Bhattacharya S K, Das N, Dasgupta G
Department of Pharmacology, Banaras Hindu University, Varanasi, India.
Indian J Exp Biol. 1990 Jul;28(7):683-5.
Earlier studies from this laboratory have indicated that CNS exerts a modulatory influence over acute inflammation in rats. The present study examines the existence of a similar modulatory effect of CNS on a subacute inflammatory paradigm, the croton oil-induced granuloma pouch in rats. The inflammatory exudate, collected on 6th day after croton oil administration, was found to be substantially less in intracerebroventricular (icv) cannulated and artificial cerebrospinal fluid administered rats as compared to their uncannulated saline (ip) administered counterparts. This effect may be due to stress induced by cannulation. Centrally administered pharmacological agents which attenuate central monoaminergic, cholinergic or prostaglandin systems had insignificant effects on the inflammatory exudate. However, induced increase in central noradrenergic activity was found to attenuate the inflammation when the treatment was done before, but not 48 hr after, the induction of the inflammation. In contrast, induced increase in central serotonergic activity had no effect on the volume of the inflammatory exudate at either time period. Steady state levels of rat brain noradrenaline and serotonin, but not dopamine, were enhanced by the inflammatory procedure. However, these effects may be attributed to the stress induced by croton oil inflammation. The investigation indicates that the modulatory influence of CNS remains limited to the acute phase of inflammation, being exerted mainly by the central noradrenergic system. Once the inflammation has progressed, this modulatory influence of CNS is no longer apparent.
该实验室早期的研究表明，中枢神经系统（CNS）对大鼠的急性炎症具有调节作用。本研究考察了CNS对亚急性炎症模型（巴豆油诱导的大鼠肉芽肿袋）是否存在类似的调节作用。在给予巴豆油后第6天收集的炎症渗出物发现，与未插管并腹腔注射生理盐水的大鼠相比，脑室内插管并注射人工脑脊液的大鼠的炎症渗出物明显较少。这种效应可能是由于插管引起的应激。中枢给予的减弱中枢单胺能、胆碱能或前列腺素系统的药物对炎症渗出物影响不显著。然而，发现当在炎症诱导前而非诱导后48小时进行处理时，中枢去甲肾上腺素能活性的诱导增加可减轻炎症。相反，在两个时间段中，中枢5-羟色胺能活性的诱导增加对炎症渗出物的量均无影响。炎症过程可提高大鼠脑内去甲肾上腺素和5-羟色胺的稳态水平，但对多巴胺无影响。然而，这些效应可能归因于巴豆油炎症引起的应激。该研究表明，CNS的调节作用仅限于炎症的急性期，主要由中枢去甲肾上腺素能系统发挥作用。一旦炎症进展，CNS的这种调节作用就不再明显。
