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At least 487 records · Page 27Linked to original sources
PubMed2000

Participation of angiotensin II in pressor response and norepinephrine release to spinal nerve stimulation in pithed rats.

Experiments were carried out to examine whether endogenous angiotensin II (A-II) is involved in the regulation of release of norepinephrine (NE) elicited by the stimulation of spinal sympathetic nerves in pithed rats. It was assessed in terms of the alterations in concentrations of arterial blood plasma A-II and NE elicited by nerve stimulation (5 Hz, 50 V, 1 msec for 45 s) in pithed rats under vehicle or captopril (3 mg/kg, i.v.) treatment. Comparative study with pentobarbital anesthetized rats showed that pithing rats have the characteristics of lower basal blood pressure and lower NE level, whereas they have higher basal A-II level. In pithed rats treated with vehicle, pressor response to nerve stimulation was accompanied by increases in both A-II and NE level. In rats treated with captopril, the nerve stimulation caused about 40% lower increases in pressor response and NE level than those observed in rats treated with vehicle. These results suggest that the sympathetic nerve-induced NE release is facilitated by endogenous A-II in pithed rats, and that captopril exerts its inhibitory effect on the pressor response to nerve stimulation through the suppression of this interaction.

Angiotensin II↗
PubMed1993

Novel surgical strategies to correct neural deficits following experimental spinal nerve root lesions.

In attempts to correct neural deficits following avulsion trauma, novel experimental strategies were developed. In rats, spinal roots were replanted superficially in the dorsal horn following dorsal root avulsion and concomitant denervation by ganglionectomy. Outgrowth from cord neurons in the dorsal horn into the implanted dorsal root was demonstrated by means of retrograde HRP labeling. Double labeling experiments showed that some of these neurons had retained their central projections while extending new processes into the implanted root. After dorsal root avulsion, sensory pathways might be reconstructed by substituting the lost input from damaged primary sensory neurons with induced peripheral outgrowths from secondary neurons. In primates, intraspinal replantation of avulsed ventral nerve roots was investigated as a surgical treatment for motor deficits that develop after severe brachial plexus injury. Two to 3 months after surgery there were EMG signs of reinnervation in previously denervated muscles, which were shortly followed by evidence of clinical recovery. A gradual improvement in the function of the affected arm occurred and motor behavior became normalized, although the EMG activity in the reinnervated muscles at maximal contraction was still reduced. The outcome of these experimental studies indicates that reconstructive surgery applied to the brachial plexus might be of value to restore functional deficits induced by traumatic spinal nerve root avulsions also in man.

Animals↗
PubMed1996

Ultrastructural changes in spinal nerve roots induced by autologous nucleus pulposus.

STUDY DESIGN: Ultrastructural changes were analyzed by transmission electron microscopy in nerve roots exposed to autologous nucleus pulposus experimentally. OBJECTIVES: To assess if ultrastructural changes were present in areas with no light microscopic changes in nerve roots exposed to autologous nucleus pulposus in a pig model. SUMMARY OF BACKGROUND DATA: Previous analyses have shown that there is focal nerve fiber damage in nerve roots exposed to autologous nucleus pulposus in the pig. These changes could not fully explain the reduction in nerve conduction velocity seen in the same nerve roots. In the present study, the parts of the nerve roots that did not display breakdown of axons or myelin sheaths at the light microscopic level were analyzed regarding ultrastructural changes. METHODS: In a previous study, nucleus pulposus was harvested from a lumbar disc and placed epidurally onto the cauda equina at the sacrococcygeal level in pigs. Retroperitoneal fat was used as control. After 1, 3, and 7 days, the nerve roots were excised and processed for light microscopy. Parts of the nerve roots that appeared normal at the light microscopic level were further processed for the present electron microscopic examination. RESULTS: Significant ultrastructural changes, such as expansion of the Schwann cell cytoplasm and intracellular edema with vesicular swelling of the Schmidt-Lanterman incisures, were observed in nerve fibers with normal axons. Although present after nucleus pulposus and control application, the changes were more pronounced after the application of nucleus pulposus. CONCLUSIONS: Epidural application of autologous nucleus pulposus without any pressure may induce not only nerve function impairment but also axonal injury and significant primary Schwann cell damage with vesicular swelling of Schmidt-Lanterman incisures. However, because axonal and Schwann cell changes affected only part of the nerve fibers, further causes of the impaired nerve conduction need to be determined.

Animals↗
PubMed1995

Repair of ruptured spinal nerve roots in a brachial plexus lesion. Case report.

A 22-year-old woman sustained a brachial plexus injury with supraganglionic rupture of the C-8 and T-1 nerve roots as a result of a traffic accident. She was operated on approximately 1 week following the accident. After a hemilaminectomy, the intradural defects in the ruptured roots were bridged with sural nerve grafts. Within 3 years she recovered function in all muscles supplied from the lower roots in the plexus except for the intrinsic hand muscles, but she had a persisting, complete sensory loss in the ulnar nerve distribution. The possibility for functional gain after repair of spinal root lesions in brachial plexus patients is discussed.

Adult↗
PubMed1994

[The surgical treatment of muscle tonus disorders by the destruction of the input areas of the posterior spinal nerve roots].

Stereotactic cryodestruction of the subcortical ganglions for microdestruction of the inlets of the radices spinales was conducted in resistant to drug and surgical treatment patients with impaired muscular tension and spastic pain syndrome (infantile cerebral paralysis, dystonia musculorum deformans, postencephalitic spastic-hyperkinetic syndrome). A total of 8 patients aged 19-46 were treated. The destruction of the segments depended on the site of the tension impairment. In cervical, upper extremity, lumbar, lower extremity involvement the segments to be destroyed were, respectively: SV--SVII, SVIII, LII--LIII, LIV, LV and SI. The surgery aimed at breaking the centripetal nociceptive and myotactic tracts. The treatment reduced muscular hypertonicity and hyperkinesis, relieved spastic pain. The paper presents anatomic and neurophysiological grounds for the procedure application.

Adult↗
PubMed2003

Neurodegenerative effect of electrocauterization on spinal nerve root: an experimental study.

We investigated the number of degenerated neurons in spinal roots of rabbits after spinal surgery to test if electrocauterization causes neuronal loss. The number of degenerated neurons was higher in study group than in control group, and the number of live neurons was higher in control group than in study group. These results suggest that electrocauterization applied during spinal surgery is hazardous to spinal neurons and should not be applied unless required.

Animals↗
PubMed1998

Supraspinal involvement in the production of mechanical allodynia by spinal nerve injury in rats.

This study examined whether or not the production of mechanical allodynia in a rat model of neuropathic pain required an involvement of supraspinal site(s). To this aim, we assessed the effect of spinal cord section at the L1 segment level on the mechanical allodynia sign (i.e. tail flick/twitch response), which was elicited by innocuous von Frey hair stimulation of the tail after unilateral transection of the tail-innervating nerve superior caudal trunk (SCT) at the level between the S3 and S4 spinal nerves. Cord transection or hemisection of the cord ipsilateral to the injured SCT drastically (though not completely) blocked the behavioral sign of mechanical allodynia (leaving noxious pinprick-elicited tail withdrawal reflex intact), whereas sham section or contralateral hemisection of the cord was without effect. These results suggest that the generation of mechanical allodynia following partial peripheral nerve injury involves transmission of the triggering sensory signal to a site(s) rostral to the L1 segment via an ipsilateral pathway(s).

Animals↗