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Biomedical subjects

K Starke

Publications and source records attributed to K Starke.

At least 271 records · Page 15Linked to original sources
PubMed1976

Enkephalin: a potential modulator of noradrenaline release in rat brain.

In slices of rat occipital cortex preincubated with 3H-noradrenaline, methioine-enkephalin diminished the overflow of tritium evoked by electrical field stimulation or by 20 mM potassium. The effect was not modified by phentolamine, but was antagonized by naloxone. Giver alone, naloxone slightly increased the potassium-evoked overflow. It is concluded that enkephalin reduces transmitter release from cerebrocortical noradrenergic nerve endings. One-function of endogenous opiate receptor ligands may be presynaptic inhibition of central noradrenergic transmission.

Animals↗
PubMed1976

[Synoptical X-ray diagnostics of pulmonary emphysema (author's transl)].

In marked chronic obstructive pulmonary emphysema, especially in the classical emphysematous type of abnormal thorax, a good correlation can be found between the anteroposterior expansion of the thorax, the reduced inspiratory capacity, the clinical state, disturbed mechanics of breathing and the x-ray-state. On the contrary, in clinical emphysema of a lower degree, especially in subclinical, i. e. in predominantly asymptomatic pulmonary emphysema of the elderly, the effectiveness of the roentgenological examination is very small.

Aged↗
PubMed1975

Morphine tolerance and dependence in noradrenaline neurones of the rat cerebral cortex.

By subcutaneous implantation of 2 or 13 morphine pellets (75 mg morphine/pellet), rats were made tolerant to, and dependent on narcotic analgesics. Occipital cortex slices from dependent animals and placebo-implanted controls were incubated with (-)-3H-noradrenaline and subsequently superfused with physiological salt solution. The accumulation of 3H-noradrenaline was not changed by pretreatment with 2, but was slightly decreased by pretreatment with 13 morphine pellets. The overflow of tritium evoked by electrical field stimulation was higher in slices from morphine-implanted rats than in those from placebo controls. Morphine and levorphanol, added in vitro, inhibited the stimulation-induced overflow of tritium at similar concentrations and to a similar degree in slices from morphineand placebo-pretreated animals.--It is concluded that, during chronic treatment with morphine, an adaptation takes place in the brain to compensate for the acute effect of narcotic analgesics, i.e. inhibition of the release of noradrenaline by nerve impulses. The chain of events from the drug-receptor interaction to the depression of the release process can be escluded as substrate of this adaptation. During withdrawal, the compensatory changes provoke an enhanced increase of extracellular noradrenaline during nerve impulses.

Animals↗
PubMed1975

Influence of morphine and naloxone on the release of noradrenaline from rat cerebellar cortex slices.

In slices of rat cerebellar cortex preincubated with (-)-3H-noradrenaline, the influence of morphine and naloxone on the efflux of tritium was investigated. The spontaneous outflow was not changed by 10(-5) M of either morphine or naloxone. On the other hand, morphine caused a concentration-dependent decrease of the overflow of tritium evoked by electrical field stimulation. Naloxone did not change the stimulation-induced overflow, but prevented its inhibition by morphine. It is concluded that morphine, through an action on opiate receptors located on cerebellar noradrenergic neurones, inhibits the secretion of the transmitter in response to nerve impulses.

Animals↗
PubMed1975

Phencyclidine and ketamine: comparison with the effect of cocaine on the noradrenergic neurones of the rat brain cortex.

In slices of rat occipital cortex, the influence of phencyclidine and ketamine on the accumulation of 3H-noradrenaline and the subsequent outflow of tritium was investigated, and was compared with the effect of cocaine.--All three drugs inhibited the accumulation of tritium during incubation of the slices with 3H-noradrenaline. Phencyclidine was slightly, whereas ketamine was much less effective than cocaine.--All three drugs accelerated the spontaneous outflow of tritium from slices preincubated with 3H-noradrenaline. The acceleration caused by low concentrations probably reflects an inhibition of the re-uptake of spontaneously released 3H-noradrenaline; in addition, high concentrations (10(-4) M phencyclidine, 3 X 10(-4)-10(-3) M cocaine and 10(-3)-3 X 10(-3) M ketamine) appear to release tritiated compounds from the neurones. The distance between uptake-inhibiting and releasing concentrations was much greater for cocaine than for phencyclidine and ketamine.--All three drugs enhanced the overflow of tritium evoked by electrical field stimulation. The increase probably reflects an inhibition of the re-uptake of released 3H-noradrenaline; in addition, phencyclidine appears to enhance the release of noradrenaline per pulse.--The actions of phencyclidine and ketamine on central noradrenergic neurones may contribute to the characteristic psychotropic side-effects of these general anaesthetics.

Animals↗
PubMed1975

Relative pre- and postsynaptic potencies of alpha-adrenoceptor agonists in the rabbit pulmonary artery.

The rabbit pulmonary artery contains postsynaptic alpha-adrenoceptors which meidate smooth muscle contraction; its noradrenergic nerves contain presynaptic alpha-adrenoceptors which mediate inhibition of the release of the transmitter evoked by nerve impulses. Dose-response curves for the pre- and postsynaptic effects of eight alpha-receptor agonists were determined on superfused strips of the artery in the presence of cocaine, corticosterone and propranolo. 1. According to the concentrations which caused 20% of the maximal contraction (EC20 post), the postsynaptic rank order of potency was: adrenaline greater than noradrenaline greater than oxymetazoline greater than naphazoline greater than phenylephrine greater than tramazoline greater than alpha-methylnoradrenaline greater than methoxamine. The pA2 values of phentolamine againstoxymethazoline, phenylephrine, alpha-methylnoradrenaline and methoxamine were 7.43, 7.48, 7.59 and 7.69, respectively. 2. For the investigation of presynaptic effects, the arteries were preincubated with 3H-noradrenaline. All agonists inhibited the overflow of tritium evoked by transmural sympathetic nerve stimulation. According to the concentrations which reduced the stimulation-induced overflow by 20% (EC20 pre), the rank order of potency was: adrenaline greater than oxymetazoline greater than tramazoline greater than alpha-methylnoradrenaline greater than noradrenaline greater than naphazoline greater than phenylephrine greater than methoxamine. 10(-5) M phentolamine shifted the presynaptic dose-response curves for moradrenaline and oxymethazoline to the right. 3. The ratio EC20 pre/EC20 post was calculated for each agonist as an index of its relative post- and presynaptic potency. According to the ratios, the agonists were arbitrarily classified into three groups. Group 1 (ratio about 30: preferentially postsynaptic agonists) comprised methoxamine and phenylephrine; group 2 (ratio near 1; similar pre- and postsynaptic potencies) comprised noradrenaline, adrenaline and naphazoline; group 3 (ratio below 0.2; preferentially presynaptic agonists) comprised oxymetazoline, alpha-methylnoradrenaline and tramazoline (as well as clonidine). 4. Preferentially presynaptic and preferentially postsynaptic agonists had opposite effects on the basoconstrictor response to nerve stimulation. Methoxamine and phenylephrine either did not change or enhanced, but never reduced, the response. In contrast, oxymetazoline, alpha-methylnoradrenaline and tramazoline at low concentrations selectively inhibited the response to stimulation at low frequency (0.25-2Hz). 5. It is concluded that alpha-adrenoceptor agonists vary widely in their relative pre- and postsynaptic potencies, possibly because of structural differences between pre- and postsynaptic alpha-receptors. Pre- and postsynaptic components contribute to their overll postsynaptic effec in actively transmitting synapses. The preferential activation of presynaptic alpha-receptors results in alpha-adrenergic inhibition of synaptic transmission.

Adrenergic alpha-Agonists↗
PubMed1975

Preferential blockade of presynaptic alpha-adrenoceptors by yohimbine.

Strips of the rabbit main pulmonary artery were preincubated with 3H-noradrenaline. 3 X 10(-8) -- 10(6) M yohimbine enhanced the overflow of tritium and the smooth muscle contraction induced by transmural sympathetic nerve stimulation. The increase of the stimulation-evoked overflow of tritium was prevented by a high concentration of oxymetazoline. The results indicate that yohimbine is more potent in blocking the presynaptic than the postsynaptic alpha-adrenoceptors of the artery.

Animals↗