rat.

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Polyamines (PA) are derived from ornithine by the enzyme ornithine decarboxylase (ODC), which is activated very rapidly as acute and delayed responses to brain ischemia and trauma. Polyamines play a role in the disruption of the blood-brain barrier (BBB) in different pathological states. This study

Effect of ifenprodil, a polyamine site NMDA receptor antagonist, on brain edema formation following asphyxial cardiac arrest in rats.

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OBJECTIVE Brain edema occurs in experimental and clinical cardiac arrest (CA) and is predictive of a poor neurological outcome. N-Methyl--aspartate (NMDA) receptors contribute to brain edema elicited by focal cerebral ischemia/reperfusion (I/R). Ifenprodil, a NMDA receptor antagonist, attenuates

The induction of erythema, edema, and the polyamine synthesis enzymes ornithine decarboxylase and S-adenosyl-L-methionine decarboxylase in hairless mouse skin by psoralens and longwave ultraviolet light.

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Melatonin attenuates the changes in polyamine levels induced by systemic kainate administration in rat brains.

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Systemically administered kainate has been demonstrated to induce neuronal damage and changes of the levels of biochemical substances related to neurotoxicity. Polyamines are thought to be important in the generation of edema and neuronal cell loss associated with various type of excitotoxicity.

Radiation brain injury is reduced by the polyamine inhibitor alpha-difluoromethylornithine.

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Alpha-difluoromethylornithine (DFMO) was used to reduce 125I-induced brain injury in normal beagle dogs. Different DFMO doses and administration schedules were used to determine if the reduction in brain injury was dependent on dose and/or dependent upon when the drug was administered relative to

Polyamine synthesis blockade in monocrotaline-induced pneumotoxicity.

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Based on the documented regulatory role of polyamines in cell growth and differentiation, we have proposed that these organic cations are involved with the development of monocrotaline (MCT)-induced hypertensive pulmonary vascular disease. Two lines of evidence support this hypothesis: (1) MCT

[Effect of polyamines on indices of oxygen toxicity in rats].

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The intraperitoneal administration of polyamines to rats before hyperbaric oxygenation decreases the rate of development of hyperoxic convulsions, prevents lung edema and stabilizes blood cell membranes.

Simultaneous assay of ornithine decarboxylase and polyamines after central nervous system injury in gerbil and rat.

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Ornithine decarboxylase (ODC) is considered the rate-limiting enzyme in polyamine biosynthesis. An increase in putrescine (a natural polyamine) synthesis after central nervous system (CNS) injury appears to be involved in blood-brain barrier dysfunction, development of vasogenic edema and neuronal

Regional distribution of ornithine decarboxylase activity and polyamine levels in experimental cat brain tumors.

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Biosynthesis of the polyamines putrescine, spermidine, and spermine, and activation of the first key enzyme ornithine decarboxylase (ODC) are closely associated with cellular proliferation. In the present study, the distribution of ODC activity and polyamine levels was investigated for the first

Regional activity of ornithine decarboxylase and edema formation after traumatic brain injury.

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This study examined ornithine decarboxylase (ODC) activity and edema formation bilaterally in brain cortices and hippocampi after lateral controlled cortical-impact injury in rats. To measure the activity of ODC, the brains of injured and control rats were frozen in situ at 30 minutes and at 6, 24,

Effect of difluoromethylornithine treatment on regional ornithine decarboxylase activity and edema formation after experimental brain injury.

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This study examined the effect of difluoromethylornithine (DFMO) on regional activities of ornithine decarboxylase (ODC) and edema formation in bilateral cerebral cortex and hippocampus after a unilateral controlled cortical-impact (CCI) injury in rats. To measure the activity of ODC, the brains of

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