PubMed · 4126059
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
J B Snow, F Suga. 1973. Labyrinthine vasodilators.. https://doi.org/10.1001/archotol.1973.00780010377001
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The locomotor hyperactivity induced by systemic or local (nucleus accumbens) D-amphetamine injections can be blocked by systemic or local (prefrontal cortex) injections of prazosin, an alpha1-adrenergic antagonist (Blance et al., 1994). Microdialysis studies performed on freely moving animals indicated that prazosin (0.5 mg/kg, i.p.) does not modify the increase in the extracellular dopamine (DA) levels in the nucleus accumbens that are induced by D-amphetamine (2.0 mg/kg, i.p.), but it inhibits the D-amphetamine-induced locomotor hyperactivity (-63%, p < 0.0001). No behavioral activation occurred after the bilateral local perfusion of 3 microM D-amphetamine in the nucleus accumbens, although it led to a fivefold increase in extracellular DA levels. This increase in extracellular DA levels was not affected by prazosin (0.5 mg/kg, i.p.). When an intraperitoneal injection of D-amphetamine (0.5 mg/kg) was superimposed to the continuous local perfusion of 3 microM D-amphetamine, it induced a 64% increase in the extracellular DA levels in the nucleus accumbens, and this response was associated with simultaneous behavioral activation. Both the increases in extracellular DA levels and in locomotor activity were completely blocked by a pretreatment with prazosin, injected either systemically (0.5 mg/kg, i.p.) or locally and bilaterally into the prefrontal cortex (500 pmol/side). Complementary experiments indicated that the focal application of D-amphetamine requires at least a 4.8-fold higher increase in DA output compared with systemic D-amphetamine for the behavioral effects to be elicited. Altogether, these results suggest that locomotor activating effects of D-amphetamine are caused by the stimulation of cortical alpha1-adrenergic receptors by noradrenaline, which increases the release of a functional part of subcortical DA.
PURPOSE: A rare case of an anaphylactoid reaction to maltose solution is presented. CLINICAL FEATURES: A 28-yr-old man underwent repair of bilateral inguinal hernia under spinal anaesthesia with dibucaine. At the end of operation, he developed generalized flush and circulatory collapse immediately after receiving Na acetate solution containing maltose, 5%, i.v. The reactions were treated with 32 mg ephedrine and 250 mg methylprednisolone i.v., and rapid infusion of 1,000 ml acetated Ringer's solution. The skin tests provoked positive responses to maltose solutions. CONCLUSION: The clinical features and skin tests suggested that the episode was an anaphylactoid reaction to maltose. Maltose is one of the dissacharides (MW: 342) produced from starch and glycogen. Maltose solutions are used frequently in Japan as a carbohydrate source. Further study is required to confirm whether maltose has an immunological antigen-eliciting activity.
We and others previously reported that the antinociceptive effect of clonidine, measured by the hot plate method, was greater in spontaneously hypertensive rats (SHRs) than in Wistar-Kyoto rats (WKYs). In the present study, we found that the difference in clonidine-induced analgesia between these two strains was abolished after lesioning the presynaptic noradrenergic neurons with N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4). Previous studies indicated that clonidine increases tissue norepinephrine (NE) content by inhibiting NE release. We found that the basal NE concentration in locus coeruleus (LC), as measured by HPLC-ECD, was not different between WKYs and SHRs. Systemic application of clonidine (0.69 mg/kg, I.P.) significantly increased the tissue content of NE in the SHRs, but not in WKYs. Using pressure microinjection and high-speed chronoamperometric recording techniques, we found that local application of KCl to the LC brain slices increased extracellular NE levels in both strains. Perfusion of slices with clonidine (1 microM) selectively attenuated KCl-evoked NE release in SHRs, suggesting that clonidine-induced presynapitc inhibition is more effective in SHRs than in WKYs. In conclusion, our data indicate that SHRs possess augmented sensitivity to clonidine to inhibit presynaptic NE release, which may be responsible for the enhanced antinociceptive effect of clonidine in this strain.