Magnetic resonance imaging study on the effect of levemopamil on the size of intracerebral hemorrhage in rats.

Elger, Bernd; Seega, Jürgen; Brendel, Ron

doi:10.1161/01.str.25.9.1836

Cited by 22 publications

(8 citation statements)

References 32 publications

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“…Although our data for nicardipine were in accordance with those previously reported for calcium and serotonin antagonists (Elger et al 1994;Rosenberg & Navratil 1994), these drugs have not been investigated for their effects on neurological deficits and blood pressure in this cerebral haemorrhage model. We examined the effects of nicardipine on neurological deficits 1 day after collagenase injection in the same intracerebral haemorrhage rats.…”

Section: Discussionsupporting

confidence: 89%

Nicardipine, a calcium antagonist, does not aggravate intracerebral haemorrhage in an intracerebral haemorrhage model in rats

Suzuki¹,

Hayashi²,

Sasamata³

2005

Journal of Pharmacy and Pharmacology

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Despite controversy over their safety in patients with intracerebral haemorrhage, calcium antagonists are widely used in the treatment of hypertensive emergencies. Here, we investigated the effects of nicardipine on haematoma size and neurological deficit in a rat model of collagenase-induced intracerebral haemorrhage. Injection of collagenase (0.014 U) into the striatum induced haematoma (19.9+/-3.4 mm(3)) in the striatum and brain oedema. Drugs were infused from 30 min after collagenase injection for 3 h under conscious conditions. Nicardipine intravenously at 0.1, 1 and 10 microg kg(-1) min(-1) affected neither haematoma size nor the degree of brain oedema. Nicardipine at these doses provided a stable and dose-dependent decrease in mean blood pressure of 6%, 13% and 33%, respectively, with an increase in heart rate that was apparently caused reflexively. Further, nicardipine did not aggravate the neurological deficits in these intracerebral haemorrhage rats, primarily forearm flexion behaviour on suspension by the tail and circling behaviour. These results indicate that nicardipine infusion stably decreased blood pressure without affecting intracerebral haemorrhage in an intracerebral haemorrhage model in rats.

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Section: Discussionsupporting

confidence: 89%

Nicardipine, a calcium antagonist, does not aggravate intracerebral haemorrhage in an intracerebral haemorrhage model in rats

Suzuki¹,

Hayashi²,

Sasamata³

2005

Journal of Pharmacy and Pharmacology

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“…Even though collagenase does not discriminate among different brain tissues, it produces massive bleeding and mortality, similar to that in human ICH. This model has been used extensively in investigations of ICH (Brown et al, 1995;DeBow et al, 2003;Del Bigio et al, 1996;Elger et al, 1994;Lyden et al, 1997;MacLellan et al, 2002;Matsushita et al, 2000;Rosenberg and Navratil, 1997;Rosenberg et al, 1992), including studies on the long-term deficits after collagenase-induced ICH (Chesney et al, 1995). Another animal model used to determine ICH pathophysiology and to evaluate therapeutic treatment (Andaluz et al, 2002) is the direct injection of autologous blood into the rat caudate nucleus (Nath et al, 1986), a model used in numerous studies (Bullock et al, 1984;Huang et al, 2002;Jiang et al, 2002;Mendelow, 1993;Nath et al, 1987;Thulborn et al, 1990;Xue and Del Bigio, 2000;Wu et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

MMP-9 Deficiency Enhances Collagenase-Induced Intracerebral Hemorrhage and Brain Injury in Mutant Mice

Tang

Zhou

et al. 2004

J Cereb Blood Flow Metab

160

141

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Summary:Matrix metalloproteinase-9 (MMP-9) participates in the disregulation of blood-brain barrier during hemorrhagic transformation, and exacerbates brain injury after cerebral ischemia. However, the consequences of long-term inhibition or deficiency of MMP-9 activity (which might affect normal collagen or matrix homeostasis) remains to be determined. The authors investigated how MMP-9 gene deficiency enhances hemorrhage and increases mortality and neurologic deficits in a collagenase-induced intracerebral hemorrhage (ICH) model in MMP-9-knockout mice. MMP-9-knockout and corresponding wild-type mice at 20 to 35 weeks were used to model an aged population (because advanced age is a significant risk factor in human ICH). Collagenase VII-S (0.5 L, 0.075 U) was injected into the right basal ganglia in mice and mortality, neurologic deficits, brain edema, and hemorrhage size measured. In addition, MMP-9 activity, brain collagen content, blood coagulation, cerebral arterial structure, and expressions of several MMPs were examined. Increased hemorrhage and brain edema that correlated with higher mortality and neurologic deficits were found in MMP-9-knockout mice. No apparent structural changes were observed in cerebral arteries, even though brain collagen content was reduced in MMP-9-knockout mice. MMP-9-knockout mice did exhibit an enhanced expression of MMP-2 and MMP-3 in response to ICH. The results indicate that a deficiency of MMP-9 gene in mutant mice increases collagenase-induced hemorrhage and the resulting brain injury. The intriguing relationship between MMP-9 deficiency and collagenase-induced ICH may reflect the reduction in collagen content and an enhanced expression of MMP-2 and MMP-3. Key Words: MMP-9-Intracerebral hemorrhage-Collagenase-Edema-Blood-brain barrier-Coagulation.Spontaneous intracerebral hemorrhage (ICH) is one of the most serious stroke events, and results in high mortality and morbidity in patients (Bernardini and DeShaies, 2001;Panagos et al., 2002;Woo and Broderick, 2002). Mortality in ICH is often as high as 50% within the first month after ICH, with 50% of these deaths occurring within 48 hours (Broderick, 1993). The mechanisms of ICH-induced early brain injury (e.g. brain edema) have been investigated (Altumbabic et al., 1998;Del Bigio et al., 1999;Xi et al., 2002); however, the complete etiology of early brain injury in ICH is incompletely understood.Matrix metalloproteinases (MMPs) are involved in the pathogenesis of cerebral vascular disorders, particularly the formation and rupture of aneurysms. For example, pro-MMP-2 has been implicated as a significant component within arterial walls of intracerebral aneurysms that leads to subarachnoid hemorrhage (Todor et al., 1998). Other studies also support elevated MMP (elastase and collagenase) activity in ruptured vessels in subarachnoid hemorrhage but not in unruptured aneurysms (Gaetani et al., 1999). MMPs are also involved in the hemorrhagic transformation after cerebral ischemia, especially after thrombolysis (Hosomi et al., 2001;M...

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“…A rat model of ICH involving the injection of collagenase into the brain ( Rosenberg et al 1990; Elger et al 1994) was used to examine the effect of TSC on hemorrhagic injury. Adult male Sprague-Dawley rats were anesthetized with Isoflurane and ventilated with Isoflurane using an FiO 2 of 50%.…”

Section: Methodsmentioning

confidence: 99%

Trans-sodium crocetinate improves outcomes in rodent models of occlusive and hemorrhagic stroke

et al. 2014

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Trans-sodium crocetinate (TSC) is a novel carotenoid compound capable of enhancing the diffusion of small molecules in aqueous solutions. TSC improves the diffusion of oxygen and glucose, and increases oxygenation in ischemic brain tissue. TSC also dampens the intensity of an ischemic challenge during an ongoing ischemic event. The current study examined the impact of TSC in rat models of ischemic and hemorrhagic stroke. Rat three vessel occlusion (3VO), and combined 3VO and one vessel occlusion (3VO/1VO) models of ischemic stroke were evaluated for structural and behavioral outcomes. The effects of TSC were also tested in a rat model of intracerebral hemorrhage (ICH). Delayed treatment with TSC reduced infarct volume in a rodent model of transient focal ischemia involving either 2 or 6 hours of ischemia. Neurological outcomes, based on a multi-scale assessment and automated gait analysis, also were improved by TSC treatment. Additionally, TSC reduced edema and hemorrhagic volume in a rat model of ICH. An optimal therapeutic candidate for early intervention in ischemic stroke should be effective when administered on a delayed basis and should not aggravate outcomes associated with hemorrhagic stroke. The current findings demonstrate that delayed TSC treatment improves outcomes in experimental models of both ischemic and hemorrhagic stroke. Together, these findings suggest that TSC may be a safe and beneficial therapeutic modality for early stroke intervention, irrespective of the type of stroke involved.

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Magnetic resonance imaging study on the effect of levemopamil on the size of intracerebral hemorrhage in rats.

Cited by 22 publications

References 32 publications

Nicardipine, a calcium antagonist, does not aggravate intracerebral haemorrhage in an intracerebral haemorrhage model in rats

Nicardipine, a calcium antagonist, does not aggravate intracerebral haemorrhage in an intracerebral haemorrhage model in rats

MMP-9 Deficiency Enhances Collagenase-Induced Intracerebral Hemorrhage and Brain Injury in Mutant Mice

Trans-sodium crocetinate improves outcomes in rodent models of occlusive and hemorrhagic stroke

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