Effect of intrathecal nimodipine on spinal cord blood flow and evoked potentials in the normal or injured cord

Imamura, Hiroyuki; Tator, Charles H.

doi:10.1038/sj.sc.3100662

Cited by 14 publications

(5 citation statements)

References 22 publications

(38 reference statements)

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“…There have been many studies on the effects of intrathecal administration of various drugs on SCBF. 10,11 Nimodipine has been investigated as a treatment for SCI. It had previously been shown that systemic nimodipine causes severe hypotension after SCI.…”

Section: Discussionmentioning

confidence: 99%

“…12 Thus, intrathecal administration of nimodipine did not prevent the hypotension encountered with systemic administration and exerted no beneficial effect on SCBF after acute SCI. 11 Papaverine has been used to protect the spinal cord from ischemic damage while operating on the descending or thoracoabdominal aorta. It was administered Figure 1 Spinal cord blood flow (SCBF) over time as assessed by the laser flow blood perfusion monitor.…”

Section: Discussionmentioning

confidence: 99%

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Effect of intrathecal papaverine on blood flow and secondary injury in injured cord

et al. 2008

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Study design: Experimental laboratory investigations with a model of neurotrauma in Macaca rhesus. Object: The present study evaluates whether intrathecal papaverine induces changes in spinal cord blood flow (SCBF) of injured spinal cord and prevents secondary injury. Setting: Institute of Spinal Cord Injury, Sun Yat-sen University, China. Methods: After laminectomy was performed and contusive spinal cord injuries were induced in adult female Macaca rhesus, three received intrathecal papaverine, and three received saline 0.9% for control. SCBF was registered by laser-Doppler recording technique continuously for 180 min after injection. Histological analyses and microvessel density (MVD) were used for evaluation of spinal cord injury, and the percentage of spared spinal cord area was calculated. Results: Mean arterial blood pressure showed no significant change in both groups. In the papaverine group, SCBF recovered to 81.35±7.8% of baseline at 15 min, 75.24±6.3% at 30 min, 73.38±2.3% at 90 min and 72.57 ± 4.1% at 180 min after the completion of infusion. SCBF was significantly higher than the control groups (Po0.01). There was no occlusion of the arteries, but occluded veins were identified at the injured site. The MVD in the spinal cord of the control group was significantly lesser than the papaverine group (Po0.01). Luxol Fast Blue staining showed that intrathecal papaverine reduced myelin loss in the lesion 2 weeks after injury (Po0.05). Conclusion: Intrathecal administration of papaverine increased SCBF in non-human primates. It is likely that the effects of papaverine can reduce secondary injury in spinal cord injured Macaca rhesus.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effect of intrathecal papaverine on blood flow and secondary injury in injured cord

et al. 2008

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“…However, several studies in rats using clip compression injury have demonstrated bene®cial eects on evoked potentials after drug treatments. 7,35,43 To check the lesion severity and evoked potential responses, we performed a preliminary study using the same aneurysm clip (50 g) for 1 min compression injury, and we were not able to analyse the amplitudes because of the large number of absent responses; thus the compression time was chosen to be 30 s. In our study, decline in the amplitudes if SSEPs occurred after clip compression signi®cantly improved in highdose magnesium treated group. However, the decreased amplitudes did not recover in saline treated and low-dose magnesium treated groups.…”

Section: Discussionmentioning

confidence: 98%

“…31 ± 33 Calcium antagonists have been shown to increase blood¯ow in the brain and spinal cord, and decrease cellular toxicity; thus, they have been extensively studied in spinal cord trauma. 1,7,33,35 Neuroprotective eects of magnesium has been shown in experimental models of permanent focal cerebral ischemia, transient global ischemia, spinal cord ischemia, traumatic brain injury, topically induced quinolinate hippocampal neurodegeneration, perinatal postasphyxial brain damage, and delayed cerebral vasospasm after subarachnoidal haemorrhage.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of magnesium on lipid peroxidation and axonal function after experimental spinal cord injury

et al. 1999

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Study design: An experimental study examining the neuroprotective eect of magnesium on axonal function and lipid peroxidation in a rat model of acute traumatic spinal cord injury. Objective: To determine the eectiveness of postinjury treatment with magnesium on evoked potentials and lipid peroxidation after spinal cord injury (SCI). Setting: Pamukkale University, Denizli, Turkey. Methods: Spinal cord injury occurred in 30 rats with an aneurysm clip at T9 and the rats were randomly assigned to undergo subcutaneous administration of one of the following at 1 h after injury: (1) Physiological saline (n=10); (2) MgSO 4 , 300 mg/kg (n=10) and (3) MgSO 4 , 600 mg/kg (n=10). Spinal somatosensory evoked potentials (SSEPs) were recorded before injury, 30 min after injury and 3 h after injections. Rats were killed 24 h after the injury, and malondialdehyde (MDA) levels were measured. Results: Following SCI, there were signi®cant decreases in the amplitudes of P1 and N1 (P50.001) and only high-dose magnesium improved the SSEPs (P50.01). On the other hand, there was signi®cant dierence in lipid peroxide content between high-dose magnesium treated group and both of saline treated and low-dose magnesium treated groups (P50.01). Conclusion: These results suggest that magnesium has a dose-dependent neuroprotective eect on SSEPs and lipid peroxidation after experimental spinal cord injury.

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“…It is known that calcium channel blockers have positive effects on microcirculation and spinal perfusion after SCI. Calcium channel blockers have been shown to increase blood flow in the spinal cord after trauma in many studies [5, 6]. They selectively inhibit peripheral vasodilatation by acting on CNS veins and prevent ischemic deficits.…”

Section: Discussionmentioning

confidence: 99%

The effects of barnidipine on an experimental ischemia reperfusion model of spinal cord injury and comparison with methyl prednisolone

Daltaban

Mısır

Türksoy

et al. 2018

North Clin Istanbul

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OBJECTIVE: Increased intracellular calcium concentration plays an important role in the secondary mechanism of spinal cord injury. In the presenting experimental study, we aimed to evaluate the healing effect of barnidipine, which has a high affinity for L-type calcium channels, on acute spinal cord injury and to compare its effects with those of methylprednisolone. METHODS: A total of 32 Spraque Dawley albino adult female rats were divided into 4 groups; group 1: sham-operated (n=8), group 2: only ischemia (n=6), group 3: barnidipine-treated (n=8), and group 4: methylprednisolone-treated (n=6). An ischemia-reperfusion model was created by clipping the abdominal aorta in the rats. Motor examination was performed 1 hour after the surgical procedure and before sacrification. Immediately following the second motor examination, rats were sacrificed and tissue samples were taken for histopathological examination and for testing of tissue malondialdehyde (MDA) levels. RESULTS: A significant correlation of motor examination was found between the sham-operated and barnidipine-treated groups and the sham-operated and only ischemia groups at the 1 st and 24 th hour (p<0.008). There was no significant difference between the only ischemia and barnidipine-treated groups and only ischemia and methylprednisolone-treated groups (p>0.008). Light microscopic examination of the sham-operated group revealed findings consistent with normal spinal cord structure. In group 2, 3, and 4, light microscopic examination revealed polymorphonuclear leukocyte infiltration and a small amount of axonal swelling. There was no significant correlation between the ischemia and barnidipine-treated groups and the barnidipine and methylprednisolone groups in terms of MDA levels (p>0.008). CONCLUSION: A single dose of barnidipine (10 mg/kg) and methylprednisolone are not effective and not sufficient to prevent spinal ischemia-reperfusion injury in rats.

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Effect of intrathecal nimodipine on spinal cord blood flow and evoked potentials in the normal or injured cord

Cited by 14 publications

References 22 publications

Effect of intrathecal papaverine on blood flow and secondary injury in injured cord

Effect of intrathecal papaverine on blood flow and secondary injury in injured cord

Neuroprotective effect of magnesium on lipid peroxidation and axonal function after experimental spinal cord injury

The effects of barnidipine on an experimental ischemia reperfusion model of spinal cord injury and comparison with methyl prednisolone

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