�ber eine hyperglyk�mische Wirkung von Reserpin

Kuschke, H. J.; Frantz, Justin

doi:10.1007/bf00249447

Cited by 18 publications

(5 citation statements)

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“…In the present work the drug caused a hyperglycemia, as reported earlier (33). This could be due to a mobilisation of glycogen, since the content of glycogen in liver and the specific radioactivity of glucose in blood serum were both diminished.…”

Section: Discussionsupporting

confidence: 87%

Incorporation of [U- 14 C]Glucose into Metabolites of Brain, Liver and Blood of Rats Pretreated with Reserpine or Phenothiazines

Raheem¹,

Gründig²,

Salvenmoser³

et al. 1979

Clinical Chemistry and Laboratory Medicine

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Summary:Parkinsonism was induced in rats by using phenothiazines (Butyrylperazin and Thioproperazin), (P-group), or reserpine, (R-group). [U-14 C)D-glucose was administered when the symptoms of Parkinsonism had become fully developed. Concentrations and radioactivities of different metabolites were studied in brain, liver and blood serum. 3. Both treatments caused a fall in the amino acid concentration of the blood serum. A rise in the specific radioactivity of blood amino acids was observed in the P^group, while a decrease in specific radioactivity was observed in the R-group. A hyperglycemia was induced in the R-group with reduced specific radioactivity of glucose in both P-and R-groups. A reduction in lipid concentration of blood serum was achieved with an increased specific radioactivity in P-group and decreased radioactivity in R-group.4. The changes in amino acids common to both treatments are also observed in human Parkinsonism. Der Einbau von [i/-14

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Section: Discussionsupporting

confidence: 87%

Incorporation of [U- 14 C]Glucose into Metabolites of Brain, Liver and Blood of Rats Pretreated with Reserpine or Phenothiazines

Raheem¹,

Gründig²,

Salvenmoser³

et al. 1979

Clinical Chemistry and Laboratory Medicine

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“…Thus Everett et at. (1957) described evanescent pilo-erection in mice or rats about half an hour after large doses of reserpine (50-100 mg/kg by mouth); RESERPINE AND SYMPATHETIC SYSTEM Kuschke & Frantz (1955) saw hyperglyeaemia in the rabbit; tachyeardia has been seen to occur in the heart-lung preparation of the dog (Plummer, Earl, Schneider, Trapold & Barrett, 1954), and many workers have observed rises in blood pressure in different species (de Jongh & van Proosdij-Hartzema, 1955;Maxwell, Ross, Plummer & Sigg, 1957;Domino & Rech, 1957). A raised level of blood adrenaline has been found in rabbits during the first hour after an intravenous dose of reserpine (Muscholl & Vogt, 1957 c).…”

Section: Discussionmentioning

confidence: 99%

The action of reserpine on the peripheral sympathetic system

Muscholl¹,

Vogt²

1958

The Journal of Physiology

232

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Reserpine causes the release of 5-hydroxytryptamine (5-HT) from all tissues in which it is normally stored. This release is shown by a fall in the tissue concentration of 5-HT and by an increase in its urinary metabolites (Pletscher, Shore & Brodie, 1955;Shore, Silver & Brodie, 1955). That reserpine may also lower the concentration of catecholamines in tissues was shown by experiments (Holzbauer & Vogt, 1956) in which the disappearance of noradrenaline from the hypothalamus was demonstrated in cats injected with small doses of reserpine (0-4 mg/kg). This depletion, however, did not occur in all organs, the denervated, in contrast to the innervated, adrenal medulla remaining unaffected by this dose of the drug.It is tempting to try to correlate the effects on behaviour and responsiveness produced by reserpine with the loss of 5-HT and noradrenaline from the brain. The tendency has been to attribute not only the sedation, but also such signs as the fall in blood pressure, the miosis and the relaxation of the nictitating membrane to central changes alone. Although all these phenomena might be due to central causes, they could also be produced, at least partly, by disturbances in the peripheral sympathetic system. Failure of another sympathetic mechanism after reserpine was described by G. M. Everett who observed (personal communication, and Everett, Toman & Smith, 1957) that cold did not produce pilo-erection in mice injected with reserpine. This failure, too, might be due to a central or to a peripheral derangement, or to both.The aim of the present paper is to determine the effect of reserpine on the peripheral sympathetic tissues: the investigation, abstracts of which have been published (Muscholl & Vogt, 1957 a, b), deals with the loss of transmitter and the damage to function produced by reserpine in adrenergic neurones. In preliminary experiments the normal range of concentrations of adrenaline and noradrenaline in various parts of the sympathetic system was established.

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“…This effect may explain the hyperglycaemic action of reserpine in rats (TAKETOMO et al, 1957) and in rabbits which is blocked by ergot alkaloids but is not abolished by splanchnic nerve sections (KUSCHKE and FRANTZ, 1955). The acute administration of reserpine to dog heart-lung preparations markedly increases the rate of beating (PLUMMER et al, 1954;KRAYER and FUENTES, 1958), but only if cardiac noradrenaline stores are intact (PAASONEN and KRAYER, 1958;LIEBMAN et al, 1962).…”

Section: Sympathomimetic Responses To Reserpinementioning

confidence: 91%