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Head-to-head association in bovine spermatozoa induced by catecholamines.

Noradrenaline, adrenaline, and isoproterenol induce head-to-head association in bovine spermatozoa in a Tris-HCl-buffered medium. Noradrenaline was the most and isoproterenol the least efficient. This effect was stimulated by Ca2+, Mg2+ and Mn2+, Ca2+ being more efficient than the other two ions. At 2 X 10(-6) M Ca2+, oxidation products of adrenaline dissociated spermatozoa associated by washing; at 2 X 10(-5) M Ca2+, the dissociating effect was transformed into association. The induction of association by adrenaline was blocked by both alpha- and beta-adrenergic blockers at low concentrations (2 X 10(-7) M). Both cAMP and dibutyryl substituted cAMP (db-cAMP) induced association in the Tris-buffered medium at 2 X 10(-6) M Ca2+. Further increase in association was brought about by increasing the Ca2+ concentration to 2 X 10(-5) M. Prolongation of the treatment with cAMP increased association. When combined with cAMP under the same conditions as used in the combination with adrenaline, L-propranolol did not inhibit association induced by cAMP. In an identical experiment, performed in Tyrode solution, L-propranolol inhibited association induced by cAMP. At 2 X 10(-5) M, theophylline, caffeine, and papaverine induced association in the presence of 2 X 10(-5) M Ca2+. The results are compatible with the hypothesis that catecholamines act via receptors and formation of cAMP.

3',5'-Cyclic-AMP Phosphodiesterases↗

Calcium and catecholamines: relevance to cardiomyopathies and significance in therapeutic strategies.

There are marked differences between human cardiomyopathies, especially of the hypertrophic variety, and animal models. There is no simple way in which a hyperadrenergic state can explain the contractile abnormalities, although additional effects of calcium overload or marked hypertrophy come somewhat closer to linking animal and human diseases. One of the best links between excess catecholamine stimulation and myocardial damage lies in the enhanced sarcolemmal permeability which is mediated by beta-adrenergic stimulation and calcium ions in an isolated rat heart model. The therapeutic success of beta-adrenergic blockade and especially calcium antagonists in no way provide firm evidence for a hyperadrenergic state nor for intracellular calcium overload. In human hypertrophic cardiomyopathy, these agents may be acting merely by enlarging cavity size. In dilated cardiomyopathy, the use of beta-adrenergic blockers is still highly controversial and calcium antagonists are not well tested. It is the lack of appropriate models for both hypertrophic cardiomyopathy and dilated cardiomyopathy which is holding up research in this important area.

Adrenergic beta-Antagonists↗

Serotonin synthesis in adrenochromaffin cells.

The inter-renal (adrenal) gland of amphibians is composed of chromaffin and steroidogenic cells which can interact through a paracrine mode of communication. We have previously shown that serotonin is present in secretory granules of frog adrenochromaffin cells; concurrently, we have demonstrated that serotonin is a potent stimulator of corticosterone and aldosterone secretion by adrenocortical cells. The aim of the present study was to determine the origin of the amine contained in frog chromaffin cells. Using 3H-labelled tryptophan as a precursor, we observed the formation of substantial amounts of serotonin and its metabolite 5-hydroxyindoleacetic acid by frog inter-renal slices. Newly synthesized serotonin was secreted into the incubation medium and the release process was enhanced by depolarizing concentrations of KCl. Fluoxetine, and inhibitor of serotonin uptake, caused an increase of 3H-labelled serotonin in the incubation medium, suggesting that the indoleamine was taken up again by adrenal chromaffin cells. The capacity of the frog inter-renal gland to synthesize serotonin was also demonstrated by incubating inter-renal slices with non-labelled tryptophan or 5-hydroxytryptophan. In these conditions, we observed that the rate of synthesis was higher when 5-hydroxytryptophan was used as a a precursor, rather than tryptophan. Taken together, these results indicate that chromaffin cells, which have the capacity for synthesizing and releasing serotonin, behave like authentic serotonergic paraneurons. As far as is known, these data provide the first evidence for the occurrence of tryptophan-5-hydroxylase activity within the adrenal gland.

5-Hydroxytryptophan↗

Dose-dependent study of liver lipid peroxidation related parameters in rats treated with pp'-DDT.

Rats treated with increasing doses of pp'-DDT (60, 100 and 180 mg/kg body wt.) i.p., for 24 h, showed a dose-independent increase in liver cytochrome P450 levels, together with an increase in lipid peroxidation, measured as production of thiobarbituric acid reactants. This oxidant condition elicited in the liver by DDT was not accompanied by any change in the activity of NADPH-cytochrome c reductase or in the rate of superoxide anion generation by liver microsomal fraction. The activities of superoxide dismutase and glutathione peroxidase were found to be increased in the higher dose DDT-treated rats, without any change in those from catalase and glutathione reductase. The results presented showed an oxidant condition in the liver elicited by DDT treatment of rats, without any adequate hypothesis proposed to explain these data.

Adrenochrome↗

Short-term delayed-release microcapsules spraycoated with acrylic terpolymers.

A series of poly(ethyl acrylate (EA)/methyl methacrylate (MMA)/2-hydroxyethyl methacrylate (HEMA)) lattices were synthesized to prepare short-term delayed-release microcapsules by employing the Wurster coating process. Latex with a HEMA molar fraction exceeding 60% could not be synthesized as an aqueous suspension due to latex particle precipitation. The effects of monomer composition on the particle size of latex and the water-uptake and glass transition temperature (T(g)) of cast films were investigated. Lattices whose T(g) ranged from 40 to 80 degrees C were used to prepare the microcapsules. Most of the lattices exhibited excellent process performance while coating particles that were smaller than 100 microm: the product yields were 85.1-90.6% and the mean particle sizes were 82-85 microm. However, since the lattices with high molar ratios of EA and HEMA were highly hydrophilic and strongly adhesive, the core particles in the coating were severely agglomerated. The microcapsules coated with lattices whose HEMA molar fractions were higher than 50% were unable to retard the release of carbazochrome sodium sulfonate, a water-soluble model drug, during the initial 0.5 min. Poly(EA/MMA/HEMA) with a molar ratio of 9:9:10 appeared to be suitable for the preparation of short-term delayed-release microcapsules by the Wurster coating process.

Acrylates↗

Failure of carbazochrome sodium sulfonate (AC-17) to prevent dengue vascular permeability or shock: a randomized, controlled trial.

OBJECTIVE: We studied the ability of carbazochrome sodium sulfonate (AC-17) to prevent capillary permeability in dengue hemorrhagic fever/dengue shock syndrome. METHOD: A randomized, placebo-controlled trial in 95 children stratified by age and sex was conducted in two hospitals during 1992. AC-17 (n = 45 cases) or B vitamins as placebo (n = 50) were given as a bolus infusion and then as a continuous drip for 24 hours; a total of 300 mg of AC-17 was administered on the first 2 days and 150 mg on the third day. RESULTS: The two groups were comparable in age, sex, duration of illness, and clinical manifestations. No significant difference in shock or pleural effusion was noted between the two groups. Shock developed in 8.9% (4/45) of patients in the AC-17 group and 6% (3/50) in the placebo group (p = 0.44). Pleural effusion was found at 0, 24, 48, and 72 hours after admission in 4.4%, 20%, 31.1%, and 20% in the AC-17 group and 2%, 14%, 28%, and 14% in the placebo group, respectively. CONCLUSION: Administration of AC-17 does not prevent plasma leakage or shock in dengue hemorrhagic fever/dengue shock syndrome.

Adrenochrome↗