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Biomedical subjects

O Kraupp

Publications and source records attributed to O Kraupp.

At least 19 recordsLinked to original sources
PubMed1996

[Effectiveness of fixed analgesic combinations exemplified by thomapyrin].

Thomapyrin has been on the German market as analgesic for the past 50 years. It is the prescription-free preparation with the highest sales there. This is an occasion to survey current state of scientific knowledge concerning combination analgesics with acetyl salicylic acid, paracetamol and caffeine. For the assessment and registration of fixed preparations authorities of different European countries and also USA have defined special criteria. Analgesic preparations must agree with these defined criteria. The importance of these combination analgesics in pain therapy is described with the respect to the latest scientific results. Combination analgesics represent an important area of self-medication by the patient. The properties of the active substances alone and in combination are set forth, with respect to pharmacokinetics and efficacy. The experimental and especially clinical results clearly show a broader spectrum of action in consequence of the different modes of action of the individual active substances. Analgesic action is 1.4 fold higher owing to added caffeine. The fixed combination of active substances does not change the profile of side effects. The conclusion is that combination analgesics such as Thomapyrine show a positive benefit/risk ratio. Furthermore such combination analgesics are appropriate for self-medications and suited to combat pain of different kinds.

Acetaminophen↗
PubMed1989

Effects of urapidil on catecholamine turnover and release in the central nervous system of the rat.

The actions of urapidil, prazosin, idazoxan, and haloperidol on the turnover of noradrenaline in the hypothalamus and dopamine in the nucleus accumbens of the rat were investigated using changes in the ratios of 3-methoxy-4-hydroxyphenyl-glycol/noradrenaline (MHPG/NA) and 3,4-dihydroxyphenylacetic acid/dopamine (DOPAC/DA), respectively, as measures for drug-induced effects. Urapidil (2.5-30 mg kg-1 i.v.) increased the ratios of MHPG/NA and DOPAC/DA. Its effects on NA turnover were maximal at 60 min (160% of control at 30 mg kg-1), and on DA turnover at 30 min (138% of control at 30 mg kg-1). Prazosin (0.5-2.5 mg kg-1 i.v.) had no effect, but the high dose of 5 mg kg-1 i.v. significantly increased the ratio of MHPG/NA in the hypothalamus. Idazoxan (2-50 mg kg-1 i.v.) and haloperidol (0.02-0.5 mg kg-1 i.v.) selectively enhanced turnover of NA and DA, respectively. In experiments on field-stimulated overflow of tritium from slices of hypothalamus and nucleus accumbens labelled with [3H]NA or [3H]DA, respectively, urapidil (1 mumol L-1) facilitated the evoked responses in both regions. Prazosin (0.1 mumol L-1) had no effect in either of the two areas. Idazoxan (0.1 mumol L-1) increased stimulated overflow of [3H]NA from the hypothalamus but not of [3H]DA from the nucleus accumbens. Conversely, haloperidol (0.1 mumol L-1) greatly enhanced evoked overflow of [3H]DA but not of [3H]NA. From the present results it is concluded that urapidil has an antagonistic effect at central alpha 2-adrenoceptors and also a weak antagonistic action at central dopamine D2-receptors.

Animals↗
PubMed1985

Characterization of vasodilators by comparison of their effects on blood pressure, counterregulation and myocardial oxygen demand in conscious normotensive dogs.

Vasodilators were characterized on the basis of their first-dose effect on systolic and diastolic blood pressure, heart rate, on the product of heart rate and systolic blood pressure and on plasma renin activity (PRA) in conscious normotensive dogs. The compounds were given orally to the animals and the effects were studied over a period of 4 h. The arterial vasodilators (propyldazine, dihydralazine and labetalol) caused a marked reduction of systolic and diastolic blood pressure with excessive stimulation of the sympathetic nervous system, leading to an increase in myocardial oxygen demand. The blood pressure effect of urapidil and prazosin resembled more the pattern seen with typical venous dilators (molsidomine and nitrates) and was not accompanied by significant increases in heart rate and in PRA. Hence, the magnitude of diastolic blood pressure reduction seems to be an essential determinant of reflex counterregulation. The results prove that some few parameters can give information about the overall pattern of hemodynamic effects of vasodilators.

Animals↗
PubMed1984

Blood pressure response and renin release following 4 days of treatment with dihydralazine and urapidil in conscious dogs.

The magnitude and the persistence of blood pressure reduction by dihydralazine and urapidil were investigated following treatment over a period of 4 days. The experiments were performed on six normotensive dogs, trained to submit to puncture of the femoral artery and to stand quietly in a special frame. The first-dose effects of orally administered dihydralazine (1.42, 7.1 mg X kg-1) and urapidil (2.0, 10.0 mg X kg-1) on heart rate, arterial blood pressure and plasma renin activity (PRA) were compared with the effects of the substances after 4 days of treatment. Both compounds caused a dose-dependent decrease in blood pressure but in contrast to urapidil the effect of dihydralazine was accompanied by large increases in heart rate and PRA. Dose-dependent tolerance to dihydralazine but not to urapidil was observed after treatment over only 4 days. However, basal blood pressure was significantly lowered after 4 days of treatment with urapidil at the high dosage and no further reduction was achieved on the fifth day. The importance of persistent counterregulation in the development of tolerance to the antihypertensive effect of dihydralazine is discussed.

Animals↗
PubMed1982

Adenosine receptor agonists: binding and adenylate cyclase stimulation in rat liver plasma membranes.

N6-Cyclohexyl[3H]adenosine([3H]CHA,[3H]adenosine, and 5'N-ethylcarboxamide[3H]adenosine ([3H]NECA), potent agonists in adenosine-responsive cellular systems, have been used to identify adenosine binding sites in rat liver plasma membranes. Endogenous ligands were removed by prior dialysis of the membranes. Specific binding of the ligands tested was characterized by rapid forward and reverse kinetics and heterogeneity as indicated by curvilinear Scatchard plots. The KD in the high affinity range was 80 nM for [3H]adenosine, 84 nM for [3H]NECA, and 168 nM for [3H]CHA; the respective binding capacities of 1.19, 1.03, and 1.05 pmol/mg protein were of virtually the same magnitude, suggesting labeling of identical sites. However, all ligands also displayed binding to large numbers of low affinity sites. This high level of apparently non-receptor binding markedly influenced the adenosine structure-activity profile of [3H]CHA displacement, which differs with pharmacological findings. - NECA and CHA stimulated hepatic adenylate cyclase with an apparent ED50 of 60 and 580 nM, respectively; adenosine was stimulatory at a concentration range from 0.1 - 2.0 microM, but inhibitory at higher concentrations. Hence, estimation of the true ED50 was not possible. Because the KD of high affinity binding and the ED50 of the biological effect of NECA and CHA are in the same range, it may be reasonable to assume that the high affinity sites represent adenosine receptors, recently classified as Ra-site receptors.

Adenosine↗
PubMed1982

The effects of NECA (adenosine-5'N-ethylcarboxamide) and of adenosine on glucagon and insulin release from the in situ isolated blood-perfused pancreas in anesthetized dogs.

The effect of adenosine-5'-N-ethylcarboxamide, (NECA), a long-lasting adenosine derivative with pronounced vasoactivity was investigated on glucagon and insulin release from the in situ isolated blood perfused pancreas in the anesthetized dog: NECA (10(-9) to 10(-5) mol/l) led to a dose-dependent glucagon release. Insulin release was inhibited by NECA at low concentrations, but significantly increased at higher concentrations of the adenosine analogue. Similar effects were observed with infusion of adenosine at 10(-7) and 10(-6) mol/l. Aminophylline (10(-4) mol/l) produced a 10-fold attenuation of the actions of NECA. The preponderance of glucagon release at low concentrations of NECA and adenosine in contrast to that of insulin release at high concentrations may represent a local pancreatic regulatory mechanism of adenosine in glucose homeostasis.

Adenosine↗
PubMed1980

The effects of adenosine-5'-ethylcarboxamide on liver blood flow and hepatic glucose, lactate and pyruvate balances in dogs.

The actions of adenosine-5'-ethylcarboxamide (744-96), a long-acting adenosine analogue, on liver, portal and intestinal balances of glucose, lactate and pyruvate and on hepatic and portal blood flow were investigated in 6 chloralose-anaesthetized mongrel dogs. 744-96 led to an increase in portal and hepatic blood flow. Glucose release by the liver and glucose uptake by the non-hepatic splanchnic area (portal balance) were markedly increased by 744-96. Hepatic lactate and pyruvate balances were reversed from uptake to release by the adenosine analogue. The changes in glucose balances compare closely to the actions of glucagon, which is known to be released by 744-96. Apart from these possible glucagon-mediated actions, a direct action of the adenosine analogue must be assume from the changes in lactate metabolism. The results of this study are indicative of a substrate-mobilising action of adenosine in addition to its well-known vasodilatory action.

Adenosine↗
PubMed1979

Effect of a 5'-substituted adenosine analogue (744c96) on insulin and glucagon release in isolated rat islets of Langerhans.

The effect of adenosine-5'-(N-ethylcarboxamide) (744-96), a highly vasoactive adenosine analogue, was investigated on insulin and glucagon release from isolated rat islets of Langerhans. The compound inhibited glucose-induced insulin release in a dose-dependent manner (concentration range 10(-8) to 10(-5 M). No effect of 744-96 was observed on basal or on arginine-induced glucagon release. By contrast, 744-96 (5 microgram/kg i.v.) produced a significant increase in plasma glucagon and glucose levels in normal as well as in reserpinized rats. The observed failure to promote glucagon release from isolated islets may be attributable to the isolation procedure, to a release of glucagon in vivo from non-pancreatic stores, or to a non-specific effect of 744-96 on glucagon secretion.

Adenosine↗
PubMed1979

Pharmacological properties of taglutimide, a new sedative-hypnotic drug.

2-[Bicyclo(2,2,1)heptane-2-endo-3-endo-dicarboximido]-glutarimide (taglutimide, K-2004) proved to be a new sedative-hypnotic drug which did not produce any toxic effects when administered orally to mice even at a very high dosage. Central-nervous depression was demonstrated by a reduction in spontaneous motor activity, potentiation of the central-depressant effect of pentobarbital, antagonism of the central-stimulant effect of amphetamine after oral administration and by narcotic activity after i.v. administration of the drug. Furthermore, oral administration of taglutimide potentiated the analgesic action of morphine without being effective on its own. Only weak potentiation of chlorpromazine-induced catalepsy, but not of reserpine-induced catalepsy was observed after taglutimide pretreatment. The drug influenced neither motor co-ordination nor the toxicity of ethanol. Taglutimide exhibited no anticonvulsant activity with respect to maximum electroshock or strychnine-induced seizures. No effect on heart rate or blood pressure was demonstrable after taglutimide treatment in conscious dogs.

Animals↗
PubMed1978

Evidence for glucagon-releasing activity of vasoactive adenosine analogues in the conscious dog.

An investigation was carried out in conscious dogs concerning the effects of three adenosine derivatives substituted at the 5'-(744-96) or 2'-, 3'-, and 5'-positions (744-98, 744-99), with pronounced and long-lasting coronary dilator activity, on glucagon release. All three compounds (10 microgram/kg i.v.) induced a sustained increase in plasma glucose and a decrease in plasma FFA concentration; concomitantly, plasma glucagon levels rose 2--3 fold. Changes in plasma insulin concentration were relatively small and of no statistical significance. A simultaneous fall in arterial blood pressure was also observed. A lowering of blood pressure of similar magnitude by sodium nitroprusside infusion in control experiments failed to show any significant effect on plasma glucagon level. These results point to a specific effect of vasoactive adenosine derivatives on glucagon release.

Adenosine↗
PubMed1978

Influence of aminophylline or beta-adrenoceptor blockade on glucagon release by a vasoactive adenosine analogue.

The glucagon-releasing activity of adenosine-5'-ethyl-carboxamide (744-96) was studied in conscious dogs pretreated either with aminophylline or with bupranolol, a beta-adrenoceptor blocking drug. The adenosine antagonist, aminophylline, inhibited both the glucagon-releasing and the blood pressure lowering effects of 744-96 (10 microgram/kg i.v.). The actions of the adenosine analogue on glucagon release and haemodynamics were not affected by bupranolol pretreatment. These results indicate that the adenosine analogue mediates glucagon release by interaction with so-called adenosine receptors. A beta-adrenoceptor mediated release secondary to 744-96-induced hypotension and baroreceptor-activation can be excluded.

Adenosine↗