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At least 433 records · Page 24Linked to original sources
PubMed2002

[Protective effect of dansheng injection on experimental rabbits' spinal cord injury].

OBJECTIVE: To investigate the protective effect of Dansheng injection on experimental rabbits' in spinal cord injury. METHODS: Thirty-two New Zealand rabbits were impacted between T12-T1 with a force of 150 g.cm-1 (10 g x 15 cm). The rabbits were randomly divided into the injury group, monitor group, L-NAME group and Dansheng group. The blood was obtained at 0 h, 4 h, 6 h to separate the serum at the end the injured spinal cord. Cord tissues were obtained for histological examination. Methyl-di-aldehyde (MDA), superoxide dismutase (SOD) and nitro oxide (NO) from the serum and spinal tissues homogenated were tested. RESULTS: MDA and NO increased in the injury group compared with the others, but SOD significantly decreased in the injury group compared with the others. Histological examination showed that neurons were degenerated and necrosed. The injury group displayed serious changes while the Dansheng group less changes. iNOS expressed in all the groups. CONCLUSION: Dansheng injection has some protective effect on spinal cord injury in the early stage.

Animals↗
PubMed2002

Participation of nitric oxide and N-methyl-D-aspartic acid receptors in the pressor response to intrathecal injected noradrenaline at the spinal cord of the rat.

In pentobarbital-anesthetized rats, intrathecal injection of noradrenaline (NA; 6, 18 and 60 nmol) induced a dose-dependent increase in the mean blood pressure. The pressor response to NA (18 nmol) was blocked by pretreatment with the selective antagonist for N-methyl-D-aspartic acid (NMDA) receptors, 2-amino-5-phosphonovaleric acid (30 nmol), but not by pretreatment with the selective antagonist for (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid/kainate receptors, 6,7-dinitroquinoxaline-2,3-dione (50 nmol). The pressor effect of NA was reduced after pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 1 micromol). The effect of L-NAME on the pressor response to NA was reverted by the precursor of nitric oxide (NO), L-arginine (5 micromol). The hypertension induced by NA was also reduced by the guanylate cyclase inhibitor methylene blue (0.3 micromol). These results suggest that spinal NMDA receptors and spinal NO are involved in the pressor response to NA.

Animals↗
PubMed1984

A new method for studying the distribution of drugs in spinal cord after intrathecal injection.

The pharmacological effect of local anaesthetic solutions in mice including their distribution within the spinal cord, were assessed following intrathecal injection at the L5-L6 interspace. A solution of 5 microliters radioactively labelled lidocaine at a concentration of 50 mg/ml or bupivacaine at 7.5 mg/ml, was used. Both drugs blocked the motor function of the hindlegs in less than 1 min. This persisted for 15.1 +/- 0.8 min. (mean +/- S.E.M.) after lidocaine and 15.2 +/- 2.7 min. after bupivacaine. The highest spinal cord concentration was adjacent to the site of injection, even if traces were present up to the lower cervical cord. The tissue concentration of bupivacaine was considerably less than that of lidocaine, despite a similar motor blockade. When the injected volume was doubled from 5 to 10 microliters, there was a tendency to a more cephalic distribution of lidocaine. When the speed of injection was increased from 2.5 sec., to 30 sec., no difference in results was seen. The drug concentration at the injection site tended to fall in animals alive until 5 min. after the injection, whereas it persisted in animals sacrificed before the intrathecal injection, suggesting that the circulatory transport is the major route of redistribution from the cord.

Anesthesia, Spinal↗
PubMed1978

Lesions in the cat spinal cord following local injections of 6-aminonicotinamide.

Lesions were made in the spinal cord of cats by means of local injections of 6-aminonicotinamide. The concentration needed to induce primary demyelination also caused extensive axonal death. In the early stages following injection there was evidence of astrocyte and oligodendrocyte destruction and with longer survival times most of the surviving demyelinated axons were remyelinated by Schwann cells. This experimental system indicates that Schwann cell remyelination of central axons follows astrocyte destruction, but it was not considered a suitable model system for the study of cellular relationships in remyelination because of the extensive concomitant axonal damage.

6-Aminonicotinamide↗
PubMed2005

Microglia activation in rat spinal cord by systemic injection of TLR3 and TLR7/8 agonists.

Here we describe activation of microglia in the rat spinal cord by systemic injections of toll-like receptor agonist polyinosine-polycytidylic acid (poly(I:C), a TLR3 ligand) and R848 (a TLR 7/8 ligand). A significant but transient increase of ED-1+ spinal cord microglia was observed 4 days after a single intraperitoneal (i.p.) injection. Immunostainings by different microglial markers, AIF-1, EMAPII, OX6, P2X(4) receptor (P2X4R), indicated that microglia were not fully activated and tracing of cell proliferation by 5-bromo-2 -deoxyuridine revealed that only a small fraction of proliferating cells were microglia (less than 5%). Thus, these stimulators of the innate immune system have, after peripheral administration, clearly effects on the innate immune system of the spinal cord. This should be considered in the design of clinical trials, as both TLR ligands have been used in patients. As injections of TLR ligands can be used to modulate immune activity in the spinal cord, such agents might be tools to modulate local regenerative processes in the spinal cord.

Analysis of Variance↗
PubMed1978

[Neurofilament hypertrophy induced in the rabbit spinal cord after intracisternal injection of aluminum chloride (author's transl)].

The cytological changes induced in the spinal cords of rabbits by intracisternal injections of aluminum chloride have been studied at the light- and electron-microscopic level for examining the progress of the 100 A filament hypertrophy. A moderate increase in the number of the 100 A filament was detected in perikarya of neurones in anterior, lateral, and dorsal horns 4--5 days after aluminum injection. Tangles of 100 A filament were seen in perikarya and proximal parts of dendrites in these neurones 1--2 weeks after the administration of aluminum. In this stage the tangles were detected as large clear spots at light-microscopic level. The 100 A filament bundles developed in between clumps of densely aggregated endoplasmic reticulum keeping close contact with this and squeezing other organella out. In high resolution studies the 100 A filament closely resembled the neurofilament in normal neurones in size and appearances and was seen to be connected with each other via side arms coming out from its wall. Relations between the endoplasmic reticulum and the 100 A filament hypertrophy was discussed referring to intoxicating effects of aluminum compounds on the nucleus of the neuron.

Aluminum↗
PubMedDate not supplied

Success rate of unilateral spinal anesthesia is dependent on injection flow.

BACKGROUND AND OBJECTIVES: The dependence of unilateral spinal anesthesia on injection flow is controversial. We hypothesized that it is possible to achieve strictly unilateral sympathetic block (as assessed by temperature measurements of the limbs) and unilateral sensory and motor block, respectively, during spinal anesthesia by a slow and steady injection of a hyperbaric local anesthetic solution. METHODS: Forty-four patients (American Society of Anesthesiologists [ASA] physical status I-III) undergoing surgery of one lower extremity were randomly assigned to one of two groups. Dependent on the patients' height, 1.4 to 1.7 mL hyperbaric bupivacaine 0.5% was injected manually with the patient in the lateral decubitus position, which was maintained for 30 minutes after injection. Injection flow was approximately 0.5 mL/min in group I ("air-buffered" injections performed by 4 mL air between the local anesthetic and the syringe's plunger, n = 25) and approximately 7.5 mL/min in group II ("conventional" injections, n = 19). Sympathetic block was defined as a temperature increase of more than 0.5 degrees C at the foot. Any reduction in the ability to move the hip, knee, or ankle as well as loss of temperature discrimination and/or pinprick even in one dermatome on the nondependent side was considered as a bilateral block. RESULTS: Before surgery, significant differences (P < .05) were observed for unilateral motor paralysis (92% in group I v 68.4% in group II), unilateral sensory block (48.0% v 10.5%), and unilateral sympathetic block (72% v 42.1%). Strictly unilateral spinal anesthesia was found to be significantly more frequent in group I (40% v 5.3%). Significant hemodynamic differences between the groups were not detected. CONCLUSIONS: For hyperbaric spinal anesthesia, the injection flow is an important factor in achieving unilateral sympathetic block. A slow injection proves useful to restrict spinal anesthesia to the side of surgery.

Adolescent↗
PubMed1976

The response of alpha-motoneurons of different size to stretch and vibration of extensor muscles after injection of 5-hydroxytryptophan in spinal cats.

1. Vibration of the GS muscle at 100/sec, and the peak-to-peak amplitude of about 100 mu, produced slight reflex activity of homonymous and heteronymous alpha-motoneurons in the spinal, unanesthetized cat. 2. Intravenous injection of the 5-HT precursor 5-HTP (25 mg/kg, L-form) performed in the spinal preparation facilitated the responses of single extensor alpha-motoneurons to both vibration and stretch of the corresponding muscle. The 5-HT antagonist methysergide (0-5 mg/kg i. v.) blocked almost completely the facilitation of the vibration and stretch induced motoneuronal discharges produced by 5-HTP in the spinal cat, indicating that the facilitation was 5-HT specific. 4. A comparison of the types of alpha-motoneurons participating in the reflex responses elicited by the different stimuli in the spinal cat following injection of 5-HTP showed that both small-tonic and large-phasic alpha-motoneurons take part in both stretch and vibration reflexes. 5. It is concluded that the alpha-motoneuron pool of the GS muscle represents an homogenous population, no matter what kind of synaptic drive is used for its activation, and that the susceptibility of a motoneuron to discharge depends on the amount of the afferent excitatory input rather than on the modalities of sensory stimulation.

5-Hydroxytryptophan↗
PubMed1991

Spinal transection reduces both spinal antinociception and CNS concentration of systemically administered morphine in rats.

Within one day after spinal transection, the antinociceptive effect of systemically administered morphine on the spinal withdrawal reflex is significantly reduced. This observation has provided important empirical support for the present model of opiate-induced analgesia. One prediction from this model is that the antinociceptive effect of intrathecal (spinal) morphine injections should not be reduced by spinalization. When examined experimentally, this prediction was not supported; the antinociceptive effect of intrathecally administered morphine was significantly enhanced after acute spinalization. This result suggested an alternate hypothesis of morphine-induced analgesia. One prediction from this new hypothesis is that the decreased behavioral response to systemic morphine in spinal rats is due to a decrease in the spinal concentration of morphine produced by spinal transection. To test this prediction separate groups of intact rats and acute (one day) spinal rats, were assessed with the tail-flick (TF) procedure 60 min after subcutaneous injection of various doses of morphine (0.75, 1.5, 3.0, 4.5, 6.0 or 9.0 mg/kg) or at different time points (30, 60, 90, 150 or 240 min) after a single injection of 9.0 mg/kg. Immediately after behavioral testing, the rats were killed and brains, spinal cords and blood samples were collected and subsequently analyzed with a morphine radioimmunoassay. The results show that the concentration of morphine in the brain and spinal cords of acute spinal rats is significantly lower than that of intact rats, whereas morphine levels in the blood do not differ. These data suggest that the decreased antinociceptive effect of subcutaneous morphine in acute rats is due to a decrease in the concentration of the opiate in the central nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

R-phenylisopropyl-adenosine increases spinal cord blood flow after intrathecal injection in the rat.

The A1-adenosine receptor agonist, R-phenylisopropyl-adenosine (R-PIA), demonstrated antinociceptive properties in animal studies after intrathecal administration. In the evaluation of a drug for possible spinal injection in humans, the effects of intrathecal R-PIA on spinal cord blood flow (SCBF) were investigated using the laser-Doppler flow-metry technique in anesthetized rats. In low doses (0.1-1 nmol), no change in SCBF was recorded, whereas larger doses (10-100 nmol) caused a significant increase in SCBF. No change in systemic arterial blood pressure could be seen, except for a decrease after administration of the largest dose of R-PIA (100 nmol). It is concluded that R-PIA in doses of 10 nmol and larger induces an increase in SCBF after intrathecal injection in anesthetized rats and that an increase in blood flow is seen before any effect on the systemic circulation is detected. It can also be deduced that the antinociceptive effects of R-PIA after intrathecal injection are not a consequence of spinal ischemia and that disturbances in local blood flow cannot be expected to constitute a neurotoxic factor.

Animals↗
PubMed1993

Neuronal degeneration and spinal cavitation following intraspinal injections of quisqualic acid in the rat.

Microinjections of quisqualic acid were made in the spinal cord to evaluate the excitotoxic effects of this excitatory amino acid agonist on spinal neurons in the rat. Animals were divided into four groups based on post injection survival times of 7-49 days. Injections ranging from 0.3 to 2.0 microL of 8.3, 83, and 125 mM quisqualic acid or normal saline were made in the lower thoracic and upper lumbar spinal cord. At all survival times evaluated unilateral injections of quisqualic acid produced unilateral or bilateral cell death and a prominent inflammatory reaction. In 23/25 animals spinal cavities were also observed. Spinal cord segments at or near quisqualate injection sites contained darkly stained, hypertrophied neuronal profiles, and increased staining for glial fibrillary acidic factor. Immunostaining for glial fibrillary acidic factor was especially intense in areas of neuronal degeneration and in border areas of spinal cavities. The results of this study suggest that the intraspinal injection of quisqualic acid may be an effective method to study the mechanisms of excitatory amino acid neurotoxicity, and the pathogenesis of spinal cavitation following neuronal injury.

Animals↗
PubMed2006

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

OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: Intra-aortic propofol injections produce the quick suppression of MEP amplitudes and protect spinal cords from ischemia during aortic cross-clamping.

Animals↗
PubMed1993

A neurotoxicologic evaluation of the spinal cord after chronic intrathecal injection of R-phenylisopropyl adenosine (R-PIA) in the rat.

Studies in animals have shown that the adenosine receptor agonist R-phenylisopropyl adenosine (R-PIA) induces antinociceptive effects after intrathecal administration. Before such a potentially antinociceptive drug could be considered for intrathecal injection in humans, a neurotoxicologic examination of the spinal cord must be performed in animal models. Rats were injected once every day for 14 consecutive days with R-PIA or saline (controls). The number and density of neuronal cells were calculated by using light microscopy, and further examined with electron microscopy. The "disector method," which is an unbiased stereologic estimator of cell number and mean cell volume, was used for quantitative morphometric analyses. With this technique no significant changes could be seen in rats that had received R-PIA as compared to control rats. We conclude that no significant histologic changes could be detected after chronic intrathecal administration of R-PIA.

Animals↗
PubMed2002

BDNF modulates sensory neuron synaptic activity by a facilitation of GABA transmission in the dorsal horn.

Topical application of brain-derived neurotrophic factor (BDNF) to the adult rat isolated dorsal horn with dorsal root attached preparation inhibited the electrically evoked release of substance P (SP) from sensory neurons. This effect of BDNF was dose dependent (EC(50) 250 pM) and reversed by the tyrosine kinase inhibitor, K-252a. BDNF-induced inhibition of SP release was blocked by the GABA(B) receptor antagonist CGP 55485 but not by naloxone. Acute application of BDNF significantly increased potassium-stimulated release of GABA in the dorsal horn isolated in vitro and this effect was blocked by K-252a. Intrathecal injection of BDNF into the rat lumbar spinal cord induced a short-lasting increase in hindpaw threshold to noxious thermal stimulation that was blocked by CGP 55485 and was associated with activation of ERK in dorsal horn. These data suggest that exogenous BDNF can indirectly modulate primary sensory neuron synaptic efficacy via facilitation of the release of GABA from dorsal horn interneurons.

Afferent Pathways↗