Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Reserpine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources

[Treatment with sympathetic intravenous block with reserpine in work-related reflex sympathetic dystrophy].

To assess the results obtained in treatment of sympathetic reflex dystrophy by sympathetic endovenous blockades with reserpine in working patients. We reviewed 170 diagnoses of sympathetic reflex dystrophy in 165 patients. One hundred seven were located in the foot, 13 were in the knee and 50 were in the hand. All were treated once a week for 3 weeks with local sympathetic endovenous blocks with reserpine (1 mg in the upper extremity and 1.5 mg in the lower extremity). We analyzed the location, etiology, course, X-rays, gammagrams, psychological state, other treatments, associated conditions, number of blocks received and side effects. The results were classified as excellent, good, fair and nil. We particularly reviewed sympathetic reflex dystrophy associated to Colles' fractures. Five hundred forty endovenous sympathetic blocks with reserpine were performed. Results obtained were excellent in 57 (34%) patients, good in 77 (45%), fair in 29 (17%) and nil in 7 (4%). Sympathetic reflex dystrophy leads to loss of 215 +/- 91 working days. In patients with Colles' fracture without sympathetic reflex dystrophy the loss is 96 +/- 31 days, although this period lengthens to 115 +/- 15 days if the two conditions are associated in stage I and to loss of 193 +/- 71 days if the association is in stage II. Results of treating sympathetic reflex dystrophy with sympathetic endovenous blocks with reserpine are satisfactory, particularly when diagnosis and treatment are early, clearly demonstrating the usefulness of this technique in workplace medicine.

Adult↗

[Lithium oxybutyrate correction of the circadian pattern of reserpine-induced depression].

Lithium oxybutyrate was studied for effects on the circadian pattern of reserpine-induced depression ("open field") in relation to the time of the drug use. Reserpine given in a single dose of 0.75 mg/kg caused a reduction of diurnal frequencies, inversion of rhythm acrophases, decrease in their mesors and amplitudes. Lithium oxybutyrate given after rhythm acrophases in reserpine-treated animals recovered the lost 24-hour harmonics phase relations between them, but when used before acrophases it did not only fail to prevent the animals from the exhausting action of reserpine, but aggravated the course of depression.

Animals↗

Magnesium and reserpine influence norepinephrine sensitivity of vas deferens in rats.

Reserpine induced supersensitivity to norepinephrine (NE) in rat vas deferens was sought by alteration of Mg++ and Ca++ concentration in incubation medium in the absence and presence of EDTA. Vas deferens incubated in Mg++ free and Mg++ excess media showed supersensitivity and subsensivity to NE respectively. Alterations in the sensitivity to NE produced by varying the concentrations of Mg++ were comparatively less. In the presence of EDTA, vas deferens obtained from reserpinized animals showed subsensitivity in normal and Mg++ excess media and supersensitivity in Mg++ free medium. In the presence of EDTA, reserpinized preparations showed slight supersensitivity in normal Mg++ medium, marked supersensitivity in Mg++ free and lesser subsensitivity in Mg++ excess medium. Probably EDTA by more effectively removing Mg++ from the membrane binding sites by chelation makes the membrane permeable to Ca++ leading to supersensitivity to NE (observed only in the presence of EDTA). These results suggest that the failure of reserpine to induce supersensitivity to NE in rat vas deferens may be due to an enhanced antagonism of Mg++ on Ca++ movements in this preparations due to the poor capacity of rat tissue to retain Ca++.

Animals↗

Autoradiographic localization of [3H]reserpine binding sites in rat brain.

[3H]Reserpine was administered (i.v.) to rats and they were killed 7 days later. At this time, the regional localization of radioactivity paralleled the distribution of specific binding sites observed in other laboratories. Autoradiographic studies of certain areas displayed a striking localization of radioactivity. There was a marked association of autoradiographic grains with areas containing catecholamine systems. In particular, the locus ceruleus, the caudate-putamen, the nucleus accumbens, the dorsolateral septum and the infundibulum had high grain densities. In the caudateputamen, there was a clear localization of grains to the neuropil. There was also a striking association of autoradiographic grains with certain hypothalamic nuclear, i.e., the dorsal premammillary nucleus, the prelateral mammillary nucleus and the lateral mammillary nucleus. In these areas, the grains were clearly localized in the cytoplasm of the cell bodies. All of the above localizations of autoradiographic grains were blocked by administration of unlabeled reserpine before injection of [3H]reserpine. The significance of these findings and their relationship to the clinical actions of reserpine are discussed.

Animals↗

Vesicular and juxtavesicular serotonin: effects of lysergic acid diethylamide and reserpine.

An extensive analysis of subcellular serotonin (5-HT) compartmentation with and without reserpine was undertaken in order to localize further the effect of LSD on rat brain 5-HT. Modification of the subfractionation procedure resulted in an increase in purity of fractions and a decrease in variability of 5-HT content. With the modified procedure, the administration of LSD produced a significant increase in 5-HT in the nerve-ending fraction prepared from rat whole brain. LSD caused a 50% increase in 5-HT in the vesicular fraction which was recovered after osmotic disruption of nerve-endings. The increase of 5-HT in the vesicular fraction after LSD was not demonstrable in rats treated with reserpine for as long as 2 weeks postreserpine. Instead, with reserpine pretreatment the LSD-induced increase in 5-HT was localized to the intrasynaptosomally derived "end supernatant" as early as 48 hours postreserpine. Thus, an unanticipated "juxtavesicular" site capable of 5-HT retention or binding was detected. In crude subcellular fractions, by contrast, significant increase in 5-HT were not observed with LSD administration until 4 days after reserpine, at which time at least a 50% 5-HT repletion had occurred. This study of drug interactions suggests a juxtavesicular compartment that may be of functional importance in presynaptic binding or transport of 5-HT.

Animals↗

Studies on hyperactivity in rats given tranylcypromine stereoisomers and reserpine.

Hyperactivity, salivation, piloerection, exophthalmia and ejaculation occurred in rats given reserpine (5 mg/kg i.p.) 2 hr after an oral dose (5 mg/kg) of trans-dl-2-phenylcyclopropylamine (tranylcypromine, dl-Tcp). The same syndrome occurred in rats given the d-isomer (d-Tcp) plus reserpine but not in rats given the l-isomer (l-Tcp) lus reserpine. Neither alpha methyl-p-tyrosine (2 X 150 mg/kg s.c.) nor parachlorophenylalanine (200 mg/kg s.c.) pretreatment prevented the hyperactivity syndrome. The results suggest that mainly MAO inhibition and release of monoamines are involved in the hyperactivity syndrome produced by dl-Tcp plus reserpine.

Animals↗

Effects of sex steroids on growth hormone responses to clonidine and GHRH in reserpine pretreated rats.

Administration of reserpine in a dose causing depletion of brain monoamines led to a complete suppression of the pulsatile secretory pattern of growth hormone (GH) in gonadectomized (GX) as well as in sham-operated male and female rats. In GX animals of both sexes treated with estradiol, but not in those treated with testosterone or dihydrotestosterone (DHT), the reserpine induced inhibition of GH release was partially antagonized. Administration of the alpha 2-adrenoceptor agonist clonidine caused secretion of GH in reserpine pretreated, sham-operated rats. In GX male rats GH responses to clonidine were blunted, while in GX males treated with testosterone or estradiol, but not in those treated with DHT, the responses were restored. In female rats gonadectomy did not significantly affect the GH releasing effect of clonidine. However, administration of estradiol to GX females led to enhanced responses to the alpha 2-agonist. Administration of the GH releasing hormone (GHRH) induced pronounced GH secretion in reserpine pretreated animals of both sexes; this effect was not significantly affected by gonadectomy. In GX males, however, GH responses to GHRH were enhanced by replacement with estradiol or testosterone, while in GX females, estradiol, but not testosterone, had the same effect.

Animals↗

Morphological and pharmacological effects of reserpine, given alone or after iproniazid, on the catechol amines of the adrenal glands of the rat.

Adrenomedullary cells, after fixation with OsO(4), are filled with well formed granules which are considered to represent their catechol amine content. The submicroscopic appearance of these cells was studied in reserpine-treated rats during the late phase of catechol amine depletion and during the period of its restoration. At 3 days after the beginning of reserpine treatment, the granules appeared to be emptied of their content and small vesicles containing scattered, dense deposits of, presumably, catechol amines began to be seen. At 9 days after the beginning of treatment, these deposits had already become granules and the cells had attained a completely normal appearance. The submicroscopic structure of the adrenomedullary cells of rats pretreated with iproniazid (before reserpine), in which a complete inhibition of monoamine oxidase activity had thus been obtained, was similar to that seen in non-treated animals. In numerous cases, however, some characteristic features were noted: the sacs which usually contained a dense granule of catechol amines appeared swollen and many fine granules could be seen around them; the latter were dispersed in a way suggesting that they may represent a partial breakdown of the large granules which, under the inhibitory action of iproniazid, do not release the catechol amines contained within them.

Adrenal Glands↗

A COMPARISON OF IMIPRAMINE, CHLORPROMAZINE AND RELATED DRUGS IN VARIOUS TESTS INVOLVING AUTONOMIC FUNCTIONS AND ANTAGONISM OF RESERPINE.

Seven structurally-related compounds consisting of three antidepressant drugs (imipramine, desmethylimipramine and amitriptyline), three tranquillizing agents (promazine, chlorpromazine and chlorprothixene) and a hybrid, desmethylpromazine, have been examined in a series of tests involving autonomic functions and antagonism of reserpine. Activities of the compounds in antagonizing reserpine-induced ptosis in rabbits and prolongation of alcohol hypnosis in mice give good correlation with their clinical actions, whilst their activities in augmenting excitation of rats by amphetamine and yohimbine toxicity in mice, and in reversing reserpine-induced bradycardia in rats offer further evidence for drug-induced sensitization to adrenergic or tryptaminic mechanisms, which is not however specific for antidepressant agents. No evidence has been obtained to indicate that a central parasympatholytic action is an important component of the antidepressant activity of imipramine and related drugs.

Alcoholic Intoxication↗

URINARY EXCRETION OF CATECHOL AMINES IN THE RAT AFTER THEIR LIBERATION BY RESERPINE OR DEXAMPHETAMINE.

Daily urinary excretion of catechol amines in normal rats and in rats from which the adrenal medullae had been removed has been determined by a photofluorimetric method. In both groups, reserpine (2 mg/kg, intraperitoneally) produces: (1) A decrease in the urinary excretion of noradrenaline which persists for more than 3 weeks; this action is not influenced by monoamine oxidase inhibitors and mecamylamine. (2) An increase, within 20 to 68 hr, in the urinary excretion of adrenaline, even though the urine of rats without adrenal medullae does not usually contain adrenaline. These effects are prevented by monoamine oxidase inhibitors and, in the normal animals, are reduced by mecamylamine. In both groups, dexamphetamine (6 mg/kg, intraperitoneally) produces an increase in the excretion of adrenaline and noradrenaline, the adrenaline appearing in the urine of the rats without adrenal medullae within 20 to 44 hr. Mecamylamine prevents the effect of dexamphetamine on the excretion of noradrenaline. Dexamphetamine, administered within a week of reserpine treatment, produces its usual effects on the urinary excretion of catechol amines in normal rats, but has no effect in rats without adrenal medullae. The results are discussed with regard to both the mechanism by which reserpine and dexamphetamine influence the peripheral stores of adrenaline and noradrenaline, and the significance of the adrenal and extra-adrenal chromaffin system.

Adrenal Medulla↗

Reserpine and breast cancer. A community-based longitudinal study of 2,000 hypertensive women.

To supplement several case-control studies questioning whether use of reserpine is associated with occurrence of breast cancer, we conducted a longitudinal study of nearly 2,000 hypertensive women residing in Rochester, Minn. Exposure to antihypertensive agents and subsequent incidence of breast cancer were ascertained. Expected numbers of cases, derived from local population data and from the Connecticut Tumor Registry, were compared with the numbers of cases observed in exposure groups of interest. No evidence was found of any association of reserpine use, thiazide use, or untreated hypertension with subsequent occurrence of breast cancer in these hypertensive women. In addition, several issues were investigated that warrant consideration in evaluating reports published to date, especially before conclusions are drawn as to the questionable contention that reserpine has caused breast cancer in women.

Benzothiadiazines↗

Effect of reserpine treatment and hypophysectomy on the nitric oxide synthase immunoreactivity and NADPH-diaphorase staining in the rat adrenal gland.

BACKGROUND: The presence of nitric-oxide-synthesising neurons in the adrenal gland has recently been described by the immunohistochemical and/or enzyme histochemical demonstration of its synthesising enzyme, nitric oxide synthase (NOS; Afework et al. 1994. Cell Tissue Res,276:133-141). In the present report, these neurons have been examined by studying the changes that occur during conditions known to affect the adrenal gland. METHODS: By using NOS immunohistochemistry and NADPH-diaphorase histochemistry, levels of NOS and/or NADPH-diaphorase containing cellular elements in the adrenal gland were studied in rats subjected to either reserpine treatment or hypophysectomy as compared with the controls. RESULTS: Reserpine treatment caused a significant decrease in immunoreactivity to the neuronal isoform of NOS in the nerve fibres that innervate adrenal medullary cells. Hypophysectomy did not cause any change in the NOS immunoreactivity, although it eliminated most of the NADPH-diaphorase-staining non-NOS-immunoreactive cortical cells. CONCLUSIONS: The reduction in the level of NOS in the reserpine treated rats may indicate a decrease in the production of nitric oxide in the gland; this action may be related to the increase in the biosynthesis and secretion of catecholamine, which follows treatment with the drug. The reduction in the NADPH-diaphorase-positive cells may reflect the elimination of adrenal cortical cells that occurs after hypophysectomy, whereas hypophysectomy by itself appears to have no effect on the level of production of nitric oxide in the gland.

Adrenal Glands↗

Lithium interferes with reserpine-induced dopamine depletion.

Long-term lithium treatment attenuated the hypokinetic effect of reserpine in a patient with tardive dyskinesia. In rats, prophylactic lithium administration inhibits reserpine-induced dopamine depletion in the brain. These data indicate that lithium may limit the therapeutic efficacy of reserpine in tardive dyskinesia.

Adult↗

In vivo administered reserpine increases piecemeal degranulation in rat adrenal chromaffin cells.

The effects of the amine-depletory agent reserpine have been evaluated by transmission electron microscopy in chromaffin cells of the rat adrenal glands. The drug has been injected intraperitoneally in the animals at a dose of 0.5 mg/kg body weight in two administrations at 24-hr interval. The observed ultrastructural changes closely reminded of piecemeal degranulation (PMD), a slow and long-lasting secretory process previously described in normal and tumor pheochromocytes. Both adrenaline- and noradrenaline-storing cells presented the following microscopic features: high granule polymorphism, due to coexistence in the same cell of normal resting granules, granules with partially mobilized components, and large empty containers; absence of granule fusion; characteristic "haloed" pattern of residual secretory contents; great amount of 30-150 nm diameter, membrane-bound, electron-dense and -lucent vesicles, free in the cytoplasm or attached to granules; and multiple vesicles budding from the granule-limiting membranes. Morphometric analysis revealed that the frequency of all these microscopic parameters was found to be significantly increased in adrenal chromaffin cells from reserpinized rats in comparison to cells from control animals. These data suggest that reserpine, besides blocking the inward transport of catecholamines in chromaffin granules, might also stimulate a complex secretory reaction, which shares many common passages with bona fide PMD.

Adrenal Medulla↗

Simultaneous determination of reserpine and hydrochlorothiazide in two-component tablet formulations by high-performance liquid chromatography.

A high-performance liquid chromatographic procedure is presented for the simultaneous determination of reserpine and hydrochlorothiazide in two-component tablet formulations. An aliquot of a tetrahydrofuran extract of the tablet, containing polylythiazide as an internal standard, is chromatographed on a microparticulate silica gel column using a mobile phase of 0.01% (v/v) diethylamine, 5% (v/v) chloroform, and 18% (v/v) 2-propanol in n-hexane. The relative standard deviations are 1.2 and 0.6% for the simultaneous determination of reserpine and hydrochlorothiazide, respectively. Seven commericial tablet formulations were found to contain 92.7--101.0% and 98.3--101.4% of the labeled amounts of reserpine and hydrochlorothiazide, respectively.

Chromatography, High Pressure Liquid↗

Liquid membrane phenomenon in reserpine action.

Reserpine was shown to generate a liquid membrane. Transport of adrenaline, noradrenaline, dopamine, 5-hydroxytryptamine, glutamic acid, and gamma-aminobutyric acid in the presence of the reserpine liquid membrane was studied. The data indicate that the phenomenon of liquid membrane formation is likely to play a role in the mechanism of reserpine action.

Amino Acids↗

Comparison of the effects of losulazine and reserpine on central aminergic neurons.

The purpose of this study was to examine the effects of both acute and chronic administration of the peripheral sympatholytic antihypertensive agent losulazine on central dopaminergic, noradrenergic, and 5-hydroxytryptaminergic neurons in the rat. For comparison, the acute effects of reserpine were also examined. Acute systemic administration of losulazine produced marked dose- and time-dependent decreases in dopamine and norepinephrine concentrations in regions outside the blood-brain barrier (i.e., the median eminence, intermediate lobe, and neural lobe), that were accompanied by an increase in plasma concentrations of prolactin and alpha-melanocyte-stimulating hormone. By comparison, losulazine caused a relatively modest, transient depletion of dopamine and norepinephrine (but not 5-hydroxytryptamine) in regions of the brain protected by the blood-brain barrier (i.e., the striatum, nucleus accumbens, and dorsomedial nucleus of the hypothalamus). In contrast to losulazine, acute systemic administration of reserpine caused a prolonged depletion of dopamine, norepinephrine, and 5-hydroxytryptamine in all brain and pituitary regions examined. These results suggest that regional differences in the response of aminergic neurons to acute administration of losulazine and reserpine reflect differences in the ability of these drugs to penetrate the blood-brain barrier. Chronic systemic administration of losulazine produced a similar decrease in dopamine and norepinephrine in the median eminence, intermediate lobe, and neural lobe, suggesting that tolerance does not develop to the ability of losulazine to deplete catecholamines in these regions. Chronic losulazine administration also decreased dopamine concentrations in the striatum, and norepinephrine concentrations in the dorsomedial nucleus, suggesting that losulazine may have cumulative effects on central catecholamine neurons terminating in these brain regions.

Animals↗

Carrier-mediated outward transport of dopamine from adrenergic varicosities of the vas deferens of reserpine-pretreated rats.

In vasa deferentia of reserpine-pretreated rats a carrier-mediated (i.e., desipramine-sensitive) outward transport of endogenous dopamine was induced by either tyramine or ouabain. The dopamine taking part in the efflux induced by tyramine (and the concomitant efflux of DOPAC) was derived from ongoing synthesis of dopamine. Inhibition of MAO trebled the rate of spontaneous efflux of dopamine and reduced the spontaneous efflux of DOPAC by 90%. After inhibition of MAO, desipramine caused a further five-fold increase in the basal efflux of dopamine with no change in the basal efflux of DOPAC. Inhibition of COMT failed to affect the spontaneous efflux of dopamine but increased that of DOPAC. It is concluded that, after depletion of the noradrenaline stores by pretreatment with reserpine, an outward transport of axoplasmic dopamine is induced by the same mechanisms that (without any pretreatment with reserpine) are known to initiate an outward transport of noradrenaline.

3,4-Dihydroxyphenylacetic Acid↗