生物羊膜移植治疗难治性角膜溃疡的护理

总结了18例生物羊膜移植治疗难治性角膜溃疡患者的护理,包括术前护理、术后护理、出院指导等,认为生物羊膜移植是治疗眼表疾病的有效方法,认真细致的护理是促进康复的重要措施.     

脊髓损伤后瘫痪肢体疼痛的康复护理

总结了1例脊髓损伤患者瘫痪肢体疼痛的康复护理经验,主要措施有:心理护理、病情观察及护理、肢体疼痛的观察及护理、肢体疼痛的预防、对家属的指导教育、出院后随访等,认为用正确的方法处理疼痛的肢体将对患者的康复起到积极的作用;患者肢体运动功能得到明显恢复;提高了生存质量;减轻了家庭和社会负担.     

脊髓损伤患者的舒适护理

总结了对31例脊髓损伤患者进行舒适护理的体会.阐述了对脊髓损伤患者实施生理、心理、社会、灵魂四方面舒适护理的具体措施,并指出运用舒适护理模式,对患者进行耐心细致的生活护理,心理护理,可使患者得到生理、心理的舒适.督促患者尽早康复训练,指导家属帮助患者积极锻炼,可使患者的康复治疗在愉快的氛围中完成,促进患者残障肢体的功能重建,防止并发症发生,提高生存和生活质量,使患者达到了社会、灵魂的舒适,早日回归家庭,回归社会.     

促吸收剂癸酸钠对黄连素在大鼠肠道吸收的促进作用

目的:探讨黄连素(Ber)在大鼠肠道的吸收动力学,阐明癸酸钠(SC)对Ber在小肠段吸收的影响.方法:雄性Wistar大鼠建立在体肠段灌流模型,HPLC法测定不同浓度Ber(50、100和200 μmol·L-1)和Ber与质量浓度为0.2%SC合用在小肠的吸收情况;测定肠灌流液中乳酸脱氢酶(LDH)活性,观察SC对肠道黏膜细胞的损伤.结果:Ber浓度在50～200 μmol·L-1范围内Ber吸收呈浓度依赖性;吸收速率常数(Ka)组间差异无统计学意义(P>0.05);SC能显著提高Ber在小肠的吸收量(P<0.05);SC对Ber吸收速率常数Ka无显著影响(P>0.05);Ber组、SC+Ber组肠循环液中LDH的含量与空白对照组比较差异无统计学意义(P>0.05).结论:Ber在小肠吸收较差,吸收机制为被动扩散,吸收过程为一级动力学过程;SC能显著促进Ber在小肠的吸收,是一种安全、有效的促吸收剂.     

浅谈脊髓损伤患者的临床护理

脊髓损伤是脊柱骨折的严重并发症,由于椎体的移位或碎骨片突出于椎管内,使脊髓或马尾神经产生不同程度的损害.主要表现为脊髓损伤平面以下的感觉运动障碍,反射异常及大小便失禁.对脊髓损伤病人加强护理,可以减少并发症,提高病人的生存质量和生活质量.     

脊髓损伤患者的排尿康复护理

目的 探讨脊髓损伤(sCI)患者进行排尿康复护理后的疗效.方法 对34例sCI患者在住院期间进行饮水计划和间歇导尿等康复护理的效果进行观察.结果 34例患者其中27例出院后能自解小便,7例出院后仍需进行饮水计划和间歇导尿.结论 饮水计划和间歇导尿等康复护理措施对脊髓损伤患者的排尿功能恢复有重要意义,值得临床推广.     

脊髓损伤致高位截瘫患者的护理对策

高位截瘫是横贯性病变发生在脊髓较高水平位上的,一般都会引起四肢瘫痪,是一种严重的创伤,如得不到妥善的护理,常因严重的并发症而死亡或常年卧床,因此对在护理高位截瘫患者中出现的患者心理异常、呼吸道低效、如何预防其他严重并发症的发生等常见问题进行分析,根据病人的临床特点制定切实可行的护理方法,使病人能够积极配合治疗及护理,让患者得到最大可能的康复是至关重要的.     

作业治疗对脊髓损伤患者日常生活活动能力的临床研究

目的:观察作业治疗(occupational therapy OT)对脊髓损伤(Spinal Cord injury SCI)患者日常生活活动能力(activities of daily living,ADL)的影响.方法:对45例脊髓损伤患者进行系统作业治疗,并对其治疗前、后的ADL评定结果进行分析.结果:治疗后ADL评定结果明显高于治疗前,差异有显著性P＜0.05.结论:作业治疗可以有效的提高脊髓损伤患者日常生活活动能力.     

早期康复治疗对脊髓损伤后痉挛性神经源性膀胱功能的影响

目的:探讨早期康复治疗对脊髓损伤后痉挛性神经源性膀胱功能的影响.方法:将60例外伤性脊髓损伤患者按康复介入开始时间分为早期康复组(术后1个月内)和对照组(术后3个月)各30例,分别在治疗前和治疗3个月后进行膀胱容量、残余尿量、尿路感染发生率进行测定,比较两组数据.结果:早期康复组患者膀胱容量增加、残余尿量减少、尿路感染发生率降低,且均优好于对照组(P<0.05).结论:早期康复治疗能有效改善脊髓损伤后痉挛性神经源性膀胱的排尿功能.     

脊髓损伤截瘫病人肠道功能训练的护理体会

总结帮助截瘫病人建立起反射性排便的护理.包括排便训练前评估,饮食的管理,肠道按摩方法,肛门刺激方法,排便时的体位配合,心理护理及排便情况的观察和记录.认为通过对脊髓损伤截瘫病人肠道功能训练,可以提高其生活质量,增加其在社交活动中的独立性,维持最佳的卫生状况,保持自尊及健康感.     

Recovery in rats after spinal cord injury

Previous studies from this laboratory have shown evidence of regeneration of long descending spinal motor tracts in rats after spinal cord transection and treatment to modify the animals' immune response. In this study, less extensive surgical lesions were combined with the most favorable drug treatment (75 mg per kilogram of cyclophosphamide in a single dose) in an effort to improve the prospects for regeneration. Less than complete spinal cord transections in the rat were frequently followed by clinical and electrophysiologic evidence of return of function. Such return of function appears to depend on a reorganization of the nervous system that results in the use of the few remaining fibers to transmit motor information rather than on regeneration. Immunosuppressive treatment had no effect on these results.     

Regional spinal cord blood flow in rats after severe cord trauma

Spinal cord blood flow (SCBF) was measured in 12 albino rats following acute cord injury produced by the extradural clip compression technique. Severe injury was produced with the clip compressing the cord with a force of 180 gm for 5 minutes, an injury previously shown to produce a severe functional deficit. Regional SCBF was measured 15 minutes, 2 hours, and 24 hours after injury by the 14C-antipyrine autoradiographic technique and a scanning microscope photometer. At 15 minutes and 2 hours, white and gray matter blood flow was severely diminished, and, at 24 hours, there was only minimal improvement. Focal decreases in blood flow were seen in white and gray matter for a considerable distance proximal and distal to the site of cord trauma. Thus, it has been confirmed in this model that severe cord compression injury produces severe posttraumatic ischemia in the cord which lasts for at least 24 hours.     

Spasticity in rats with sacral spinal cord injury

We have investigated sacral spinal cord lesions in rats with the goal of developing a rat model of muscular spasticity that is minimally disruptive, not interfering with bladder, bowel, or hindlimb locomotor function. Spinal transections were made at the S2 sacral level and, thus, only affected the tail musculature. After spinal transection, the muscles of the tail were inactive for 2 weeks. Following this initial period, hypertonia, hyperreflexia, and clonus developed in the tail, and grew more pronounced with time. These changes were assessed in the awake rat, since the tail is readily accessible and easy to manipulate. Muscle stretch or cutaneous stimulation of the tail produced muscle spasms and marked increases in muscle tone, as measured with force and electromyographic recordings. When the tail was unconstrained, spontaneous or reflex induced flexor and extensor spasms coiled the tail. Movement during the spasms often triggered clonus in the end of the tail. The tail hair and skin were extremely hyperreflexive to light touch, withdrawing quickly at contact, and at times clonus could be entrained by repeated contact of the tail on a surface. Segmental tail muscle reflexes, e.g., Hoffman reflexes (H-reflexes), were measured before and after spinalization, and increased significantly 2 weeks after transection. These results suggest that sacral spinal rats develop symptoms of spasticity in tail muscles with similar characteristics to those seen in limb muscles of humans with spinal cord injury, and thus provide a convenient preparation for studying this condition.     

The effects of aging on mu and delta opioid receptors in the spinal cord of Fischer-344 rats

The lordosis-inhibiting effects of the 5-HT1A receptor agonist, (+/-)8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), were examined in ovariectomized rats, hormone primed with 2.5, 7.5, or 25 micrograms estradiol benzoate plus 500 micrograms progesterone. 8-OH-DPAT (50, 100 or 200 ng per bilateral site) infused into the ventromedial nucleus of the hypothalamus (VMN), inhibited lordosis behavior in all hormone-treated conditions. However, animals primed with 2.5 micrograms estradiol benzoate were significantly more affected by the infusion than rats primed with 7.5 or 25 micrograms of the hormone. These findings strengthen prior speculations that 5-HT1A receptor function is modulated by estrogen.     

Alteration of thromboxane A2/prostacyclin and their effect on spinal cord blood flow in experimental spinal cord injury in rats

In order to document the contribution of Thromboxane (TXA2) and Prostacyclin (PGI2) to the secondary damage following spinal cord injury (SCI) and their effects on spinal cord blood flow (SCBF), the alteration of SCBF, TXB2 and 6-keto-PGF1 alpha concentration in injury site (T13-L1) and adjacent cords (upper: T12, under: L2) were studied using a rat SCI model induced by Allen's weight drop method (50g-cm). The result showed that after SCI the SCBF in injury site significantly reduced during 1-2 hrs and reduced further during 4-8 hrs. The SCBF in adjacent cords also decreased during 4-8 hrs. TXB2 levels significantly increased at 1 hr and reached peak value at 4 hrs. The 6-keto-PGF1 alpha concentration also significantly increased at 1 hr and maintained that level for 24 hrs. The TXB2/6-keto-PGF1 alpha ratio was significantly elevated at 1 hr and reached its peak at 4 hrs after SCI, then gradually decreased to the preinjury level during 8-24 hrs. The negative correlation of SCBF with TXB2 concentration and TXB2/6-keto-PGF1 alpha ratio were appeared. The experimental results indicated that the imbalance of TXB2/6-keto-PGF1 alpha could be the main cause of microcirculatory disturbance and secondary damage in SCI.     

Central nuclei and spinal pathways in feedback inhibitory spinal cord potentials in ketamine-anaesthetized rats

It has been suggested that heterosegmentally activated slow positive potentials (HSP), recorded from the spinal cord of rat and humans, are feedback inhibitory potentials. The present study was carried out to define ascending and descending spinal tracts and the sites of central nuclei involved in the production of these HSP, and the effects of ketamine on these central nuclei. The spinal cords in ketamine-anaesthetized rats were transected to determine the ascending and descending tracts involved in the production of hindpaw (HP) and forepaw (FP) HSP, respectively. Lesions of the brain at various levels were performed stereotactically during ketamine anaesthesia. Dorsal one-third resection of the cord at the T8-9 level did not affect HSP significantly, while contralateral lesion of the dorsal two-thirds of the cord decreased FP-HSP but not HP-HSP during ketamine. Bilateral transection of the ventral one-third of the cord abolished both HSP. Ablation of the cerebral cortex, cerebellum, thalamus, midbrain and pons did not affect HSP significantly. However, transection of the middle medulla decreased, while transection of the most caudal part of the medulla completely abolished both HSP. Ketamine decreased HSP even in the medulla-spinal cord preparation and the segmental slow positive wave in spinalized animals. In ketamine-anaesthetized rats, ascending and descending spinal tracts involved in the production of HP-HSP and FP-HSP are located bilaterally in the ventrolateral quadrant and in the contralateral lateral funiculus and ventrolateral quadrant, respectively. Principal central nuclei feeding back HSP might be situated diffusely in the medulla down to the caudal part. Ketamine is suggested to suppress these inhibitory feedback potentials predominantly at, and partly even below, the level of the medulla.     

Role of neutrophil elastase in compression-induced spinal cord injury in rats

Myeloperoxidase (MPO) is an essential component of the oxygen-dependent microbicidal system of neutrophils and monocytes. Hereditary deficiency of MPO occurs in 1 in 2,000 to 4,000 individuals in the general population and has been generally considered an autosomal recessive trait. Previous studies have used the peroxidase activity of blood leukocytes to assess the phenotype of affected family members. Eosinophil peroxidase (EPO) also contributes to the peroxidase activity of blood leukocytes. Because EPO expression is normal in MPO-deficient subjects, eosinophil contamination can significantly contribute to peroxidase activity in leukocytes from family members of an MPO-deficient subject and thereby undermine correct interpretation of the inheritance pattern. To avoid this potential problem, we used cytochemical, immunochemical, and genetic techniques to assess the inheritance pattern of MPO deficiency in sixteen individuals from five unrelated kindreds. Each kindred had an index case with MPO deficiency and the R569W missense mutation, a genotype that causes MPO deficiency. Our analysis demonstrated that MPO deficiency was not inherited as a simple autosomal recessive trait. Most subjects were compound heterozygotes with respect to the R569W mutation and demonstrated a spectrum of phenotypes. Our data demonstrate the broad phenotypic impact of compound heterozygosity on the expression and function of a multimeric protein such as MPO.     

Spontaneous long-term remyelination after traumatic spinal cord injury in rats

The capability of the central nervous system to remyelinate axons after a lesion has been well documented, even though it had been described as an abortive and incomplete process. At present there are no long-term morphometric studies to assess the spinal cord (S.C.) remyelinative capability. With the purpose to understand this phenomenon better, the S.C. of seven lesionless rats and the S.C. of 21 rats subjected to a severe weight-drop contusion injury were evaluated at 1, 2, 4, 6, and 12 months after injury. The axonal diameter and the myelination index (MI = axolemmal perimeter divided by myelinated fiber perimeter) were registered in the outer rim of the cord at T9 SC level using a transmission electron microscope and a digitizing computer system. The average myelinated fiber loss was 95.1%. One month after the SC, 64% of the surviving fibers were demyelinated while 12 months later, only 30% of the fibers had no myelin sheath. The MI in the control group was 0.72 +/- 0.07 (X +/- S.D.). In the experimental groups, the greatest demyelination was observed two months after the lesion (MI = 0.90 +/- 0.03), while the greatest myelination was observed 12 months after the injury (MI = 0.83 +/- 0.02). There was a statistical difference (p < 0.02) in MI between 2 and 12 months which means that remyelination had taken place. Remyelination was mainly achieved because of Schwann cells. The proportion of small fibers (diameter = 0.5 micron or less) considered as axon collaterals, increased from 18.45% at 1 month to 27.66% a year after the contusion. Results suggest that remyelination is not an abortive phenomenon but in fact a slow process occurring parallel to other tissue plastic phenomena, such as the emission of axon collaterals.