PubMed · 9640513
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S Gazzola. 1998. Preparing LET solution.. https://pubmed.ncbi.nlm.nih.gov/9640513/
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A previous study demonstrated that microinjection of carbachol (CCh) into the dorsal periaqueductal gray matter (dPAG) of rats increases the latency for the tail flick reflex. Several other studies have implicated the raphe magnus (NRM) and the reticularis paragigantocellularis (NRPG) nuclei as relay stations through which descending pathways from the PAG project to the spinal cord via the dorsolateral funiculus (DLF). In the present study, the effects of microinjecting CCh into the dPAG on the tail flick test were examined in rats in which the ipsilateral DLF was previously lesioned, or saline or lidocaine (2%) was microinjected into the NRM or ipsilateral NRPG. The DLF lesion did not change the baseline threshold of the animals in the test, but abolished the CCh-induced increase in the tail flick latency from the dPAG. The neural block of the NRM or NRPG with lidocaine also did not change significantly the latency for the tail flick reflex. The increase in the tail flick latency produced by CCh from the dPAG was not changed by the neural block of the NRPG, but was significantly reduced by the neural block of the NRM. These results are interpreted as indicative that the central antinociceptive mechanisms activated by CCh from the dPAG depend on a descending pathway that projects to the spinal cord via DLF utilizing at least the NRM, but not the NRPG, as an intermediary relay station.
The present study describes the simultaneous determination of seven different kinds of local anesthetics and one metabolite by GC-MS with solid-state extraction: Mepivacaine, propitocaine, lidocaine, procaine (an ester-type local anesthetics), cocaine, tetracaine (an ester-type local anesthetics), dibucaine (Dib) and monoethylglycinexylidide (a metabolite of lidocaine) were clearly separated from each other and simultaneously determined by GC-MS using a DB-1 open tubular column. Their recoveries ranged from 73-95% at the target concentrations of 1.00, 10.0 and 100 microg/ml in plasma, urine and water. Coefficients of variation of the recoveries ranged from 2.3-13.1% at these concentrations. The quantitation limits of the method were approximately 100 ng/ml for monoethylglycinexylidide, propitocaine, procaine, cocaine, tetracaine and dibucaine, and 50 ng/ml for lidocaine and mepivacaine. This method was applied to specimens of patients who had been treated with drip infusion of lidocaine, and revealed that simultaneous determination of lidocaine and monoethylglycinexylidide in the blood and urine was possible.
Activation of neurons in the ventromedial medulla by electrical stimulation or by microinjection of opioid or cholinergic agonists produces antinociception that is mediated in part by spinally-projecting noradrenergic neurons. Several lines of evidence indicate that these noradrenergic neurons are located in the pontine A7 catecholamine cell group. For example, anatomical studies have demonstrated that neurons in the ventromedial medulla project to the noradrenergic neurons in the A7 catecholamine cell group that provide the major noradrenergic innervation of the spinal cord dorsal horn. In addition, electrical and chemical stimulation of A7 neurons produces antinociception that can be reduced by intrathecal injection of alpha2-adrenoceptor antagonists. The present studies provide more direct evidence that activation of neurons in the ventromedial medulla produces antinociception by activating noradrenergic neurons in the A7 cell group. Neurons in the ventromedial medulla were stimulated by microinjecting the cholinergic agonist carbachol (5 microg) into sites in the nucleus raphe magnus or the nucleus gigantocellularis pars alpha of pentobarbital anesthetized Sprague-Dawley rats. In some experiments, the local anesthetic tetracaine (10 microg) was then microinjected near the A7 cell group to inactivate the spinally-projecting noradrenergic neurons. In other experiments, cobalt chloride (100 mM) was microinjected near the A7 cell group to block synaptic activation of spinally-projecting noradrenergic neurons. Microinjection of carbachol into sites in the ventromedial medulla produced antinociception, assessed using the tail flick test, that lasted more than 60 min. However, the effects of carbachol were attenuated by microinjection of either tetracaine or cobalt into sites near the A7 cell group neurons identified by tyrosine hydroxylase-immunoreactivity. Similar injections of tetracaine or cobalt more than 500 microm from the A7 neurons did not alter the antinociceptive effect of carbachol. These results support the conclusion that the antinociception produced by activating neurons in the ventromedial medulla is mediated in part by the subsequent activation of spinally-projecting noradrenergic neurons in the A7 cell group.