Alkali burns of the rabbit cornea. I. A histochemical study of beta-glucuronidase, beta-galactosidase and N-acetyl-beta-D-glucosaminidase.

In alkali burned rabbit corneas activities of beta-glucuronidase, N-acetyl-beta-D-glucosaminidase and acid beta-galactosidase were studied histochemically in various time intervals after the traumatization. The technic with semipermeable membranes was employed. Within four days after the injury enzyme activities in the traumatized area were almost lacking. The corresponding activities in the unaffected part of the cornea were within the norm. On the 7th day enzyme activities were on an increase (but still subnormal) in the traumatized area. This area was surrounded by a zone of keratocytes with high levels of enzyme activities. This was particularly remarkable in keratocytes subjacent to the epithelium. The activation of all enzymes studied was present in the basal layer of the epithelium and in the endothelium as well. On the 14th day enzyme activities in the traumatized area were nearly restored and on the 32nd day they could not be distinguished from the normal cornea. Beta-galactosidase displayed a relatively maximal increase in the activity of all enzymes investigated.     

Leukotriene B4 Release and Polymorphonuclear Cell Infiltration in Spinal Cord Injury

Activation of arachidonic acid occurs after spinal cord injury. Leukotriene B4 is a lipoxygenase metabolite of arachidonic acid. In a rat model of experimental spinal cord injury, we found that the leukotriene B4 content was less than the sensitivity of our assay (8 pg/mg of protein) in non-traumatized spinal cord. Leukotriene B4 was detectable in traumatized cord (mean +/- SE, 25 +/- 5 pg/mg of protein; n = 3). Release of leukotriene B4 from spinal cord slices into the incubation medium was also noted after trauma (9 +/- 1 pg/mg of protein; n = 12) and was enhanced by exposure of traumatized spinal cord slices to the calcium ionophore A23187 (375 +/- 43 pg/mg of protein; n = 12). The amount of leukotriene B4 released corresponded to the extent of post-traumatic polymorphonuclear cell infiltration determined by a myeloperoxidase assay. Results from this study suggest that the source of leukotriene B4 in spinal cord injury is infiltrating polymorphonuclear cells.     

Altered levels of PGF in cat spinal cord tissue following traumatic injury.

Previous studies by others indicated that PGs were present in brain, spinal cord, and c.s.f. of several mammalian species. In the present study we compared levels of PGE and PGF by R.I.A. in spinal cord tissue from traumatized cats and cats pretreated with indomethacin prior to trauma to those of baseline and sham operated controls in order to assess for the first time, to our knowledge, whether meaningful changes in levels of PGE and PGF could be detected which might shed new light on the etiology of spinal cord trauma. Levels of PGF (nanograms/gram wet wt) in the cord segment immediately adjacent to the point of trauma were 8.05 +/- 1.50, and 13.13 +/- 1.38 for baseline and sham operated cats respectively. Spinal trauma led to more than a 100% increase in PGF levels to 29.26 +/- 3.58. Although pretreatment with indomethacin 30 min prior to trauma gave the expected blockade of the PGF response to trauma, a measurable level of PGF (2.55 +/- 0.17) was found in the cord after indomethacin. Cord levels of PGF declined after 3 hr in both sham operated and traumatized animals. PGF was maximally stimulated by trauma during the first 3 hr with little effect at 72 hr. Although carefully examined, PGE levels in cat spinal cord appeared to be virtually unaffected by trauma. These findings clearly demonstrate for the first time that traumatic injury to the spinal cord is accompanied by marked increases in PG levels at the site of trauma, and that the observed elevation in PGF in response to trauma can be blocked by indomethacin in vivo. Whether PGF changes are causally related to the etiology of spinal cord trauma, or merely represent a manifestation of PG release as a result of non-specific tissue injury, remains to be seen.     

Noradrenergic mediation of traumatic spinal cord autodestruction

Acute spinal injury initiates hemorrhagic necrosis (HN), a novel tissue destructive process, within traumatized cord tissues. HN assures permanent paralysis within 24 hours by locally destroying the injured cord. It results from microvascular failure and subsequent lethal tissue hypoxia. Norepinephrine (NE) a normal spinal cord transmitter material rapidly increases (four to tenfold) at the injury site. This vasoactive substance has been implicated in post wounding vascular stasis and permanent spinal paralysis because: 1. Direct spinal NE injections reproduce histological HN. 2. Phenoxybenzamine (alpha receptor blockade) pretreatment significantly diminishes traumatic lesion size. 3. NE synthesis inhibition by alpha methyl tyrosine (acts upon tyrosine hydroxylase), alpha methyl dopa (acts upon L dopa decarboxylase) and FLA-63 (acts upon dopamine beta hydroxylase) all variously protect the wounded cord against HN traumatic lesions. 4. Reserpine (NE depletion) provides significant tissue protection. This drug restores some useful spinal function after severe experimental injuries which consistently paralyze untreated animals.NE bulbospinal fibers are modulated, as determined by tissue lesion size, by two other neural systems. 1. Facilitation occurs from afferent dorsal rootposterior spinal column fibers (non-catecholamine) because prior surgical interruptions significantly diminish traumatic lesions. 2. Inhibition by dopaminergic (DA) fibers was detected by: a. Cord protection with apomorphine DA receptor stimulation. b. Aggravation of traumatic lesions by Pimozide DA receptor blockade. Although these studies are early and incomplete, there is convincing evidence for NE post wounding involvement. As this system is better understood we believe treatments will be developed for spinal injured man.     

Formation of spinal cord cicatrix under various experimental conditions

Structure of the cat spinal cord scar has been studied by means of light and electron microscopy after its lateral hemisection, complete dissection and hemisection in combination with autotransplantation of the sympathetic ganglion, which keeps its connection with the sympathetic trunk, into the cut of the spinal cord. Three zones are revealed in the scar: central (connective tissue), intermediate (glio-connective tissue) and peripheral (zone of glio-cystous and reactive changes of the nervous tissue). Peculiarities of intercellular reactions are revealed in the process of formation of various zones in the scar and their dependence on the type of the experiment. In the experiments with autotransplantation of the sympathetic ganglion into the spinal cord, a definite possibility to restrict scarry changes of the spinal cord is demonstrated in connection with improving reinnervation and revascularization of the traumatized segment.     

Triphosphopyridine nucleotide-dependent enzymes in the developing spinal cord of the rabbit

Abstract— Total lipid and the activity of five enzymes closely related to the generation of NADPH have been measured in the anterior horn region and dorsal columns of rabbit spinal cord during the period of rapid myelination. Lipid deposition progressed to a much greater extent in the dorsal columns than in the anterior horn region; however, the age at which one-half of the total adult level of lipid accumulated in both regions was the same, i.e. 19-20 days after birth. During the first 15 days of postnatal development of the dorsal columns, glucose-6-phosphate dehydrogenase changed in parallel with lipid content; however, in the anterior horn region changes in lipid were not accompanied by increases in glucose-6-phosphate dehydrogenase. In contrast to changes in glucose-6-phosphate dehydrogenase, the activity of malic enzyme increased in the anterior horn region but remained relatively constant in the dorsal columns during development. The activities of two other enzymes of the pentose phosphate pathway, 6-phosphogluconate dehydrogenase and transketolase, measured at various intervals after birth, did not directly parallel changes in the activity of glucose-6-phosphate dehydrogenase in the dorsal columns. In both areas of the developing spinal cord the activity of NADP⁺-dependent isocitrate dehydrogenase was greater than the activities of the other three dehydrogenases but it did not parallel changes in lipid content of either region. A relationship between the requirements for reducing equivalents and the activities of the four NADP⁺-dependent dehydrogenases is suggested by the finding that both areas of the adult spinal cord contained lower activities of these enzymes than those observed during the initial 26 days of development. The differences noted in the two areas of the spinal cord during development suggest that mechanisms for the generation of NADPH differ in gray and white matter.     

Change in acetylcholinesterase during early phase of experimental spinal cord trauma in primates

Specific activity of acetylcholinesterase has been shown to be decreased following experimental spinal cord trauma (200 gcm) in primates. The decrease in activity was evident at 8, 24, 48 hr and 1 week after injury to the traumatized segments of spinal cord.     

Alkali burns of the rabbit cornea

Summary In alkali burned rabbit corneas activities of -glucuronidase, N-acetyl--D-glucosaminidase and acid -galactosidase were studied histochemically in various time intervals after the traumatization. The technic with semipermeable membranes was employed. Within four days after the injury enzyme activities in the traumatized area were almost lacking. The corresponding activities in the unaffected part of the cornea were within the norm. On the 7th day enzyme activities were on an increase (but still subnormal) in the traumatized area. This area was surrounded by a zone of keratocytes with high levels of enzyme activities. This was particularly remarkable in keratocytes subjacent to the epithelium. The activation of all enzymes studied was present in the basal layer of the epithelium and in the endothelium as well. On the 14th day enzyme activities in the traumatized area were nearly restored and on the 32nd day they could not be distinguished from the normal cornea. -galactosidase displayed a relatively maximal increase in the activity of all enzymes investigated.     

Altered levels of PGF in cat spinal cord tissue following traumatic injury

Previous studies by others indicated that PGs were present in brain, spinal cord, and c.s.f. of several mammalian species. In the present study we compared levels of PGE and PGF by R.I.A. in spinal cord tissue from traumatized cats and cats pretreated with indomethacin prior to trauma to those of baseline and sham operated controls in order to assess for the first time, to our knowledge, whether meaningful changes in levels of PGE and PGF could be detected which might shed new light on the etiology of spinal cord trauma.Levels of PGF (nanograms/gram wet wt) in the cord segment immediately adjacent to the point of trauma were 8.05 ± 1.50, and 13.13 ± 1.38 for baseline and sham operated cats respectively. Spinal trauma led to more than a 100% increase in PGF levels to 29.26 ± 3.58. Although pretreatment with indomethacin 30 min prior to trauma gave the expected blockade of the PGF response to trauma, a measurable level of PGF (2.55 ± 0.17) was found in the cord after indomethacin. Cord levels of PGF declined after 3 hr in both sham operated and traumatized animals. PGF was maximally stimulated by trauma during the first 3 hr with little effect at 72 hr. Although carefully examined, PGE levels in cat spinal cord appeared to be virtually unaffected by trauma.These findings clearly demonstrate for the first time that traumatic injury to the spinal cord is accompanied by marked increases in PG levels at the site of trauma, and that the observed elevation in PGF in response to trauma can be blocked by indomethacin $\text{in vivo}$. Whether PGF changes are causally related to the etiology of spinal cord trauma, or merely represent a manifestation of PG release as a result of non-specific tissue injury, remains to be seen.     

Effect of axotomy on cholinergic enzyme activities in the spinal cord and sciatic nerve of the dog

Choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activity measured in the ventral and dorsal part of the dog spinal cord (L6-S2) and in the stumps of the sciatic nerve 5, 10, 15 and 21 days after its transection were compared with the corresponding activities in the intact contralateral nerve and in sham-operated animals. AChE was also examined histochemically. Changes in the enzyme activities in the central nerve stump were correlated with activity changes in the spinal cord. In the central nerve stump, a marked (25%) increase in AChE activity was found on the fifth day after transection, but by the 21st day it fell below control value levels; up to the 15th day it showed good correlation with AChE activity in the ventral spinal cord. Histochemically, pronounced reduction of enzymatic activity was found in the ipsilateral part of the spinal cord. On the 15th day, ChAT activity in the ventral spinal cord was also significantly decreased and the accumulation of the enzyme in the central nerve stump was negligible. On the contrary, at the last 21-day interval examined, a significant increase in ChAT activity and a nonsignificant increase in AChE activity was found in the spinal cord, but their activities in the central nerve stump were decreased. In the degenerated peripheral nerve stump ChAT activity dropped by an average of 99% and AChE activity by 48% during the first 15 days after transection but, on the 21st day, AChE activity was 22% higher than at the preceding interval.     

Effect of ischemia in vivo and oxygen-glucose deprivation in vitro on NOS pools in the spinal cord: comparative study

1. This study was performed to compare both the Ca(2+)-dependent nitric oxide synthase (NOS) activity and the neuronal nitric oxide synthase immunoreactivity (nNOS-IR) in the rabbit lumbosacral spinal cord after 15 min abdominal aorta occlusion (ischemia in vivo) and oxygen-glucose deprivation of the spinal cord slices for 45 and 60 min (ischemia in vitro). All ischemic periods were followed by 15, 30 and 60 min reoxygenation in vitro. 2. Catalytic nitric oxide synthase activity was determined by the conversion of (L)-[(14)C]arginine to (L)-[(14)C]citrulline. Neuronal nitric oxide synthase immunoreactivity in the spinal cord was detected by incubation of sections with polyclonal sheep-nNOS-primary antibody and biotinylated anti-sheep secondary antibody. 3. Our results show that ischemia in vivo and the oxygen-glucose deprivation of spinal cord slices in vitro result in a time-dependent loss of constitutive NOS activity with a partial restoration of enzyme activity during 15 and 45 min ischemia followed by 30 min of reoxygenation. A significant decrease of enzyme activity was found during 60 min ischemia alone, which persisted up to 1 h of oxygen-glucose restoration. The upregulation of neuronal nitric oxide synthase was observed in the ventral horn motoneurons after all ischemic periods. The remarkable changes in optical density of neuronal nitric oxide synthase immunoreactive motoneurons were observed after 45 and 60 min ischemia in vitro followed by 30 and 60 min reoxygenation. 4. Our results suggest that the oxygen-glucose deprivation followed by reoxygenation in the spinal cord is adequately sensitive to monitor ischemia/reperfusion changes. It seems that 15 min ischemia in vivo and 45 min ischemia in vitro cause reversible changes, while the decline of Ca(2+)-dependent nitric oxide synthase activity after 60 min ischemic insult suggests irreversible alterations.     

Kininogen and Kinin in Experimental Spinal Cord Injury

Activation of the kallikrein-kinin system has been implicated in the pathogenesis of vasogenic brain edema and posttraumatic vascular injury. We determined the levels of kininogen and kinin in an experimental spinal cord injury model in the rat. Kininogen content in traumatized cord segments increased in a time-dependent manner. Western blot analysis showed that the kininogen in traumatized cord comigrates with 68K low-molecular-weight kininogen or T-kininogen. Trypsin treatment of the kininogen in traumatized cord released both bradykinin and T-kinin, which were separated by HPLC and quantified with a kinin radioimmunoassay. Endogenous kinin levels in the frozen spinal cord also increased up to 40-fold 2 h after injury as compared with controls. The results demonstrate an increased accumulation of kininogen and its conversion to vasoactive kinins in experimental spinal cord injury.     

A Threshold Dose of Heavy Ion Radiation that Decreases the Oxidative Enzyme Activity of Spinal Motoneurons in Rats

The effect of heavy ion radiation exposure of the spinal cord on the properties of the motoneurons innervating the slow soleus and fast plantaris muscles was investigated. A 15-, 20-, 40-, 50-, or 70-Gy dose of carbon ions (5 Gy/min) was applied to the 2nd to the 6th lumbar segments of the spinal cord in rats. After a 1-month recovery period, the number and cell body size of the irradiated motoneurons innervating the soleus and plantaris muscles did not differ from that of the non-irradiated controls, irrespective of the dose received. However, the oxidative enzyme activity of these motoneurons was decreased by heavy ion radiation at doses of 40, 50, and 70 Gy compared to that of the non-irradiated controls. This decrease in oxidative enzyme activity levels in the motoneurons returned to that of the non-irradiated controls after a 6-month recovery period. We conclude that heavy ion radiation at doses of 40–70 Gy reversibly decreases the oxidative enzyme activity of motoneurons in the spinal cord of rats.     

Neuroprotective Effects of Ebselen on Experimental Spinal Cord Injury in Rats

Spinal cord injury (SCI) results in rapid and significant oxidative stress. This study was aimed to investigate the possible beneficial effects of Ebselen in comparison with Methylprednisolone in experimental SCI. Thirty six Wistar albino rats (200–250 g) were divided in to six groups; A (control), B (only laminectomy), C (Trauma; laminectomy + spinal trauma), D (Placebo group; laminectomy + spinal trauma + serum physiologic), E (Methylprednisolone group; laminectomy + spinal trauma + Methylprednisolone treated), F (Ebselen group; laminectomy + spinal trauma + Ebselen treated), containing 6 rats each. Spinal cord injury (SCI) was performed by placement of an aneurysm clip, extradurally at the level of T11–12. After this application, group A, B and C were not treated with any drug. Group D received 1 ml serum physiologic. Group E received 30 mg/kg Methylprednisolone and, Group F received 10 mg/kg Ebselen intraperitoneally (i.p.). Rats were neurologically examined 24 h after trauma and spinal cord tissue samples had been harvested for both biochemical and histopathological evaluation. All rats were paraplegic after SCI except the ones in group A and B. Neurological scores were not different in traumatized rats than that of non-traumatized ones. SCI significantly increased spinal cord tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) enzyme activities compared to control. Methylprednisolone and Ebselen treatment decreased tissue MDA and PC levels and prevented inhibition of the enzymes SOD, GSH-Px and CAT in the tissues. However, the best results were obtained with Ebselen. In groups C and D, the neurons of the spinal cord tissue became extensively dark and degenerated with picnotic nuclei. The morphology of neurons in groups E and F were very well protected, but not as good as the control group. The number of neurons in the spinal cord tissues of the groups C and D were significantly less than the groups A, B, E and F. We concluded that the use of Ebselen treatment might have potential benefits in spinal cord tissue damage on clinical grounds.     

Decidual cell reaction: relative response to traumatization in uterus of rat, hamster and guinea pig

Relative decidual cell response to traumatization was studied in the uterus of immature rat, hamster and guinea pig. A single dose of progesterone (1.0 mg/animal) caused 285 +/- 41 and 459 +/- 58% uterotrophy in traumatized horn of rat and hamster respectively, while in guinea pig increasing doses of progesterone (1, 2 and 5 mg/animal), several combinations of estrogen and progesterone or alteration in treatment schedule of the two hormones as well as extending the day of traumatization failed to elicit comparable uterotrophic response. Uterus of immature hamster was found to be most responsive to traumatization and that of guinea pig the least.     

Mechanism of formation of intramedullary cavities and their role in the regeneration of the spinal cord

The spinal cord preparations of 38 dogs and 20 rabbits have been studied with the aim to investigate the influence of the cerebrospinal fluid on the spinal cord nervous tissue. The spinal cord preparations of 8 patients having trauma of the vertebral column with interruption of the spinal cord have also been studied. As demonstrate histological investigations, the cerebral tissue of the pieces, put into the flask with liquor, in the subarachnoidal space of the canine spinal cord, in diastasis between the ends of the cut spinal cord during 6 h up to 7 days, swells, becomes edematous. Cavities occupying about 30% of the area in the slices studied appear in it. At hemisection of the rabbit spinal cord without closure of the defect in the meninx vasculosa with the glue MK-6, the area of the cavity formation varies from 24 up to 35%, comparing the whole area of the preparation, while in rabbits with hemisection and successive gluing of the defect in the meninx vasculosa the area of the nervous tissue destruction makes 13-18%. It has been proved that the scar forming in the traumatized segment of the spinal cord does not present a continuous formation, but contains a large amount of cavities that prevent regeneration of nerve fibers. The experimental data concerning lysing effect of the cerebrospinal fluid on the traumatized nervous tissue are confirmed by the results obtained at investigating the preparations of the spinal cord of the patients died as the cause of the spinal cord trauma.     

Selective Neurotoxic Lesions of Descending Serotonergic and Noradrenergic Pathways in the Rat

The ability of neurotoxic substances to induce selective lesions of the descending monoaminergic pathways in rats was investigated. Saline, 6-hydroxydopamine, 5,6-dihydroxytryptamine, or 5,7-dihydroxytryptamine were administered into the lumbar subarachnoid space through a chronically indwelling catheter. The lesions were evaluated 2-3 weeks later by in vitro uptake of [3H]noradrenaline and [14C]5-hydroxytryptamine into synaptosomal preparations from the frontal cortex, brainstem, cervical spinal cord, and lumbar spinal cord of each animal. There was no difference in uptake between saline-injected and noncatheterized controls and no significant changes in cortical uptake after any of the treatments (dose range of neurotoxins: 0.6-80 micrograms). In the lumbar spinal cord, 6-hydroxydopamine (5-80 micrograms) reduced the [3H]noradrenaline uptake by approximately 90% with no effects on [14C]5-hydroxytryptamine uptake, whereas 5,6-dihydroxytryptamine reduced the uptake of [14C]5-hydroxytryptamine by 90% (20-80 micrograms). [3H]Noradrenaline uptake was unaffected by lower doses of 5,6-dihydroxytryptamine but fell by 45-55% after 40-80 micrograms. 5,7-Dihydroxytryptamine (10-80 micrograms) reduced [3H]noradrenaline uptake by 90-95% and [14C]5-hydroxytryptamine uptake by approximately 80% (5-80 micrograms) in the lumbar cord. It is concluded that intrathecal administration of suitable doses of neurotoxins may produce extensive selective lesions of descending noradrenergic and serotonergic pathways.     

TYROSINE–ALPHA-KETOGLUTARATE AMINOTRANSFERASE ACTIVITY IN RAT LIVER AFTER SPINAL CORD SECTION

Spinal cord section brings about early and late changes in rat liver tyrosine-alpha-ketoglutarate aminotransferase activity. Early effects (4 h after surgery): spinal cord section at C₇ level causes an unreactiveness of rat liver tyrosine-alpha-ketoglutarate aminotransferase both to endogenously and exogenously elevated plasma glucocorticoid levels. Induction of tyrosine–alpha-ketoglutarate aminotransferase by hydrocortisone administration is almost completely inhibited. This unreactiveness of the rat liver enzyme to hydrocortisone is not due to delayed resorption of hydrocortisone by the peritoneum as tested with [³H]hydrocortisone, to changes in the secretion of hypophyseal hormones or to changes in the levels of glucose in blood or liver. L₃ level section of the spinal cord or sham operation results in a stress-like enzyme pattern (an increase at 4 h with return to normal level at 24 h). The stress elevation of tyrosine–alpha-ketoglutarate aminotransferase at 4 h after the operation is absent in C₇ level sectioned rats. This effect is not due to a decreased plasma corticosterone level since it is 4.1-fold higher in C₇ level sectioned rats and 2.7-fold higher in sham-operated controls (as measured 2.5 h after the operation). Late effects (24 h after the surgery): C₇ level section of the spinal cord brings about a nine-fold increase in a tyrosine–alpha-ketoglutarate aminotransferase activity in animals with intact adrenals and three-fold increase in adrenalectomized rats at 24 h after the operation. This increase is abolished almost completely by cycloheximide, irrespective of the time of administration. Experiments with actinomycin D, injected at different times after C₇ level section have shown that there exists a period of higher sensitivity of the amino-transferase toward the antibiotic (lasting about 3 h), followed by a period of lower sensitivity (lasting 16 h or longer). These results can be explained by assuming the existence of two tyrosine-alpha-ketoglutarate aminotransferase mRNAs with different lifetime. A direct participation of the CNS in the changes in enzymic activity observed after section of the spinal cord above the segments innervating the liver is suggested.     

肢体远程预处理通过上调机体抗氧化酶活性诱导兔脊髓缺血耐受

目的:证实抗氧化酶活性上调是肢体远程预处理(remote preconditioning,RPC)诱导兔脊髓缺血耐受效应的主要机制之一。方法:60只雄性新西兰大白兔随机分成对照组、远程预处理组、缺血组及RPC 缺血组(对照组n=6,余组n=18)。RPC组行双下肢短暂缺血2次(每次10min,间隔10min);缺血组仅行脊髓缺血模型;RPC 缺血组在远程预处理后1h行脊髓缺血;对照组为假手术组。对照组于脊髓缺血再灌注后48h行神经功能评分后取脊髓,作为对照。余三组分别于再灌注后6h、24h及48h评分后取材,各时间点各取6只。所有动物于缺血前、缺血20min、再灌注20min及再灌注6h采动脉血测血清抗氧化酶活性和丙二醛(MDA)含量;于取材后测定脊髓匀浆抗氧化酶活性和MDA含量。结果:再灌注后6h、24h及48h时对照组、远程预处理组及远程预处理 缺血组神经功能评分均明显高于缺血组(P<0.05)。血浆超氧化物歧化酶(SOD)活性和过氧化氢酶(CAT)活性在每个时间点RPC组均高于对照组,RPC 缺血组高于缺血组(P<0.05);其中缺血20min时,缺血组血浆SOD、CAT活性低于对照组,RPC 缺血组低于RPC组(P<0.05);而与缺血前相比,缺血20min时缺血组及RPC 缺血组SOD和CAT活性显著下降(P<0.05)再灌注24h和48h时,脊髓匀浆SOD、CAT活性对照组低于RPC组,缺血组低于RPC 缺血组(P<0.01);而MDA含量再灌注24h时对照组高于RPC组,缺血组高于RPC 缺血组(P<0.05)。脊髓匀浆SOD、CAT活性与神经功能评分具有显著相关性。结论:RPC诱导脊髓缺血耐受的机制可能为上调抗氧化酶活性,增强机体在缺血再灌注过程中清除氧自由基的能力,从而减少氧自由基介导的损伤,发挥脊髓保护作用。     

Uterine estradiol and progesterone receptor concentration in relation to circulating hormone levels and histoarchitecture during high endometrial sensitivity and induced decidualization in guinea pigs

Alterations in nuclear and cytosolic estradiol (ER) and progesterone (PR) receptor concentration in the antimesometrial (AM) and mesometrial (M) segments of the uterus in relation to circulating hormone levels, histology and surface topography during the period of high endometrial sensitivity and development of trauma-induced decidualization in cyclic guinea pigs were investigated. The period of high endometrial sensitivity (i.e. day 5 of the estrous cycle) was characterized by elevated plasma estradiol and progesterone and their receptors in the nuclear and cytosolic fractions of the uterus. There was, however, no difference in the concentration of these receptors or the surface ultrastructure in the AM and M segments. Unilateral traumatization by scissor cut along the AM length of the uterus on day 5 of the estrous cycle induced decidual cell reaction resulting in a marked increase in weight of the decidualized (traumatized) uterine horn with advancing decidualization to reach maximum levels (926% of the contralateral nontraumatized uterine horn) 7 days after traumatization. This was associated with decidual transformation and a marked increase in nuclear and cytosolic ER and PR concentration in the AM segment of the traumatized uterine horn. An increase in receptor concentration in the M segment of the traumatized uterine horn or the AM segment of the nontraumatized uterine horn was transitory and of a low order. Receptor concentration in the M segment of the nontraumatized uterine horn remained low throughout days 8–12 of the cycle. Findings indicate a possible role of both estradiol and progesterone in induction of endometrial sensitivity and development and maintenance of decidua in the guinea pig.