Treatment of acute spinal cord injuries: comparison of thyrotropin-releasing hormone and nimodipine

İlbay, Konuralp; Baykal, Süleyman; Ceylan, Savaş; Şener, Uğur; Ozmenoglu, M.; Kalelioğlu, Müfit; Aktürk, Fadil; Komşuoğlu, Sezer; Ozoran, A

doi:10.1007/bf02576254

Cited by 18 publications

(11 citation statements)

References 23 publications

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“…(C) A significant correlation was detected between lesion volume values obtained with the two methods (P < 0.05, regression ANOVA). a variety of experimental models of CNS trauma in a number of species (Akdemir et al, 1993;Arias MJ, 1987;Behrmann et al, 1994;Ceylan et al, 1990Ceylan et al, , 1992Faden, 1989Faden, , 1993Faden et al, 1981Faden et al, , 1990Fukuda et al, 1979;Puniak et al, 1991;Takami et al, 1991;Wang and Zhu, 1991). A small clinical study confirmed these beneficial effects in human spinal cord injury (Pitts et al, 1995).…”

Section: Figmentioning

confidence: 99%

Neuroprotective and Nootropic Actions of a Novel Cyclized Dipeptide after Controlled Cortical Impact Injury in Mice

Faden

Fox

et al. 2003

J Cereb Blood Flow Metab

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Summary: 1-ARA-35b (35b) is a cyclized dipeptide that shows considerable neuroprotective activity in vitro and improves neurologic recovery after fluid percussion-induced traumatic brain injury in rats. The authors evaluated the effects of treatment with 35b in mice subjected to controlled cortical impact brain injury. Animals treated with intravenous 35b after traumatic injury showed significantly enhanced recovery of beam walking and place learning functions compared with vehicle-treated controls, in addition to reduced lesion volumes. Beneficial effects were dose related and showed an inverted U-shaped dose-response curve between 0.1 and 10 mg/kg. Protective actions were found when the drug was administered initially at 30 minutes or 1, 4, or 8 hours, but not at 24 hours, after trauma. In separate experiments, rats treated with 35b on days 7 through 10 after injury showed remarkably improved place learning in comparison with injured controls. These studies confirm and extend the neuroprotective effects of this diketopiperazine in traumatic brain injury. In addition, they show that 35b has a relatively wide therapeutic window and improves cognitive function after both acute and chronic injury.

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Section: Figmentioning

confidence: 99%

Neuroprotective and Nootropic Actions of a Novel Cyclized Dipeptide after Controlled Cortical Impact Injury in Mice

Faden

Fox

et al. 2003

J Cereb Blood Flow Metab

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“…OFR and intracellular trypsin activation are the key factors in the pathogenesis of acute pancreatitis [8,13,17]. However, the side effect of the CCB is a decrease in blood pressure [2] and results in ischemia of the pancreas [8,13]. We observed in our study that the use of CCB caused hypotension in sham and pancreatitis groups.…”

Section: Discussionmentioning

confidence: 82%

“…Nimodipine as a CCB (Nimotop produced by Bayer, Istanbul) was given 0.02 mg/kg per hour for 6 h intravenously [2]. Infusion syringes were protected from light with aluminium foil because of the photosensitivity of nimodipine.…”

Section: Modelmentioning

confidence: 99%

The effects of calcium channel blocker and thyrotropin releasing hormone on acute necrotizing pancreatitis in rats

et al. 1999

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The main purpose of this study was to investigate the influence of nimodipine, a calcium channel blocker (CCB) and thyroid-releasing hormone (TRH) on acute necrotizing pancreatitis (ANP) induced by glycodeoxycholic acid in rats. CCB decreased blood pressure in rats in the control and pancreatitis groups. TRH corrected this decrease. CCB alone had no effect on PO2 serum amylase activity, calcium concentration, liver transaminases, lactate dehydrogenase or the degree of pancreatic damage, except for the serum concentration of creatinine. CCB+TRH reduced the concentrations of serum urea and creatinine, the degree of pancreatic damage, and increased PO2 and serum calcium concentration. CCB and CCB+TRH had no effect on pancreatic myeloperoxidase activity. CCB alone had no effect on the course of ANP, but CCB+TRH had beneficial effects on the course of the ANP and various systems.

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“…7,9,10 In our opinion, failure to counteract post-traumatic hypotension was an important reason for the lack of improvement seen with nimodipine in some studies of spinal cord injury. 5,6,8,11,13,17 In our laboratory, when adjuvant therapy was given to counteract post-traumatic hypotension, nimodipine produced an improvement in SCBF. 7,9,10 For example, when adrenalin was used to maintain the posttraumatic MABP at a normal level, there was 60% recovery of SCBF with nimodipine.…”

Section: Introductionmentioning

confidence: 82%

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

Imamura

Tator

1998

Spinal Cord

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A method was developed for administering intrathecal pharmacotherapy in a rat model of spinal cord injury. The eects of intrathecal administration of nimodipine on spinal cord blood¯ow (SCBF) and evoked potentials (EPs) were measured in the normal and injured spinal cord. It had previously been shown that systemic nimodipine caused severe hypotension after spinal cord injury. After baseline SCBF and EPs, 15 uninjured rats were blindly allocated to one of three groups: one placebo group (n=5); and two groups with intrathecal nimodipine, 0.05 mg/kg (n=5), or 0.2 mg/kg (n=5). Ten other rats received a 35 g acute clip compression injury of the spinal cord for 1 minute and, were allocated to one of two groups: placebo (n=5); and intrathecal nimodipine 0.05 mg/kg (n=5) given 60 min after injury. In the uninjured groups, neither 0.05 nor 0.2 mg/kg of nimodipine increased SCBF during, or 30 min after, intrathecal infusion. However, the mean arterial blood pressure (MABP) decreased signi®cantly to 69.73.1% after the infusion of 0.2 mg/kg nimodipine and did not recover by 98 min. In all three groups of uninjured rats, the amplitude of the cerebellar EP was decreased 30 min after infusion. After spinal cord injury, there were signi®cant decreases in MABP, SCBF and EP amplitude in both placebo and treatment groups, but there was no therapeutic bene®t from nimodipine. Thus, intrathecal infusion of nimodipine did not prevent the hypotension encountered with systemic administration and exerted no bene®cial eect on SCBF or EPs after acute spinal cord injury.

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Treatment of acute spinal cord injuries: comparison of thyrotropin-releasing hormone and nimodipine

Cited by 18 publications

References 23 publications

Neuroprotective and Nootropic Actions of a Novel Cyclized Dipeptide after Controlled Cortical Impact Injury in Mice

Neuroprotective and Nootropic Actions of a Novel Cyclized Dipeptide after Controlled Cortical Impact Injury in Mice

The effects of calcium channel blocker and thyrotropin releasing hormone on acute necrotizing pancreatitis in rats

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

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