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C G Dacke

Publications and source records attributed to C G Dacke.

At least 37 records · Page 2Linked to original sources
PubMed1986

A comparison of the effects of bovine parathyroid hormone 1-34 and methylated prostaglandin E2 analogues on plasma calcium and inorganic phosphate levels in immature chickens and rats.

The relative effects of bovine parathyroid hormone 1-34 (bPTH-(1-34] and prostaglandin (PG)E2 analogues, 16,16-dimethyl PGE2 and 11,16,16-trimethyl PGE2, on plasma calcium, inorganic phosphate (Pi), and osmolality in 12-day-old chickens were compared. bPTH-(1-34) and 16,16-dimethyl PGE2 were similarly tested for effects on plasma Ca and Pi in immature (3-week-old) rats. PGs administered iv in a saline vehicle (20 micrograms 16,16-dimethyl PGE2 or 125 micrograms 11,16,16-trimethyl PGE2/100 g body wt, respectively) produced significant hypercalcaemic effects in chicks compared with vehicle-injected controls at times ranging from 15 to 90 min, similar to those obtained with bPTH-(1-34) (3.3 micrograms/100 g body wt). The PGE2 analogues injected in chicks also produced significant increases in plasma Pi compared with controls at 15 and 45 min, while those treated with PTH showed smaller, nonsignificant plasma Pi responses. Little change in plasma osmolality was seen in chicks following injection with either bPTH-(1-34) or 16,16-dimethyl PGE2, although a small but significant increase in this parameter was seen in chicks treated with 11,16,16-trimethyl PGE2. Acute labelling of chicks with 32P incorporated into the 16,16-dimethyl PGE2 injection vehicle indicated a decreased exit of Pi from the blood as the mechanism underlying the PG-mediated hyperphosphataemic response. This type of response was not seen following bPTH-(1-34) injection in chicks.(ABSTRACT TRUNCATED AT 250 WORDS)

16,16-Dimethylprostaglandin E2↗
PubMed1986

Evidence of saturable uptake mechanisms at maternal and fetal sides of the perfused human placenta by rapid paired-tracer dilution: studies with calcium and choline.

Rapid uptake and efflux of 45Ca2+ and [3H]choline at the maternal and fetal interfaces of the syncytiotrophoblast in the dually-perfused human placenta was investigated by application of the single circulation paired-tracer dilution method (Yudilevich, Eaton, Short & Leichtweiss 1979). Cotyledons were perfused with Krebs-bicarbonate containing dextran (30 g/l; MW = 60-70,000) at 20 and 6 ml/min on maternal and fetal sides, respectively. The paired-tracer (test substrate and extracellular marker) technique consisted of an intra-arterial injection of a tracer bolus, followed by venous sampling over 5-6 min. There was a rapid (sec) uptake of 45Ca2+, followed by backflux (efflux into the ipsilateral circulation) which, over 5-6 min, was 59-100% on the fetal side. It was more variable but generally lower on the maternal interface. At 0.1 mM calcium, 45Ca2+ maximal uptake (Umax) was about 53% on the fetal side but on the maternal side it was variable and averaged 17%. At 2.4 mM calcium fetal side Umax was reduced to 40%. However, on the maternal side the effect was not consistent. Unidirectional influx (nmol/min per g) appeared to be not different on the two sides of the placenta. For [3H]choline (in choline-free perfusates) Umax was about 50% and 30% on fetal and maternal sides, respectively; tracer backflux was variable on the maternal side and averaged 50% on the fetal side. [3H]Choline uptake was highly inhibited by either 1.0 mM choline or the specific competitive inhibitor, hemicholinium-3 (0.1 mM). Specific transplacental transfer of 45Ca2+ (i.e. in excess of the extracellular marker) was not significant in either direction. For [3H]choline there was an apparent small excess (about 4%) preferential towards the fetal circulation. These findings in the human placenta are similar to those demonstrated previously in the guinea-pig placenta which suggested the existence of specific transport systems for choline and calcium on both sides of the syncytiotrophoblast.

Biological Transport, Active↗
PubMed1985

Evidence for a novel inhibition of calcium uptake into chick bone in response to bovine parathyroid hormone (1-34) or 16, 16-dimethyl prostaglandin E2 in vivo.

Mechanisms of initial hypercalcaemic responses to parathyroid hormone (PTH) and 16,16-dimethyl prostaglandin (PG) E2 have been investigated in 10-to 12-day-old chicks in vivo using a combination of acute 45Ca injection and microwave fixation to stabilize tissue isotope levels. Single i.v. injection of 16,16-dimethyl PGE2 (20 micrograms/100 g body wt) caused an approximately 100% increase in soft tissue 45Ca levels compared with vehicle control injected chicks at 30 min. 45Ca levels were lowered in calvarium by 26% and in femur by 60% with this treatment. Bovine PTH (1-34) (3.3 micrograms/100 g body wt) had no effect on soft tissue 45Ca levels, but in calvarium it had a similar effect to the PG. In femur this dose of PTH lowered 45Ca by 19%. When expressed on an absolute basis (c.p.m./100 mg tissue wt), responses to the PG in soft tissue were only 3 and 10% respectively of those in femur and calvarium. The duration of inhibitory responses in bone were examined and those to PTH found to be transient (less than 45 min) compared with the responses to the PG (greater than 135 min). Dose-response curves for PTH- and PG-induced inhibition of 45Ca uptake into femur at 15 min were essentially parallel and indicated that the lowest doses of PTH and PG used (0.74 micrograms and 1.1 micrograms/100 body wt respectively) produced significant responses. In a separate experiment it was found that inhibition of 45Ca uptake into femur was evident as early as 3 min following PTH or PG injection.(ABSTRACT TRUNCATED AT 250 WORDS)

16,16-Dimethylprostaglandin E2↗
PubMed1984

Release of labelled taurine from the rat dorsal medulla and cerebellum in vivo.

Stimulus-induced release of labelled taurine has been studied in the superfused rat cerebellar cortex and dorsal medulla in vivo. In the cerebellum both elevated potassium and electrically induced depolarization consistently produced marked increases in the efflux of exogenously applied taurine in a calcium-dependent fashion. Veratridine-stimulation evoked a large Ca2+-independent taurine efflux which was, however, prevented by tetrodotoxin. In the dorsal medulla, both high K+ and veratridine induced a clear Ca2+-independent increase in taurine efflux. Electrical stimulation was always ineffective in changing taurine efflux from the dorsal medulla. These data strongly support a possible neurohumoral role for taurine in the cerebellum but not in the dorsal medulla.

Animals↗
PubMed1983

Hypercalcaemic responses to 16,16-dimethyl prostaglandin E2, a stable prostaglandin E2 analogue in chicks.

Intravenous injection of 6.7-60 micrograms of stable prostaglandin E2 analogue, 16,16-dimethyl prostaglandin E2, into 10-day-old chicks caused profound, long-lasting hypercalcaemia. Simultaneous i.v. loading with 50 mumol Ca/bird enhanced the peak response. The responses were accompanied by sedation and lowered skin temperature. Use of acute (simultaneous) 45Ca labelling indicated that the hypercalcaemic responses were due primarily to inhibition of Ca exit from extracellular fluid pools, while chronic (6-day) 45Ca labelling indicated a slower but distinct increase in mobilization of bone Ca pools.

16,16-Dimethylprostaglandin E2↗
PubMed1979

A possible neuronal release of [14C] GABA from the rat cerebellum in vivo.

Release patterns for exogenously applied [14C] labelled alpha-amino-n-butyric-acid (GABA) have been investigated in rat cerebellar cortex in vivo. An increase in [14C] GABA release could be evoked by stimulating with high (40 mM) K+ or veratridine (10(-4)M) but not with direct electrical stimulation. Biphasic patterns for high K+ and possibly veratridine stimulated release of GABA suggest the existence of two separate anatomical sources of isotope which are sensitive to these depolarising stimuli. Both K+ and veratridine-evoked GABA release are calcium dependent. Studies involving partial replacement of Na+ with HEPES, (N-2-hydroxyethyl-piperazine-N-2-ethane-sulphonic acid), sucrose or choline chloride also reveal a sodium dependency of [14C] GABA release. These studies collectively indicate a neuronal source for evoked GABA release, a criterion for transmitter identification not previously satisfied in the cerebellar cortex.

Animals↗
PubMed1977

Calcium-dependent increase in efflux of [1-3H] taurine from the superfused rat cerebellar cortex in vivo.

High (40 mM) potassium stimulation has been shown to increase the efflux in vivo of [1-3H] taurine from the superfused rat cerebellar cortex by 46%, P less than 0.001. During superfusion with calcium-free media this increase in efflux is abolished. The cellular location of [1-3H] taurine in the cerebellar cortex is not yet known, but this region of the brain contains exceptionally high levels of endogenous taurine. The calcium dependency of the release of labelled taurine raises the possibility that taurine has some neuro-humoral role in the cerebellar cortex.

Animals↗