The effects of cocaine on the contractile response of isolated human nasal mucosal blood vessels to field stimulation and methoxamine were investigated. Results showed that cocaine antagonized methoxamine and inhibited field stimulation. The drug increased resting tension in human nasal mucosa in vitro through direct actions and potentiated mucosal contractions by norepinephrine and epinephrine. The study indicated that high concentrations of cocaine may actually antagonize alpha-adrenoceptors, but these concentrations are not necessary in eliciting desired degrees of vasoconstriction in nasal blood vessels while being applied as a local anesthetic.
The glyoxylic catecholaminergic histofluorescence method was employed on tissues from five cases of juvenile nasopharyngeal angiofibroma in order to study the sympathetic innervation present. There was no sympathetic innervation identified in tumor parenchyma while some scant noradrenergic fibers were found in the tumor border. These findings indicate that keeping a dissection surface out of tumor during planned excisions may be very important, as vessels there have more sympathetic innervation which will then result in good vessel contraction in controlling bleeding. Non-diseased nasal mucosa from each patient was used as control tissue, with its submucosa seen to be filled with noradrenergic innervation. Some noradrenergic fibers were also found to innervate the muscle layers of arterioles or venules adjacent to the sphenopalatine foramen.
Methamphetamine (MA) and ethanol (EtOH) are two commonly abused drugs. Previous behavioral studies indicated that MA may synergistically alter EtOH responses. In the present study, we found that local application of MA did not potentiate ethanol-induced depressions of the spontaneous activity of Purkinje neurons in urethane-anesthetized rats. We and others previously found that, in cerebellar Purkinje neurons, EtOH and gamma-amino-butyric acid (GABA)-mediated depressions can be enhanced by norepinephrine (NE) acting via beta-adrenergic receptors while these responses are decreased by activation of alpha-adrenergic receptors. In the present experiment, after blocking alpha-adrenergic receptors with prazocin, MA significantly enhanced EtOH responses in most of neurons studied. It has been reported that MA may directly and indirectly enhance alpha-adrenergic and beta-adrenergic receptor-mediated responses. The present study may suggest that MA can negatively modulate (antagonize) the depressant effects of ethanol via the alpha-adrenergic receptor, which oppose the positive modulatory mechanism (potentiation of EtOH depression) via actions of the beta-adrenergic receptors. We found that lesioning NE neurons with N-chloroethyl-N-ethyl-2-bromobenzylamine hydrochloride (DSP4), a selective noradrenergic neurotoxin, enhance the MA-facilitated ethanol responses, suggesting that this action of MA may not require NE. Since it has been reported that MA increases serotonin (5-HT) and catecholamine release from their nerve terminals, MA may potentiate EtOH depressions by facilitating the release of NE and 5-HT. Taken together, our data suggested that MA may modulate EtOH responses via catecholaminergic and serotonergic mechanisms in cerebellar Purkinje neurons.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.