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PubMed1987

[Transient vision loss caused by scandicaine with added arterenol in the excision of basalioma of the side of the nose].

In facial dermatosurgery, the addition of sympathomimetics to local anaesthetics produces a desirable topical effect by creating an almost bloodless operation field due to transitory vasoconstriction. In an 87-year-old woman suffering from a meningioma that had caused blindness of the left eye, a basal-cell carcinoma was removed from the right side of the nose. The local anaesthetic contained noradrenaline at a concentration of 1:50,000. After the operation, the patient complained of headache and a transient loss of vision. We suggest that noradrenaline caused vasoconstriction of the arteria centralis retinae via arterial periorbital anastomoses. Patients with severe vision disorders should be considered a risk group, in whom sympathomimetics should not be added to local anaesthetics used in skin surgery of the middle and upper face.

Aged↗
PubMed1988

Reactivity of catecholamines and related substances in the mouse lymphoma L5178Y cell assay for mutagens.

Using the L5178Y mouse lymphoma cell thymidine kinase locus and the Salmonella his locus assays, the mutagenic potentials of several catecholamines and related compounds were examined. No supplementary metabolic activation systems were used. In the mouse lymphoma assay, the dihydroxybenzenes catechol and hydroquinone had similar and appreciable mutagenic potentials, whereas resorcinol was less active. Derivatives of catechol, such as dopamine and epinephrine, were mutagenic, whereas the related monohydroxylated compounds tyramine and synephrine were inactive. The primary amine, arterenol, and the corresponding secondary amine, epinephrine, induced similar mutagenic responses. Carboxylation of the side chain of dopamine, giving L-dopa, reduced the maximum mutagenic response. The introduction of charged groups directly on to the aromatic ring also reduced mutagenic activity, while an intervening methylene reversed this effect. Thus, 3,4-dihydroxyhydrocinnamic acid was more active than 3,4-dihydroxybenzoic acid. The compound active at the lowest doses was 4-tert-butyl catechol. The activities of these compounds are highly dependent upon substituent groups. Experiments with superoxide dismutase gave circumstantial evidence for some of the mutagenic activity being due to superoxide anion. Active oxygen species might be responsible for some of the observed effects, but this cannot be concluded from the superoxide dismutase experiments. Mutagenic responses in Salmonella were very low but were significant for L-dopa in three strains and for epinephrine and arterenol in one strain. Limited DNA association studies of 14C-dopamine suggest interactions in L5178Y and Salmonella cells and in mouse liver. The mutagenicity of dopamine in L5178Y is reduced by high serum concentrations during the exposure period, while the apparent association with DNA is unaffected.

Animals↗
PubMed2001

Regulation of apolipoprotein E secretion in rat primary hippocampal astrocyte cultures.

Apolipoprotein E isoforms may have differential effects on a number of pathological processes underlying Alzheimer's disease. Recent studies suggest that the amount, rather than the type, of apolipoprotein E may also be an important determinant for Alzheimer's disease. Therefore, understanding the regulated synthesis of apolipoprotein E is important for determining its role in Alzheimer's disease. We show here that in rat primary hippocampal astrocyte cultures, dibutyryl-cAMP increased apolipoprotein E secretion with time in a dose-dependent manner (to 177% at 48 h) and that retinoic acid potentiated this effect (to 298% at 48 h). Dibutyryl-cAMP also gave a rapid, albeit transient, increase of apolipoprotein E mRNA expression (to 200% at 1 h). In contrast, the protein kinase C activator phorbol 12-myristate 13-acetate decreased both apolipoprotein E secretion (to 59% at 48 h) and mRNA expression (to 22% at 1 h). Phorbol 12-myristate 13-acetate also reversed the effects of dibutyryl-cAMP. Apolipoprotein E secretion was also modulated by receptor agonists for the adenylyl cyclase/cAMP pathway. Isoproterenol (50 nM, a beta-adrenoceptor agonist) enhanced, while clonidine (250 nM, an alpha2-adrenoceptor agonist) decreased, secreted apolipoprotein E. We also analysed the effects of agonists for the phospholipase C/protein kinase C pathway. Arterenol (1 microM, an alpha1-adrenoceptor agonist) and serotonin (2.5 microM) enhanced, whereas carbachol (10 microM, an acetylcholine muscarinic receptor agonist) decreased secreted apolipoprotein E. The effects of these non-selective receptor agonists were modest, probably due to effects on different signalling pathways. Arterenol also potentiated the isoproterenol-mediated increase. We also show that phorbol 12-myristate 13-acetate and dibutyryl-cAMP have opposite effects on nerve growth factor, as compared to apolipoprotein E, secretion, suggesting that the results obtained were unlikely to be due to a general effect on protein synthesis. We conclude that astrocyte apolipoprotein E production can be regulated by factors that affect cAMP intracellular concentration or activate protein kinase C. Alterations in these signalling pathways in Alzheimer's disease brain may have consequences for apolipoprotein E secretion in this disorder.

Alzheimer Disease↗
PubMed1997

The delta-opioid receptor in SK-N-BE human neuroblastoma cell line undergoes heterologous desensitization.

The human neuroblastoma cell line SK-N-BE expresses delta-opioid receptors negatively coupled to adenylyl cyclase. Prolonged treatment (2 h) of the cells with 100 nM etorphine leads to an almost complete desensitization (8.2 +/- 5.9 vs. 45.8 +/- 8.7% for the control). Other receptors negatively coupled to adenylyl cyclase, namely, D2-dopaminergic, alpha 2-adrenergic, and m2/m4-muscarinic, were identified by screening of these cells, and it was shown that prolonged treatment (2 h) with 1 microM 2-bromo-alpha-ergocryptine or 1 microM arterenol resulted in a marked desensitization of D2-dopaminergic and alpha 2-adrenergic receptors, respectively. Cross-desensitization experiments revealed that pretreatment with etorphine desensitized with the same efficiency the delta-opioid receptor and the D2-dopaminergic receptor, and pretreatment with 2-brorno-alpha-ergocryptine also desensitized both receptors. In contrast, pretreatment with etorphine desensitized only partly the alpha 2-adrenergic receptor response, whereas pretreatment with 1 microM arterenol partly desensitized the delta-opioid receptor response. It is concluded that the delta-opioid receptor-mediated inhibitory response of adenylyl cyclase undergoes heterolgous desensitization, and it is suggested that delta-opioid and D2-dopaminergic receptors are coupled to adenylyl cyclase via a G12 protein, whereas alpha 2-adrenergic receptor could be coupled to the enzyme via two G proteins, G12 and another member of the G1/G0 family.

Adenylyl Cyclases↗
PubMed1986

Ovarian steroid modulation of norepinephrine action on luteinizing hormone release. Analogous effects in male and female rats.

The modulatory actions of ovarian steroids on the norepinephrine (NE) induced alterations in luteinizing hormone (LH) secretion were examined in male and female rats. Long-term (4 weeks) castrated male and female rats bearing chronic third-ventricle cannulae were implanted with intra-atrial catheters. Animals were bled sequentially at 5- or 15-min intervals for 4-6 h, and plasma LH secretory patterns were determined by radioimmunoassay. After a 2- to 3-hour control bleeding period, castrated unprimed rats received an intracerebroventricular (ICV) infusion of 0.3 mumol of arterenol bitartrate or vehicle. Blood sampling was continued for an additional 2-3 h after infusion. In female rats NE caused a rapid and potent inhibition of episodic LH secretion which was characterized by decreases in mean plasma LH, mean pulse amplitude, and pulse frequency. Similarly, ICV infusion of NE into male rats resulted in decreased mean plasma LH and pulse frequency. In a second series of experiments, castrated male and female rats were primed with estrogen and progesterone 2 days prior to the bleeding/infusion session. Animals were bled sequentially and infused with 0.3 mumol arterenol bitartrate or vehicle during a morning or afternoon session. ICV infusion of vehicle had no effect on plasma LH in either sex regardless of the time of day. NE infusion into estrogen and progesterone primed female rats resulted in significant elevations of plasma LH during both morning and afternoon periods. In estrogen and progesterone primed male rats, NE infusion resulted in a marked facilitation of LH release, similar to that observed in female rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Activity Cycles↗