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PubMed1987

The treatment of intraarterial pentazocine injection injuries with intraarterial reserpine.

From 1979 to 1983, 14 patients were treated at the University of Maryland Hospital for injuries sustained as a result of the injection of crushed pentazocine tablets partially dissolved in water into the arterial system of the upper extremity. Eight patients received intraarterial reserpine within 15 hours of the injury and had no functional or tissue loss. Six patients either received no treatment or were given the reserpine more than 15 hours after the injury; they sustained notable functional or tissue loss. The results of this review would indicate that there may be a role for the use of intraarterial reserpine in the treatment of impending tissue loss from intraarterial drug injections.

Adult↗
PubMed1978

Reserpine treatment of Raynaud's disease.

Six patients with primary Raynaud's disease were investigated with magnification hand arteriography, measurement of finger systolic pressure and response to a newly devised local cooling test. They were treated with reserpine 0.5 mg injected into the brachial artery, and the clinical effects were followed by a scoring system and by the change in digital arterial tone during local cooling. The latter was registered as the change in systolic finger blood pressure measured indirectly by a finger-plethysmograph during stepwise decrease in finger temperature, until at a critical temperature complete closure of the digital arteries occurred. Shortly after injection the clinical condition improved, and closure of the digital arteries during local cooling was impeded. But within a week the cooling test showed a transient deterioration with closure of the digital arteries at the same or a somewhat higher temperature than before the reserpine injection. The clinical score followed this trend. According to animal experiments the shortlasting vascular effect of reserpine on primary Raynaud's disease might be due to depletion of the sympathetic nerve terminals for norepinephrine.

Adult↗
PubMed1984

Delayed onset of experimental allergic neuritis in rats treated with reserpine.

In delayed-type hypersensitivity most of the invading cells are not specifically sensitized against the initiating antigen but are augmenting cells called in by inflammatory mediators. It has been suggested that vasoactive amines, such as the monoamine serotonin, released by the action of sensitized T-cells on mast cells, may participate in the perivascular emigration of these cells that do not normally leave the blood. To test this hypothesis in experimental allergic neuritis (EAN), Lewis rats sensitized on day zero were treated with a single dose of the monoamine-depleting drug reserpine (2.5 mg/kg) immediately before the onset of early clinical signs on day nine (reserpine day 9, Rd9); during the onset of early clinical signs on day ten (Rd10); or immediately after the onset of early clinical signs on day 11 (Rd11). The results showed that the onset of early clinical signs was delayed in the Rd9 treated rats until approximately day thirteen whereas no effect on the course of the disease was observed in the Rd11 rats, and variable results were obtained in the Rd10 animals. Infiltration of mononuclear cells and leakage of 125I-albumin into the peripheral nerve was reduced in the Rd9 rats killed during the suppressed period. The delay in the onset of early clinical signs in the Rd9 rats correlated well with the time-course of serotonin depletion as reflected by levels in the peripheral blood of reserpine-treated normal animals. Although a role for histamine could not be demonstrated, the results suggest that other vasoactive amines are involved in the reaction. These results, therefore, would support the hypothesis that vasoactive amines play a role in the perivascular transit of inflammatory cells in EAN.

Albumins↗
PubMed1981

Intravenous reserpine for treatment of reflex sympathetic dystrophy.

The efficacy of reserpine in relieving the pain of reflex sympathetic dystrophy was tested in 25 patients--21 with upper extremity and four with lower extremity involvement. Injection of the drug relieved the acute signs and symptoms in the upper extremity in 12 of 17 patients. Four patients with quiescent reflex sympathetic dystrophy of upper extremities had prophylactic injection at the time of reconstructive surgery; they had no flare of symptoms. Relief was obtained in the four cases of lower extremity dystrophy. Our patients had no significant side effects. The drug is confined to the extremity by a pneumatic tourniquet as used for intravenous regional anesthesia. After the extremity is exsanguinated and the cuff is inflated, 1 mg of reserpine diluted to 50 ml with normal saline is injected intravenously into the upper extremity. In the lower extremity, 2 mg of reserpine diluted to 100 ml is injected. The tourniquet is removed after 15 minutes. The procedure is safe and can be done in an office setting.

Anesthesia, Conduction↗
PubMedDate not supplied

Effect of reserpine on relaxant responses of canine femoral arterial strips.

1. We studied relaxant responses to adenosine, glyceryl trinitrate, and hydralazine in control (n=5) and reserpine pretreated (1 mg/kg i.m., 24 h prior; n=5) canine femoral arterial strips contracted with noradrenaline. 2. Reserpine did not alter contractile responses to noradrenaline. 3. Reserpine pretreated tissues were supersensitive to glyceryl trinitrate, but not to adenosine or hydralazine.

Adenosine↗
PubMed1989

Effects of reserpine treatment on arrhythmogenesis during ischaemia and reperfusion in the isolated rat heart.

1. The effects of reserpine treatment on the myocardial contents of catecholamines and enkephalins and the incidence of ventricular arrhythmias during ischaemia and reperfusion in the isolated rat heart were studied. 2. Reserpine treatment almost completely depleted the heart of noradrenaline (NA). It also significantly depleted the heart of adrenaline and dopamines. It did not, however, alter the myocardial contents of enkephalins. 3. Reserpine-treatment attenuated significantly, but did not abolish, cardiac arrhythmias induced by ischaemia and reperfusion in the isolated heart preparation. 4. The results of the present study indicate that myocardial catecholamines especially NA are a contributing factor to arrhythmogenesis during ischaemia and reperfusion.

Animals↗
PubMed2006

Reserpine-induced model of stress suppresses mucosal immunity.

Stress contributes significantly to the development of many diseases. In clinical studies, a strong correlation between depression and immune dysfunction has been shown. Our previous studies indicated that sympathetic innervation can regulate intestinal mucosal immunity through sympathetic synapses, but the mechanism in stress/depression-induced intestinal immune deficiency was unclear. Using a mouse model in which behavioural stress/depression is chemically induced by reserpine, it is found that there is a substantial deficiency of intestinal local humoral and particularly specific antibody response to the antigen stimulation in reserpine-treated group. No significant difference of CD4+, CD8+ or Mac1+ cells between reserpine-treated and control groups was detected in the intestine. This deficiency is closely correlated with stress/depression. A possible correlation between stress, cytokine secretion and humoral immunity in vivo is postulated.

Animals↗
PubMed1983

[3H]dopamine depletion from osmotically defined storage sites: effects of reserpine, 53 mM KCl, and d-amphetamine.

A crude synaptosome-containing fraction (P2') prepared from rat striatal slices incubated with [3H]dopamine was exposed to hypoosmotic conditions and rapidly subjected to Millipore filtration. P2'-associated [3H]dopamine trapped on the filters was defined as hypoosmotic resistant, whereas P2'-associated [3H]dopamine that washed through the filters was defined as hypoosmotic sensitive. Electron microscopic examination of sections prepared from a P2' pellet that had been exposed to hypoosmotic conditions revealed extensive synaptosomal lysis. [3H]Dopamine accumulation and retention by the hypoosmotic-resistant fraction were reduced by reserpine. The proportional distribution of [3H]dopamine between hypoosmotic-resistant and -sensitive fractions was measured following in vitro exposure of the preloaded P2' fraction to reserpine, 53 mM KCl, and d-amphetamine. Each of these treatments resulted in a time-dependent loss of [3H]dopamine from the loaded P2' fraction without eliciting an alteration in the proportional distribution of [3H]dopamine between hypoosmotic-resistant and -sensitive fractions. Release induced by reserpine and d-amphetamine was independent of extrasynaptosomal Ca2+, whereas 53 mM KCl-induced release was dependent on extrasynaptosomal Ca2+. These results suggest that dopamine may be rapidly equilibrated between osmotically defined storage compartments, and thus specific compartmental depletion of loaded [3H]dopamine cannot be identified on the basis of osmotic lability.

Animals↗
PubMed1987

Effects of reserpine and tetrabenazine on catecholamine and ATP storage in cultured bovine adrenal medullary chromaffin cells.

The in vivo storage relationship between catecholamines and ATP in chromaffin vesicles of cultured bovine adrenal medulla cells was investigated using drugs that block vesicular catecholamine uptake. Three-day treatments with reserpine and tetrabenazine causing 85-90% depletion of catecholamines resulted in 41-46% reductions in cellular ATP content. Subcellular fractionation of reserpine-treated cells indicated that the ATP is lost from the chromaffin vesicle pool. This was confirmed in experiments using metabolic inhibitors to differentiate the vesicular and extravesicular ATP pools. The vesicular ATP loss was not proportional to that of catecholamines, resulting in a reduction by 50% in the chromaffin vesicle mole ratio of catecholamines to ATP after 48 h of treatment. In metabolic labeling studies, it was found that reserpine treatment reduced the incorporation of [3H]adenosine into vesicular ATP selectively, but it reduced the incorporation of 32Pi into both the vesicular and extravesicular pools. The reduction of the [3H]adenosine incorporation was not due to diminished vesicular nucleotide uptake resulting from low catecholamine levels, because when the catecholamines were depleted by tetrabenazine pretreatment followed by removal of the drug before labeling, no reduction in [3H]adenosine incorporation was observed. When present during the labeling, tetrabenazine was found to be a reversible inhibitor of plasma membrane adenosine uptake. The observed loss of adenine nucleotides from catecholamine-depleted chromaffin vesicles in vivo provides evidence that interactions between ATP and catecholamines are important in the vesicular storage of high concentration of these compounds.

Adenosine↗
PubMed1987

Secretion of [Met]enkephalyl-Arg6-Phe7-related peptides and catecholamines from bovine adrenal chromaffin cells: modification by changes in cyclic AMP and by treatment with reserpine.

Investigations into the effects of culturing bovine adrenal chromaffin cells in the presence (72 h) of dibutyryl cyclic AMP, forskolin, and reserpine on the level and release of [Met]enkephalyl-Arg6-Phe7 immunoreactivity, noradrenaline, and adrenaline are reported. The assay for [Met]enkephalyl-Arg6-Phe7 immunoreactivity recognises both peptide B, the 31-amino acid carboxy-terminal segment of proenkephalin, and its heptapeptide fragment, [Met]enkephalyl-Arg6-Phe7. Treatments that elevate cyclic AMP increase the amount of peptide immunoreactivity in these cells; this is predominantly peptide B-like immunoreactivity in both control cells and cyclic AMP-elevated cells. Treatment with reserpine gives no change in total immunoreactivity levels, but does not result in increased accumulation of the heptapeptide [Met]enkephalyl-Arg6-Phe7 at the expense of immunoreactivity that elutes with its immediate precursor, peptide B. Cyclic AMP treatment causes either no change or a decrease in levels of accumulated noradrenaline and adrenaline. However, the release of [Met]enkephalin-Arg6-Phe7 immunoreactivity, noradrenaline, and adrenaline is increased by 72-h pretreatment with forskolin or dibutyryl cyclic AMP, whether release is stimulated by nicotine or elevated potassium. In each case the molecular form of [Met]enkephalyl-Arg6-Phe7 immunoreactivity that is released approximately reflects the cell content. Pretreatment with reserpine has no effect on the total [Met]enkephalyl-Arg6-Phe7 immunoreactivity released, but does result in an increased release of the heptapeptide and a decrease in release of peptide B-like immunoreactivity. The studies suggest that the levels of [Met]enkephalyl-Arg6-Phe7 and peptide B available for release are controlled both at the level of proenkephalin synthesis and at the level of double-basic residue proteolysis.

Adrenal Medulla↗
PubMed1987

Amphetamine and reserpine deplete brain biogenic amines and alter blow fly feeding behavior.

HPLC with electrochemical detection was used to determine the levels of p-hydroxyphenylethanolamine (octopamine), 3,4-dihydroxyphenylethylamine (dopamine), and 5-hydroxytryptamine (5-HT) in the brains of control, reserpine, and d-amphetamine-treated blow flies, Phormia regina Meigen. Parallel studies were carried out to assess the effects of the two drugs on fly feeding behavior, measured as mean acceptance threshold: the minimum sucrose concentration to which the average fly in a population will respond by proboscis extension when its tarsi contact the solution. In saline-injected control flies, all three amines were found at levels of approximately 2 pmol/brain. Thirty minutes after injection with d-amphetamine (12 micrograms/fly), brain octopamine was depleted by 85%, whereas dopamine and 5-HT were depleted by 70%. Reserpine (5 micrograms/fly) caused 70% depletion of dopamine and greater than 90% depletion of both octopamine and 5-HT 24 h after injection. However, the effect of reserpine was much slower in onset (hours versus minutes) and more persistent (days versus hours) than was the effect of d-amphetamine. With either drug, the time course of amine depletion closely matched the time course of the increase in feeding threshold observed in drug-treated flies. These results suggest that CNS pools of the biogenic amines, octopamine, dopamine, and 5-HT are important in governing blow fly responsiveness to food stimuli.

Amines↗
PubMed1990

Tyrosine hydroxylase mRNA concentration in midbrain dopaminergic neurons is differentially regulated by reserpine.

Tyrosine hydroxylase (TH)-mRNA, assayed by in situ hybridization combined with TH immunocytochemistry, showed a selective increase in the ventral tegmental area (A-10) but not in the substantia nigra (A-9) midbrain dopaminergic (DAergic) neurons 3 days after reserpine treatment. TH-mRNA in locus ceruleus noradrenergic (A-4) neurons was increased by reserpine, as confirmed by RNA blot hybridization. These findings show that TH-mRNA is differentially regulated in midbrain DAergic neurons in response to reserpine.

Animals↗
PubMed1980

The use of an irreversible beta-adrenoreceptor antagonist to examine reserpine- and hypothermia-induced supersensitivity of guinea-pig atria.

1 Positive inotropic and chronotropic responses to guinea-pig isolated left and right atria respectively to the sympathomimetic amine orciprenaline were recorded. 2 Pretreatment of animals with reserpine for 3 days produced supersensitivity of both the inotropic and chronotropic responses. Lowering the bath temperature from 38 degrees to 30 degrees C produced supersensitivity of untreated atria to the inotropic responses only. 3 Irreversible beta-adrenoreceptor antagonism of orciprenaline by Ro 03-7894 was demonstrated by a persistent depression of the maximum inotropic and chronotropic responses after a prolonged washout from the bath (3 h). 4 The depression of the maximum rate and tension responses by Ro 03-7894 was less in atria from reserpine-pretreated animals. 5 The maxima were also depressed less at the lower bath temperature of 30 degrees C. However, when atria were cooled during the incubation with Ro 30-7894, the maxima were still depressed to the 38 degrees C level. 6 That these results suggest either a receptor proliferation or change in efficacy as possible mechanisms for reserpine- and hypothermia-induced supersensitivity is discussed.

Adrenergic beta-Antagonists↗
PubMed1957

Effects of reserpine on blood-pressure responses evoked from the hypothalamus.

Different areas of the hypothalamus were stimulated by a stereotaxic technique before and after reserpine in unanaesthetized cats. Reserpine in a dose of 1 mg./kg. body weight increased the threshold of stimulation of hypothalamic areas in cats giving an initial pressor response. It decreased the threshold of stimulation of areas of the hypothalamus in animals giving an initial depressor response. Reserpine thus appeared to affect the hypothalamus directly in two ways. It depressed the sympathetic centres in the diencephalon and facilitated the parasympathetic ones.

Animals↗
PubMed1959

The effect of reserpine on the acetylcholine content of different areas of the central nervous system of the dog.

The acetylcholine content of the frontal and temporal lobes, hippocampus, hypothalamus, cerebellum and spinal cord was estimated in 18 dogs 3 hr. after the intravenous administration of reserpine. Another group of 7 dogs served as control. After reserpine (0.5 mg./kg. body weight) there was an increase of acetylcholine in all the areas under study except in the hippocampus. The increase was specially marked in the hypothalamus. In the hippocampus, however, reserpine caused a significant decrease of acetylcholine.

Acetylcholine↗
PubMed1960

Effects of reserpine, chlorpromazine and sodium salicylate on the enzymic activity of rat liver.

The effects of reserpine, chlorpromazine and sodium salicylate on oxidative phosphorylation, stimulation of glutamic acid oxidation and adenosinetriphosphatase activity have been compared in vitro with those of 2,4-dinitrophenol using rat liver preparations. All three drugs inhibit oxidative phosphorylation, slightly stimulate glutamic acid oxidation and stimulate adenosinetriphosphatase activity at high concentrations. Reserpine has no effect on adenosinetriphosphatase activity. It is suggested that the characteristic depressant effects of reserpine on isolated tissues in vitro may be due to interference with production of energy by oxidative phosphorylation.

2,4-Dinitrophenol↗
PubMed1962

Response of normal, denervated, and reserpine-treated arteries to sympathomimetic amines and nicotine in dogs.

The sensitivity of normal, denervated carotid arterial segments, and of carotid arteries of dogs previously treated with reserpine, to sympathomimetic amines and nicotine has been compared using isolated perfused segments of these vessels. Arteries from animals and arterial segments treated with reserpine, denervated by peri-arterial stripping or by re-anastomosing of segments removed and reversed, both showed an increased sensitivity to noradrenaline which correlated well with a decrease in tissue noradrenaline content. Tyramine did not produce vasoconstriction in denervated vessels, but some constriction was observed when the vessels had been pretreated with noradrenaline or with dopamine or dopa. The effect of nicotine upon dog carotid arterial segments was recorded 130 times. The most frequent response was vasodilatation. This involved both the arterial wall per se and the vasa vasorum. The vasodilatation in response to nicotine was seen in arteries from normal and reserpine-treated animals and in denervated vessels.

Animals↗
PubMed1962

Depletion and replacement of the adrenaline and noradrenaline contents of the rat adrenal gland, following treatment with reserpine.

The effect of reserpine on the adrenaline and noradrenaline contents of rat adrenal glands has been studied. Given subcutaneously to male albino Wistar rats in 3 daily doses of 1 mg/kg, it caused, 24 hr after the final dose, a similar percentage loss of adrenaline and noradrenaline of approximately 50%. Subsequently the adrenaline content slowly increased, until at 14 days from the begining of the experiment there was no significant difference between the reserpine-treated and the control glands. In contrast, the recovery of the noradrenaline content was rapid, exceeding the control value at 7 days by approximately 250%. This increased content of noradrenaline declined to the normal level by 21 days. The total amine content returned to normal by 7 days and remained at this level subsequently. The effect of re-depleting the glands of their amine content was investigated. It was found that re-depletion at 7 days caused a preferential release of noradrenaline, followed at 14 days by a peak of noradrenaline at least as high as that obtained following the initial depletion only. Re-depletion at 21 days caused an effect similar to that obtained initially. Denervation of the left adrenal gland did not alter the degree of depletion caused by reserpine, nor did it alter the subsequent replacement of the amines as compared with that in the innervated right gland.

Adrenal Glands↗