We used pharmacological and surgical methods to determine the contribution of several neural components to joint injury in rats with adjuvant-induced arthritis. Both neonatal administration of ...capsaicin, which eliminates small-diameter afferents, and peripheral sympathectomy, which depletes catecholamines, attenuated joint injury. In contrast, the arthritis was more severe in spontaneously hypertensive rats, which have increased sympathetic tone. To address the contribution of the central vs peripheral afferent terminal selectively, a group of rats underwent unilateral dorsal rhizotomy. These rats developed a more severe arthritis in the deafferented limb. The increase in arthritis severity produced by dorsal rhizotomy could be reduced by prior sympathectomy or, less effectively, by prior treatment with capsaicin. The latter observation suggests that large-diameter afferents that are cut during dorsal rhizotomy also influence inflammation. Finally, intracerebroventricular injection of morphine attenuated the severity of arthritis, possibly through activation of bulbospinal sympathoinhibitory circuits. Taken together, these data indicate that no one class of nerve fiber is wholly responsible for the neurogenic component of inflammation in experimental arthritis but that large- and small-diameter afferents, sympathetic efferents, and CNS circuits that modulate those fiber systems all influence the severity of joint injury in arthritic rats.
Nuances in percutaneous discectomy Onik, G M; Helms, C
The Radiologic clinics of North America,
05/1998, Letnik:
36, Številka:
3
Journal Article
Recenzirano
This article presents an update of the field of percutaneous discectomy and a perspective as to where percutaneous discectomy currently fits in the treatment of patients with herniated discs. The ...future of minimally invasive disc surgery is also entertained, and a novel approach to lumbar disc surgery is presented.
We assessed the contribution of ATP and adenosine (i) to a major sign of acute inflammation, plasma extravasation (PE), in the rat knee joint and (ii) to the severity of joint injury in ...adjuvant-induced experimental arthritis, a chronic inflammatory disease. PE induced by local infusion of bradykinin, which we have previously shown to depend on the sympathetic postganglionic neuron terminal, was markedly enhanced by coinfusion of either ATP or the adenosine A2-receptor agonist 2-4-(2-carboxyethyl)phenylethylamino-5'-N-ethylcarboxamidoadenosine. Bradykinin-induced PE was inhibited by coinfusion of the ATP receptor antagonist adenosine 5'-α,β-methylenetriphosphate, the A2-receptor antagonist 3-(5H-thiozolo2,3bquinazolin-3-yl)phenol monohydrochloride, or the adenosine A1-receptor agonist N6-cyclopentyladenosine. The joint injury associated with experimental arthritis, which is reduced in severity in sympathectomized rats, was also markedly attenuated by daily administration of either ATP (40% reduction) or adenosine (55% reduction). These results demonstrate that the purines ATP and adenosine (acting at the A2receptor), cotransmitters in the sympathetic postganglionic neuron terminal, enhance bradykinin-induced sympathetic postganglionic neuron terminal-dependent PE but inhibit the joint injury of arthritis. These opposing purinergic effects on PE and joint injury suggest that enhanced PE protects against joint injury.
β 2-adrenergic Mechanisms in Experimental Arthritis Levine, Jon D.; Coderre, Terence J.; Helms, Clyde ...
Proceedings of the National Academy of Sciences - PNAS,
06/1988, Letnik:
85, Številka:
12
Journal Article
Recenzirano
Odprti dostop
We have studied (i) the contribution of specific adrenergic receptors to the proinflammatory effects of the sympathetic nervous system in experimental arthritis and (ii) the phases of the disease ...during which the sympathetic nervous system influences joint injury. Severity of joint injury was measured radiographically 28 days after induction of adjuvant arthritis in control rats and in rats treated with a variety of sympatholytic agents at various times during the course of the disease. Rats treated with a nonspecific catecholamine depletor (reserpine) or a β -adrenergic receptor antagonist (propranolol) had a delayed onset and significantly less severe joint injury than saline-treated controls when treatment began prior to injection of the adjuvant and continued to day 28 after the injection. When administered over the same treatment period, neither nonselective (phenoxybenzamine) nor selective prazosin (α 1) and yohimbine (α 2) α -adrenergic receptor antagonists affected the onset or severity of joint injury. Metoprolol, a β 1 antagonist, was also without effect. In contrast, two β 2 antagonists (butoxamine and ICI 118,551) significantly retarded disease onset and reduced the severity of joint injury. When reserpine or butoxamine treatment was initiated after the onset of clinically apparent arthritis, it was still possible to favorably influence the course of the disease. These data indicate an important contribution of the β 2-adrenergic receptor to joint injury in experimental arthritis.
Automated percutaneous discectomy is a new, safe procedure for treating herniated lumbar discs still contained by the annulus or posterior longitudinal ligament. In 1985, one of the authors reported ...a percutaneous nucleus aspiration technique using a 2-mm aspiration probe. This small probe produced minimal tissue damage, allowing the procedure to be done on an outpatient. In this series, 518 patients were treated using this technique for an overall success rate of 85%. Compensation patients, elderly patients, and patients with previous surgery were treated successfully using percutaneous discectomy on an outpatient basis. No intraoperative or postoperative complications occurred.
This study assessed the receptor site at which high systemic doses of epinephrine act to reduce the severity of adjuvant-induced arthritis in the rat. To this end we examined the effect of selective ...adrenergic antagonists on the reduction of arthritis by epinephrine, and also assessed whether high doses of selective adrenergic agonists mimicked the effect of epinephrine. The decrease in arthritis induced by epinephrine (0.5 mg/kg in chronic implant injected every 3 days) was significantly antagonized by the selective alpha 2-adrenergic antagonist, yohimbine, but not by selective alpha 1 (prazosin), beta 1 (metoprolol) or beta 2 (butoxamine) antagonists. In addition, chronic infusion of the alpha 2-adrenergic agonist clonidine, but not selective alpha 1 (phenylephrine), beta 1/beta 2 (isoproterenol) or beta 2 (salbutamol) agonists, resulted in decreased arthritis severity. These data suggest that the suppressive effect of high-dose epinephrine on joint injury in experimental arthritis is mediated by action at the alpha 2-adrenergic receptor.
We studied the effects of two non-steroidal anti-inflammatory analgesics (NSAIAs), acetylsalicylic acid (ASA) and acetaminophen, on sleep patterns in rats with adjuvant-induced arthritis. We found ...that in the normal rat both NSAIAs reduced non-rapid eye movement (NREM) sleep. In arthritic rats ASA and acetaminophen had opposite effects on sleep. ASA increased wakefulness and decreased all sleep stages and acetaminophen decreased wakefulness and increased NREM sleep and paradoxical sleep during the light hours (the hours of maximal sleep in the normal rat). When the effects of severity of arthritis were factored out, both drugs still had large and significant effects on sleep and wakefulness. Thus, two prostaglandin synthetase inhibitors showed differential effects on sleep and wakefulness in the normal rat and in rats experiencing chronic pain. Although ASA is important in the treatment of pain in rheumatic diseases, it may contribute to abnormal sleep patterns.
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