Number Of Normal Motor Neurons Research Articles

Protective Effect of Catechin Hydrate on Spinal Cord Ischemia-reperfusion Injury in Rats

Background: Aortic artery stenosis leads to Ischemia-Reperfusion (I-R) injury, which can cause certain clinical expressions, such as paraplegia. Objectives: To appraise the effect of Catechin Hydrate (CH) against spinal cord I-R injury. Materials & Methods: A total of 35 male rats (250-300 g) were divided randomly into five groups: intact, sham surgery, dimethyl sulfoxide (I-R+DMSO), low-dose CH (I-R+10 mg/kg CH), and high-dose CH (I-R+20 mg/kg CH). Abdominal aorta clamping was done for 60 min. Seventy-two hours after I-R, animals were evaluated for neurologic function, biochemical analysis, and histology. The data analysis was conducted by SPSS v. 16 using ANOVA and Kruskal-Wallis and Mann-Whitney U tests. Results: The mean Motor Deficit Index (MDI) score and white matter damage in the CH (20 mg/kg) group were lower than in the DMSO group (P=0.032). The mean plasma levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the CH groups were lower than that of the DMSO group (P<0.05). The plasma level of Total Antioxidant Capacity (TAC) in the CH (20 mg/kg) group was higher than in the DMSO group (P=0.032). In addition, the plasma level of catalase in the CH (20 mg/kg) group was higher than in the DMSO and CH (10 mg/kg) groups (P<0.001). The average number of normal motor neurons in the experimental groups was lower than in the sham surgery group (P<0.001).

Profound Hypotension before Aortic Clamping Can Exacerbate Spinal Cord Ischemic Injury after Aortic Surgery in Rats.

Spinal cord ischemia is one of the most serious complications of aortic repair in patients with acute aortic syndrome. However, the effect of hypotension before aortic clamping on spinal cord injury has not been documented. A total of 48 male Sprague-Dawley rats were randomly divided into four groups: the sham group; control group (mean arterial pressure (MAP) < 90% of baseline value before aortic clamping); mild hypotension group (MAP < 80%); and profound hypotension group (MAP < 60%). Spinal cord ischemia was induced using a balloon-tipped catheter placed in the descending thoracic aorta. Neurological function of the hind limbs was evaluated for seven days after reperfusion and recorded using a motor deficit index (MDI). The spinal cord was then harvested for histopathological examination and evaluation of oxidative stress and inflammation. The profound hypotension group demonstrated a significantly higher MDI 48 h post-reperfusion and lower number of normal motor neurons than the other groups (p < 0.001). The levels of tissue malondialdehyde and tumor necrosis factor-α (TNF-α) were also significantly increased in the profound hypotension group compared with other groups. Profound hypotension before aortic clamping can aggravate neurologic outcomes after aortic surgery by exacerbating neurologic injury and reducing the number of normal motor neurons.

Protective effect of lutein on spinal cord ischemia-reperfusion injury in rats.

Objective(s):Paraplegia is deterioration in motor or sensory function of the lower limbs that can occur after modification of a thoracoabdominal aortic aneurysm. The purpose of this survey was to determine the protective action of lutein on spinal cord ischemia-reperfusion (I-R) damage. Materials and Methods:Thirty-five male rats were distributed into five groups: intact, sham, dimethyl sulfoxide (I-R+DMSO), low dose lutein (I-R+0.2 mg/kg lutein), and high dose lutein (I-R + 0.4 mg/kg lutein). Thirty minutes before surgery, a single dose lutein or DMSO was administered to rats of experimental groups. Next, the abdominal aorta was clamped exactly under the left renal artery and proximal to the abdominal aortic bifurcation for 60 min. All animals were evaluated by neurological function and histological and biochemical examinations at 72 hr after I-R.Results:The mean motor deficit index (MDI) scores in lutein groups were lower compared with the DMSO group (P<0.001). Plasma level of malondialdehyde in lutein groups decreased compared with the DMSO group (P<0.05). Plasma level of total antioxidative capacity was increased in the high lutein group compared with low dose lutein and sham groups (P<0.05). Mean number of normal motor neurons in lutein groups was greater compared with the DMSO group (P<0.001). There was a significant negative correlation between MDI scores and the number of normal neurons (r= -0.764, P<0.001).Conclusion:Findings of the present study demonstrate that lutein may support spinal cord neurons from I-R damage.

Protective Effect of Contralateral, Ipsilateral, and Bilateral Remote Ischemic Preconditioning on Spinal Cord Ischemia Reperfusion Injury in Rats.

To evaluate the effect of different remote ischemic preconditioning (RIPC) methods in spinal cord ischemia-reperfusion (IR) injury. A total of 36 rats were distributed to the 6 groups: sham surgery, control (only spinal cord IR), unilateral (hind limb RIPC before spinal cord IR), bilateral (hind limbs RIPC before spinal cord IR), ipsilateral (hind and fore limbs RIPC to the right before spinal cord IR), contralateral (right hind limb and left fore limb as RIPC before spinal cord IR). Thirty minutes after RIPC, the spinal cord was subjected to ischemia for 60 minutes. Seventy two hours after IR, all rats were evaluated by neurological function, histological and biochemical examinations. The mean Motor Deficit Index (MDI) scores in the ipsilateral, contralateral, and bilateral groups were lower than that of the unilateral group (p < 0.05). The mean malondialdehyde (MDA) in ipsilateral group was lower than were control group (p < 0.05). The mean total antioxidant capacity (TAC) and the mean number of normal motor neurons in the experimental groups were significantly higher than increased control group (p < 0.05). The mean plasma levels of catalase in the contralateral, ipsilateral, and bilateral groups were significantly increased compared to control group (p < 0.05). The mean scores of white matter damage in contralateral, bilateral, and unilateral groups were lower than control group (p < 0.05). The results of this study show that contralateral, ipsilateral, and bilateral limb RIPC may reduce the complications of spinal cord ischemic injury.

The attenuation of neurological injury from the use of simvastatin after spinal cord ischemia-reperfusion injury in rats

BackgroundSpinal cord ischemic injury remains a serious complication of open surgical and endovascular aortic procedures. Simvastatin has been reported to be associated with neuroprotective effect after spinal cord ischemia-reperfusion (IR) injury. The aim of this study was to determine the therapeutic efficacy of starting simvastatin after spinal cord IR injury in a rat model.MethodsIn adult Sprague-Dawley rats, spinal cord ischemia was induced using a balloon-tipped catheter placed in the descending thoracic aorta. The animals were then randomly divided into 4 groups: group A (control); group B (0.5 mg/kg simvastatin); group C (1 mg/kg simvastatin); and group D (10 mg/kg simvastatin). Simvastatin was administered orally upon reperfusion for 5 days. Neurological function of the hind limbs was evaluated for 7 days after reperfusion and recorded using a motor deficit score (MDS) (0: normal, 5: complete paraplegia). The number of normal motor neurons within the anterior horns of the spinal cord was counted after final MDS evaluation. Then, the spinal cord was harvested for histopathological examination.ResultsGroup D showed a significantly lower MDS than the other groups at post-reperfusion day 1 and this trend was sustained throughout the study period. Additionally, a greater number of normal motor neurons was observed in group D than in other groups (group D 21.2 [3.2] vs. group A: 15.8 [4.2]; group B 15.4 [3.4]; and group C 15.5 [3.7]; P = 0.002).ConclusionsThe results of the current study suggest that 10 mg/kg can significantly improve neurologic outcome by attenuating neurologic injury and restoring normal motor neurons after spinal cord IR injury.

Protective effect of aqueous spinach (Spinacia oleracea L.) extract on spinal cord ischemia-reperfusion injury in rats.

Operation on the thoraco-abdominal aorta may lead to paraplegia or paraparesis is after spinal ischemia/reperfusion (I/R) injury. In this study, we investigated the protective effect of the spinach extract on spinal cord I/R injury. Thirty-five male Sprague-Dawley rats were divided into five groups: Intact, sham surgery, normal saline (NS), low dose spinach extract (20 mg kg-1), high dose spinach extract (50 mg kg-1). Neurological function, biochemical and histological evaluations were performed in 72 hr after ischemia. The mean motor deficit index scores of the spinach extract groups were significantly lower than in the NS group at 72hr after spinal cord ischemia. In addition, Spinach extract groups significantly increased plasma level of total antioxidative capacity and decreased the plasma level of malondialdehyde than the NS group. The spinach extract groups displayed a significantly large number of normal motor neurons compared with the NS group. In conclusion, the present study showed that the spinach extract may preserve more neurons in a rat model of spinal cord I/R injury.

Effects of drug volume on the model for regional drug protection against spinal cord ischemiareperfusion injury in rabbits

Objective To compare the effects of different drug volume on the model for regional aorta-infused drug protection against spinal cord ischemia-reperfusion injury in rabbits.Methods Spinal cord ischemia model was induced in New Zealand white rabbits by infrarenal abdominal aorta occlusion with a balloon catheter for 30 min.Another polycarbonate catheter was inserted into the abdominal aorta with the tip close to the site of occlusion via the femoral artery.During the ischemic period,nothing (V0 group) or different volume (1.5,3.0 or 6.0 ml/kg) of normal saline containing methylene blue (V1.5,V3 and V6 groups) was consecutively infused into the occluded aortic segments via the polycarbonate catheter at different rate of 3.0,6.0,or 12.0 ml/(kg·h).The bilateral common iliac arteries were clamped simultaneouly to prevent drug solution leakage.Thirty min later,blood flow was regained for reperfusion.The change of mean aortic pressure distal to the occluded site was measured throughout the operation.Neurological function was assessed according to the modified Tarlov scales at the moment of palinesthesia and 6,24 and 48 h after reperfusion.Lumbar segements of the spinal cord (L4-5) were harvested at 48 h after reperfusion for histopathologic evaluation,and the total number of normal motor neurons in the anterior horn was counted.Results The abdominal aorta was not completely occluded in V6 group.In V3 and V6 groups,the distal aortic pressure during ischemia was higher than in V0 and V1.5 groups with (41.0 ± 5.5) and (49.4 ± 4.5) vs.(17.9±2.6) and (22.5±1.7) mmHg [1 mmHg=0.133kPa,P＜0.05],while the difference value between ischemia and the first 10 min of reperfusion was lower than in V0 and V1.5 groups with (44.9±8.9)and (32.3±9.4) vs.(62.5±6.3) and (61.8±4.5) mmHg (P＜0.05).Tarlovscores were higher in V6 group than in V0 group at all intervals (P ＜ 0.05).The number of normal motor neurons was greater in V6 group than in V0 group with 10 (5.0-12.0) vs.0 (0-4.5) (P＜0.05).There was no significant difference between other groups and V0 group (P ＞ 0.05).Conclusion Drug volume lower than 3 ml/kg can ensure the model stability of spinal cord injury when infused into the occluded aortic segments during the ischemic period.The optimal volume was 1.5 ml/kg. Key words: Spinal cord ischemia; Reperfusion injury; Arterial infusions; Models,animal

A peroxisome proliferator-activated receptor gamma agonist attenuates neurological deficits following spinal cord ischemia in rats

Neuroprotective effects of the peroxisome proliferator-activated receptor gamma (PPARγ) agonist in cerebral ischemia have been reported, but the effect of a PPARγ agonist on spinal cord ischemia has not been investigated. The objective of this study was to investigate the effect of a PPARγ agonist on spinal cord ischemia. Pioglitazone, a PPARγ agonist, was administered in a rat model of spinal cord ischemia, and the extent of neurological damage and histological alterations were assessed. Forty-five rats were randomly enrolled into one of the three groups: (1) pioglitazone group (group PIO): rats were treated with pioglitazone 24 hours before ischemia; (2) control group (group C): rats were treated with the same volume of saline 24 hours before ischemia; and (3) sham group (group sham): rats were treated with the same volume of saline 24 hours before the sham surgery. Spinal cord ischemia was induced using a balloon-tipped catheter placed on the proximal descending aorta. Neurologic function was assessed using the motor deficit index (0 = normal, 6 = complete paralysis) during the 48 hours after reperfusion. Histological and biochemical evaluations were then performed. Compared with group C, group PIO presented with lower motor deficit index 48 hours after reperfusion (5.0 [4.0-6.0] vs 3.0 [2.0-3.0]; group C vs group PIO, respectively; P < .001). Group PIO presented with a higher number of normal motor neurons (10.7 [8.1-11.9] vs 14.7 [14.0-15.3]; group C vs group PIO, respectively; P = .009) and a smaller area of infarcts (48.4% [46.3%-54.0%] vs 16.8% [11.5%-18.3%]; group C vs group PIO, respectively; P = .009) when compared with group C. The degree of inflammatory reactions, assessed by microglia activities, was significantly reduced in group PIO. Oxidative stress level, assessed using malonydialdehyde assay, was significantly reduced in group PIO relative to group C (192.21% [173.5%-206.4%] of sham vs 141.1% [131.7%-152.1%] of sham; group C vs group PIO, respectively; P = .007). The sham group exhibited no abnormality upon neurological or histological examination. PPARγ agonist pioglitazone pretreatment significantly reduces infarct volume and attenuates neurological deficits following spinal cord ischemia. The possible mechanism of neuroprotection by PPARγ agonist may involve modulation of inflammatory reaction and oxidative stress.

Neuroprotection following mild hypothermia after spinal cord ischemia in rats

We examined the hypothesis that a 1°C reduction in body temperature would reduce gray and white matter injury induced by spinal cord ischemia in rats. In addition, we evaluated the relationship between reactive astrogliosis and gray or white matter injury after spinal cord ischemia with a 1°C reduction in body temperature or normothermia. Rats were randomly divided into hypothermia (1°C decrease in body temperature to 36.3°C), normothermia (37.3°C), and sham surgery groups (n=6/group). Hypothermia was induced 15 minutes before ischemia and maintained during ischemia. Animals were then rewarmed to normothermia. Spinal cord ischemia was induced by a balloon catheter in the thoracic aorta, and the proximal mean arterial blood pressure was maintained at 40 mm Hg for 14 minutes. Hind limb motor function was assessed at 2, 7, 14, 21, and 28 days after reperfusion. At 28 days after reperfusion, gray matter damage was assessed by counting the number of normal motor neurons and white matter damage by the extent of vacuolation. The glial fibrillary acidic protein (GFAP)-positive area fraction (GFAP%) was determined in white and gray matter structures to measure reactive astrogliosis. Compared with normothermia, hypothermia significantly improved hind limb function at all assessments (P<.01) and increased numbers of normal gray matter motor neurons (39±20 vs 99±13, respectively; P<.001), decreased the percentage area of white matter vacuolation (9.0%±2.7% vs 1.6%±1.3%, respectively; P=.001), and decreased the GFAP% in gray (P=.003) and white matter (P=.009). Prophylactic mild hypothermia (1°C reduction in body temperature) preserved hind limb motor function and reduced neuronal death, white matter vacuolation, and astrogliosis in gray and white matter induced by spinal cord ischemia in rats. Thus, mild hypothermia may be useful for perioperative management of thoracoabdominal aortic surgery.

Effect of Pretreatment With Simvastatin on Spinal Cord Ischemia-Reperfusion Injury in Rats

The aim of this study was to evaluate the pretreatment effect of simvastatin on spinal cord ischemia-reperfusion injury. Prospective, interventional study. University research laboratory. Forty-five male Sprague-Dawley rats. Rats were treated with oral simvastatin, 10 mg/kg (simvastatin group; n = 15) or saline (control group; n = 15) for 5 days before ischemia. Spinal cord ischemia was induced using a balloon-tipped catheter placed in the proximal descending aorta in the control and simvastatin groups, but not in the sham group (n = 15). Neurologic function was assessed daily using the motor deficit index until 7 days after reperfusion. After the last neurologic evaluation, a histologic examination of the spinal cord was performed. At day 1 after reperfusion, the simvastatin group showed a significantly lower motor deficit index compared with the control group (2.0, 2.0-2.0, v 4.0, 3.5-5.0; p < 0.001). This trend was sustained at day 7 (2.0, 1.5-2.0, v 4.0, 3.0-4.0; p < 0.001). The simvastatin group displayed a significantly larger number of normal motor neurons compared with the control group (mean ± SD, 31.7 ± 6.1 v 20.4 ± 4.4; p < 0.001). However, compared with the sham group, the simvastatin group displayed fewer intact motor neurons (sham group, 38.5 ± 5.1; p = 0.005). Pretreatment with simvastatin, 10 mg/kg, given orally for 5 days before the ischemia-reperfusion insult, improved the neurologic outcome and preserved more normal motor neurons compared with the control group in a rat model of spinal cord ischemia-reperfusion.

Magnesium Sulfate Does Not Protect Spinal Cord Against Ischemic Injury

ABSTRACTObjective: We tested various doses of MgSO4 to investigate the effect of Mg on a spinal cord ischemia. Methods: Rats were treated with either MgSO4 (30, 100, or 300 mg/kg; group Mglow, group Mgmedium, group Mghigh, respectively, n = 10 for each) or saline (control group; n = 10) before ischemia. Spinal cord ischemia was induced using a balloon-tipped catheter placed on proximal descending aorta. During surgery, hemodynamic variables were recorded before ischemia, during aortic occlusion and after reperfusion. Neurologic function was assessed using the motor deficit index (MDI; 0 = normal, 6 = complete paralysis) until seven days after reperfusion, and histologic examination of spinal cord was performed. Results: After reperfusion, the mean arterial pressure in the group Mghigh was significantly lower than other groups. Compared to the control group, the groups Mglow and Mgmedium did not show any difference in MDI and the group Mghigh showed significantly higher MDI. The number of normal motor neurons was similar among other groups except the group Mghigh had a significantly fewer normal motor neurons. Conclusions: Intravenous MgSO4 with low or medium dose (30, or 100 mg/kg) did not improve neurological injury following spinal cord ischemia. Furthermore, higher dose of MgSO4 (300 mg/kg) resulted in hemodynamic instability and aggravated neurologic outcome.

New method for absolute spinal cord ischemia protection in rabbits

This study aims to establish a superior procedure to prevent spinal cord damage after severe spinal cord ischemia during aortic surgery. We examined the synergistic effect of topical hypothermia of the spinal cord combined with radical scavenger infusion into the clamped segment of the aorta to prevent spinal cord damage in an animal model. Spinal cord ischemia was induced in rabbits by clamping the aorta between the renal artery and aortic bifurcation for 30 minutes. Rabbits were divided into four groups of 16 each: group I, sham-operated; group II, edaravone (6 mL, 4°C, 1 mg/kg); group III, saline (6 mL, 4°C) with transvertebral cooling pads; group IV, edaravone (6 mL, 4°C, 1 mg/kg) and transvertebral cooling pads. Solutions were injected into the clamped segment of the aorta. Postoperative assessments included the Tarlov score, spinal cord histopathology, and measurement of malondialdehyde levels in the spinal cord tissue. At 48 hours after reperfusion, the mean Tarlov scores in groups I, II, III, and IV were 4.0, 1.5, 1.9, and 4.0, respectively. The mean number of normal motor neurons was significantly higher in groups I (54.1) and IV (53.7) than in groups II (32.8) and III (36.3; P < .001). The mean malondialdehyde level in groups I (19.8 nmol/mL) and IV (22.6 nmol/mL) was significantly lower than in groups II (64.8 nmol/mL) and III (60.9 nmol/mL; P < .001). At 168 hours after reperfusion, the mean Tarlov scores in groups I, II, III, and IV were 4.0, 1.1, 1.3, and 4.0, respectively. The mean number of normal motor neurons was significantly higher in groups I (52.9) and IV (50.8) than in groups II (22.4) and III (25.9; P < .001). The mean malondialdehyde level in groups I (20.7 nmol/mL) and IV (23.4 nmol/mL) was significantly lower than in groups II (68.9 nmol/mL) and III (61.6 nmol/mL; P < .001). In a rabbit model with aortic clamping up to 30 minutes, which consistently produces complete paraplegia in rabbits, spinal cord damage was partially reduced by topical cooling with transvertebral cooling pads or the injection of edaravone into the clamped segment of aorta, but was more effectively protected by a combined use of these two strategies.

Effect of repeated hyperbaric oxygen preconditioning on expression of hypoxia-inducible factor-1 alpha and erythropoietin following spinal ischemia-reperfusion in rats

Objective To investigate the effect of repeated hyperbaric oxygen preconditioning (HOP) on the expression of hypoxia-inducible factor-1 alpha (HIF-1a) and erythropoietin (EPO) following spinal ischemiareperfusion (I/R) in rats. Methods Forty-eight male SD rats weighing 250-300 g were randomly divided into 3 groups (n = 16 each): sham operation group (S group); I/R group and repeated HOP group (HOP group). The animals in HOP group were pretreated with O2 ( ＞ 98 % ) at 2.5 ATA I h/d for 5 consecutive days at 24 h before spinal cord I/R. The animals were anesthetized with intraperitoneal pentobarbital sodium 35 mg/kg. Spinal cord ischemia was produced by cross-clamping of abdominal aorta distal to renal artery for 20 min in I/R and HOP groups. Hind-limb motor function was assessed and scored st 48 h of reperfusion. The animals were then sacrificed and the L5-7 segment of the spinal cord was removed for determination of the expression of HIF-1 α and EPO mRNA and protein and microscopic examination. Results Compared with group S, the hind-limb motor function scores and the number of normal motor neurons in the anterior horn of the spinal cord were significantly decreased, and the expression of HIF-1α and EPO mRNA and protein was up-regulated in I/R and HOP groups ( P ＜ 0.05). Compared with group I/R, the hind-limb motor function scores and the number of normal motor neurons in the anterior horn of the spinal cord were significantly increased, and the expression of HIF-1α and EPO mRNA and protein was up-regulated in group HOP ( P ＜ 0.05). The spinal cord injury was attenuated in group HOP compared with group I/R. Conclusion Repeated HOP can reduce the spinal cord I/R injury though up-regulating the expression of HIF1α and EPO in rats. Key words: Hyperbaric oxygenation; Ischemic preconditioning; Hypoxia-inducible factor 1, alpha subunit; Erythropoietin; Reperfusion injury; Spinal cord

Delayed preconditioning effect of isoflurane on spinal cord ischemia in rats

Paraplegia is one of the most common complications following aortic aneurysmal surgery. This study was designed to determine if isoflurane-induced delayed preconditioning is mediated by nuclear factor kappaB (NF-kappaB) in the rat spinal cord. The animals were divided into four groups: the control group, the pyrrolidinedithio carbamate (PDTC, an NF-kappaB inhibitor)-treated group, the isoflurane-treated group, and the PDTC/isoflurane-treated group. In the PDTC-treated groups, 2% 100mg/kg PDTC was administered intraperitoneally at 1h before operation and at 24h and 48 h after reperfusion. The rats in the isoflurane-treated groups received 30 min inhalation of 2.8% isoflurane at 24h before spinal cord ischemia. Pretreatment with NF-kappaB inhibitor significantly reduced NF-kappaB expression and the number of intact motor neurons when compared to the control group. Preconditioning with isoflurane increased the number of normal motor neurons, whereas pretreatment with both PDTC and isoflurane significantly decreased them, compared to the isoflurane-treated group. Isoflurane-induced delayed preconditioning on spinal cord ischemia improved histopathological outcomes. This neuroprotective effect of isoflurane preconditioning on spinal cord ischemia is associated with NF-kappaB expression.

The adverse effect of back-bleeding from lumbar arteries on spinal cord pathophysiology in a rabbit model

The purpose of this study was to evaluate the adverse effect of back-bleeding from the lumbar arteries on spinal cord pathophysiology in a rabbit model. White rabbits were divided into 3 groups. Through laparotomy, the abdominal aorta was clamped below the renal artery and above the aortic bifurcation for 15 minutes. In group 1 (n = 13), back-bleeding from the lumbar arteries was drained from the aorta during aortic clamping. In group 2 (n = 10), back-bleeding was not drained. Group 3 (n = 6) was the sham-operated group. Postoperative hind limb function was evaluated using the modified Tarlov scale, and cell damage was analyzed by counting the number of intact motor neurons and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive neurons. At 4 hours after operation, all animals were neurologically impaired in group 1 and normal in group 2. Motor neurons were significantly damaged in group 1 compared with groups 2 and 3 (P < .05). Forty-eight hours later, almost all animals were neurologically and pathologically damaged in groups 1 and 2. There was no difference in the number of normal motor neurons between the two groups, but the number of TUNEL-positive cells in group 2 was significantly larger than those in group 1. Rabbits with 15-minute aortic clamping in the infrarenal portion showed delayed paraplegia, and those with back-bleeding from lumbar arteries showed early onset of paraplegia. The prevention of back-bleeding from intercostal arteries and lumbar arteries during thoracoabdominal aortic surgery was considered to reduce spinal ischemic injury.

Intra-aortic injection of propofol prevents spinal cord injury during aortic surgery☆

We investigated whether propofol, a widely used anesthetic, injected into clamped aortic segments quickly attenuated transcranial spinal motor-evoked potential (MEP) amplitudes and protected against spinal cord injury during thoracoabdominal aortic surgery. Eighteen beagle dogs were divided into three groups (n=6, each group): group 1 (20 ml of saline, intra-aortic injection), group 2 (1.5 mg/kg of propofol, intravenous injection), and group 3 (1.5 mg/kg of propofol, intra-aortic injection). Aortic cross-clamping was performed for 30 min. In each group, MEP amplitudes were recorded before, during, and after aortic cross-clamping. Tarlov score and histopathological examination were used to evaluate the protective effects of intra-aortic propofol injections. MEP amplitudes in group 3 attenuated to a value that was 60% of the control in just a minute after aortic cross-clamping, but maintained 40% of the control value during aortic cross-clamping. However, MEP amplitudes in groups 1 and 2 gradually attenuated and almost disappeared. Groups 1 and 2 amplitudes were lower than those in group 3, 30 min after aortic cross-clamping (p<0.001). Twenty-four hours after ischemia, the Tarlov score in group 3 was 3.5+/-0.5 and was higher than scores from groups 1 and 2, which were 0.5+/-0.5 and 1.3+/-1.2 (mean+/-SD, p<0.001, and p<0.001), respectively. Histopathologically, normal spinal cord motor neurons in group 3 were preserved to a significantly greater extent than in groups 1 and 2 (p=0.0031, and p=0.0282, respectively). There was a strong correlation between Tarlov scores at 24h and the number of normal motor neurons in the anterior horns of spinal cords (r=0.897; p<0.001). Intra-aortic propofol injections produce the quick suppression of MEP amplitudes and protect spinal cords from ischemia during aortic cross-clamping.