putrescine/edema

The neurotoxin 2-chloropropionic acid (2CPA, 750 mg/kg, per os) induces ataxia in rats causing neuropathological changes (necrosis and edema) localized mainly in the cerebellum (CB). It has been described that putrescine (PUT) is a good marker of severe brain damage. We measured the concentration of

After treatment with putrescine (PUT) 200 mg/kg, i.p., male rats displayed a behavioural pattern that included wet dog shakes and motor inco-ordination. The concentration of PUT in the brain paralleled the severity of clinical signs. Histological examination showed the presence of perivascular edema

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

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

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,

The effect of putrescine on oleic acid-induced RDS were studied in rat, it was found that preadministration of putrescine to rat with RDS significantly improved its hypoxemia, pulmonary edema and histologic injury; inhibited the leakage of protein from plasma; lowered increase of pulmonary lipid

OBJECTIVE To explore the effect of exogenous putrescine on renal function and cell apoptosis in rats. METHODS Ninety SD rats were randomized into control group (n=10), high-dose putrescine group (P1 group, n=40), and low-dose putrescine group (P2 group, n=40) with intraperitoneal injections of 2 ml

OBJECTIVE To explore the influence of exogenous putrescine on the function of liver and apoptosis of liver cells in rats. METHODS Ninety healthy clean SD rats were divided into control group (C, n = 10, intraperitoneally injected with 2 mL normal saline), low dosage putrescine group (LP, n = 40),

Brain polyamines have been associated with posttraumatic vasogenic edema and blood-brain barrier (BBB) breakdown seen in some models of brain injury. We hypothesized that the inhibition of the enzyme responsible for polyamine production with the decarboxylase difluoromethylornithine (DFMO) may

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

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.

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

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

Polyamines are derived from ornithine by the actions of ornithine decarboxylase (ODC), which is the rate-limiting step in this pathway. Polyamines play a role in cell growth, neoplasia, differentiation, and response to injury. We have shown that transient cerebral ischemia gives rise to increased

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