PubMed · 14243098
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G PICKROTH. 1964-07-09. [INHALATION ANESTHESIA].. https://pubmed.ncbi.nlm.nih.gov/14243098/
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OBJECTIVES: The peripheral administration of granulocyte macrophage colony-stimulating factor (GM-CSF), widely used for the treatment of cytopenias, is often associated with neurological effects [Lieschke et al., N Engl J Med 1992;327:28-34]. This cytokine has recently been reported to affect neurotransmitter metabolism in the nervous system [Bianchi, Neuroreport 1997;8:3587-3590]. To further investigate the neuromodulatory effect of GM-CSF we studied the influence of GM-CSF on the efferent electric activity in the splenic nerve and the integral neuronal activity in medullary gigantocellular reticular formation (MGRF) in rats. METHODS: Anaesthetized (sodium thiopental 70 mg/kg, i.p.) Wistar rats were injected subcutaneously with 1 microg/kg of hr GM-CSF. Efferent electric activity in the splenic nerve and integral electric activity in MGRF were analyzed. The effectiveness of the applied dose of GM-CSF was verified by determining the elevation of the white blood cell count in peripheral blood 60 min after injection. RESULTS: We found that GM-CSF increases efferent electric activity in the splenic nerve and decreases that of MGRF as is evident by the frequency of electric discharges. The latency of both effects was 5-15 min. CONCLUSIONS: This data support the view that GM-CSF exerts a neuromodulatory effect and may provide a new link of neuroimmune communication.
Despite common use of narcotics in the clinical management of severe traumatic brain injury (TBI), in experimental models rats treated with fentanyl have exhibited worse functional outcome and more CA1 hippocampal death than rats treated with standard isoflurane anesthesia. We hypothesized that greater post-traumatic excitotoxicity, reflected by cerebral glucose utilization (CMRglu), may account for detrimental effects of fentanyl vs. isoflurane. Rats were anesthetized with either isoflurane (1% by inhalation) or fentanyl (10 mcg/kg iv bolus then 50 mcg/kg/h infusion). 14C-deoxyglucose autoradiography was performed 45 min after controlled cortical impact (CCI) to left parietal cortex (n=4 per anesthetic group) or in uninjured rats after 45 min of anesthesia (n=3 per anesthetic group). Uninjured rats treated with fentanyl vs. isoflurane showed 35-45% higher CMRglu in all brain structures (p<0.05) except CA3. After TBI in rats treated with isoflurane, CMRglu increased significantly only in ipsilateral CA1 and ipsilateral parietal cortex (p<0.05 vs. isoflurane uninjured). Conversely, after TBI in rats treated with fentanyl, CMRglu increased markedly and bilaterally in CA1 and CA3 (p<0.05 vs. fentanyl uninjured), but not ipsilateral parietal cortex. In contralateral CA1, CMRglu was nearly two times greater after TBI in fentanyl vs. isoflurane treated rats (p<0.05). Hyperglycolysis was exacerbated in CA1 and CA3 hippocampus after TBI in rats treated with fentanyl vs. isoflurane anesthesia. This post-traumatic hyperglycolysis suggests greater excitotoxicity and concurs with reports of worse functional outcome and more CA1 hippocampal death after TBI with fentanyl vs. isoflurane anesthesia.