Effect of Steroid Therapy on Ischaemic Brain Oedema and Blood to Brain Sodium Transport

Betz, A. Lorris; Coester, Hans C.

doi:10.1007/978-3-7091-9115-6_86

Cited by 14 publications

(12 citation statements)

References 11 publications

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“…The neuroprotective efficacy of PROG in functional and morphological recovery has been confirmed both permanent and transient stroke models by our recent studies (Sayeed et al, 2006; 2007) and previous studies of others (Betz and Coester, 1990; Jiang et al, 1996; Chen et al, 1999; Murphy et al, 2002; Gibson and Murphy, 2004; Gibson et al, 2005). In addition to animal studies, two recent randomized, double-blind, placebo-controlled clinical trials using 3 or 5 days of intravenous PROG to treat patients with moderate to severe traumatic brain injury (TBI) demonstrated both safety and efficacy compared to patients given standard of care treatment plus placebo (Wright et al, 2007; Xiao et al, 2008).…”

Section: Introductionsupporting

confidence: 67%

Effects of progesterone administration on infarct volume and functional deficits following permanent focal cerebral ischemia in rats

et al. 2009

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Recent experimental evidence indicates that progesterone (PROG) protects against various models of brain injury, including ischemic stroke. Most human studies of pharmacologic treatments for acute cerebral stroke have failed despite initial success in animal models. To simulate better the typical human stroke without reperfusion, the present study was conducted to examine the efficacy of PROG on infarct volume and functional outcome in a permanent model of stroke, using direct cauterization of the middle cerebral artery (MCA). Twenty-four male adult Sprague-Dawley rats underwent pMCAO by electro-coagulation and sham operation. After induction of permanent MCA occlusion (pMCAO), the rats received an initial intraperitoneal injection of PROG (8 mg/kg) or vehicle at 1h post-occlusion followed by subcutaneous injections at 6, 24 and 48 h. Functional deficits were tested on the rotarod and grip strength meter at 24, 48 and 72 h after pMCAO. The rats were killed 72 h after surgery and isolated brain was sectioned into coronal slices and stained with 2, 3, 5-triphenyltetrazolium chloride (TTC). PROG-treated rats showed a substantial reduction (54.05%) in the volume of the infarct (% contralateral hemisphere) compared to vehicle controls. In addition there was a significant improvement in ability to remain on an accelerating rotarod and increased grip strength observed in the pMCAO rats treated with PROG compared to vehicle. Taken together, these data indicate that PROG is beneficial in one of the best-characterized models of stroke, and may warrant further testing in future clinical trials for human stroke.

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Section: Introductionsupporting

confidence: 67%

Effects of progesterone administration on infarct volume and functional deficits following permanent focal cerebral ischemia in rats

et al. 2009

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“…23,24 Although wet to dry measurements did not differ between groups, we found that PRO tended to reduce ratios of both ipsilateral and contralateral cerebral hemispheres compared with VEH. Interestingly, brains of sham animals had a greater wet weight than either injured group.…”

Section: Commentscontrasting

confidence: 55%

Neuroprotective effects of progesterone in traumatic brain injury: blunted in vivo neutrophil activation at the blood-brain barrier

Pascual

Murcy

et al. 2013

The American Journal of Surgery

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BACKGROUND Progesterone (PRO) may confer a survival advantage in traumatic brain injury (TBI) by reducing cerebral edema. We hypothesized that PRO reduces edema by blocking polymorphonuclear (PMN) interactions with endothelium (EC) in the blood-brain barrier (BBB). METHODS CD1 mice received repeated PRO (16 mg/kg intraperitoneally) or vehicle (cyclodextrin) for 36 hours after TBI. Sham animals underwent craniotomy without TBI. The modified Neurological Severity Score graded neurologic recovery. A second craniotomy allowed in vivo observation of pial EC/PMN interactions and vascular macromolecule leakage. Wet/dry ratios assessed cerebral edema. RESULTS Compared with the vehicle, PRO reduced subjective cerebral swelling (2.9 ± .1 vs 1.2 ± .1, P <.001), PMN rolling (95 ± 1.8 vs 57 ± 2.0 cells/100 μm/min, P <.001), total EC/PMN adhesion (2.0 ± .4 vs .8 ± .1 PMN/100 μm, P <.01), and vascular permeability (51.8% ± 4.9% vs 27.1% ± 4.6%, P <.01). TBI groups had similar a Neurological Severity Score and cerebral wet/dry ratios (P > .05). CONCLUSIONS PRO reduces live pericontusional EC/PMN and BBB macromolecular leakage after TBI. Direct PRO effects on the microcirculation warrant further investigation.

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“…However, the ability of mannitol to reduce ICP is fairly unpredictable and temporary. Corticosteroids can reduce oedema 14,15 but are ineffective in improving outcome in experimental and clinical studies and may even worsen outcome 16 . Barbiturates have not been extensively shown to reduce oedema or ICP 17 and may only be of limited and brief efficacy 18 and appear to only be protective at doses high enough to depress spontaneous respiration 19 .…”

Section: Cerebral Oedemamentioning

confidence: 99%

Inhibition of Neurogenic Inflammation as a Novel Treatment for Ischemic Stroke

Turner¹,

Vink²

2007

Drug News &Amp; Perspectives

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Each year, 15 million people suffer a stroke, of which 5 million die and 5 million are left permanently disabled. Cerebral swelling is of particular concern following stroke as it accounts for much of the death and disability. However, the mechanisms leading to cerebral swelling are not yet fully understood. Recent studies from our laboratory suggest that neuropeptides, and specifically substance P, may be involved in the injury processes that occur following acute insults to the brain such as stroke and trauma, and may be responsible, in part, for edema formation. Levels of substance P are increased following CNS injury, indicative of neurogenic inflammation, and this is associated with injury to the blood-brain barrier, the development of cerebral edema, cell death and functional deficits. Subsequent studies inhibiting neuropeptide release have consistently shown decreased cerebral edema and improved neurological outcome, while substance P antagonists administered after the insult are efficacious in reducing post-stroke cerebral edema and neurological deficits. The current review summarizes the evidence supporting the benefits of inhibiting neurogenic inflammation to treat ischemic stroke.

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Effect of Steroid Therapy on Ischaemic Brain Oedema and Blood to Brain Sodium Transport

Cited by 14 publications

References 11 publications

Effects of progesterone administration on infarct volume and functional deficits following permanent focal cerebral ischemia in rats

Effects of progesterone administration on infarct volume and functional deficits following permanent focal cerebral ischemia in rats

Neuroprotective effects of progesterone in traumatic brain injury: blunted in vivo neutrophil activation at the blood-brain barrier

Inhibition of Neurogenic Inflammation as a Novel Treatment for Ischemic Stroke

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