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Biomedical subjects

V J Nickolson

Publications and source records attributed to V J Nickolson.

28 records · Page 2Linked to original sources
PubMed1977

On the oscillatory decay of the myotonic action of 9-anthroic acid. Influence of cholinesterase inhibition.

The effects of the myotonic agent, 9-anthroic acid (ANCA), and the acetylcholinesterase (AChE) inhibitor, soman, on the isolated phrenic nerve--diaphragm preparation of the rat have been studied. ANCA induced after-contractions which followed the twitches evoked by either direct or indirect stimulation. In the intermittently stimulated muscle the height of the after-contractions decreased rather rapidly and in an oscillatory fashion. The maximum height of each after-contraction was attained after the twitch had reached its peak. AChE inhibition changed the shape of these after-contractions in the indirectly, but not in the directly stimulated diaphragm. After AChE inhibition, the after-contractions decreased more slowly and in a non-oscillatory manner. Similar phenomena were observed in vivo in the gastrocnemius--soleus muscles. The effects of ANCA in the AChE-inhibited and in the non-inhibited diaphragm could be mimicked by incubation in low chloride media. Addition of ouabain to the non-inhibited diaphragm treated with ANCA, caused an immediate and striking enhancement followed by a rapid loss of the after-contractions, whereas the twitches remained fairly constant. In the AChE-inhibited diaphragm treated with ANCA, ouabain caused no increase but only a rapid and complete decay of the after-contractions with a decrease of the twitches. It is suggested that after inhibition of the AChE in the ANCA-treated muscle fibre, the site of initiation of the repetitive action potentials which cause the after-contractions shifts from the transverse tubular system to the motor end-plate. Moreover, it is suggested that the sodium pump is involved in the gradual decay of the myotonic action of ANCA.

Animals↗
PubMed1975

Further studies on the therapy of organophosphorous anti-cholinesterase intoxication with veratrinic compounds; the role of calcium.

Experiments were carried out to investigate the role of calcium in the therapy of soman intoxication with 9-anthroic acid (ANCA), a compound with veratrine-like pharmacological properties. The effects of ANCA on the respiratory paralysis and on the calcium content of the blood and that of the hindleg muscles were determined in anaesthetized, atropinized rats injected with 4 times LD50 soman. The respiratory paralysis which in control animals occurs within a few min after the injection of soman can be delayed about 2.5 hr by treatment with ANCA. It was found that ANCA causes a small decrease of the blood calcium content, an effect which is potentiated by soman. A comparison was made between the calcium accumulation in the indirectly stimulated gastrocnemius-soleus muscles in these animals with that in the non-stimulated muscles on the other side. Whereas the injection of soman or ANCA alone caused no change, the combination of the two drugs induced a two-fold increase in the accumulation of calcium in the stimulated muscles. The non-stimulated muscles remained unaffected. The accumulation of calcium in the stimulated muscles induced by soman and ANCA could be partly antagonized by lowering the free calcium concentration of the blood by EDTA. Moreover, treatment with EDTA improved the therapeutic effects of ANCA. It is concluded that the therapy of soman poisoning with ANCA falls short in completely preventing respiratory failure since ANCA causes an accumulation of calcium in the stimulated muscles of soman-poisoned animals.

Animals↗
PubMed1973

Preferential release of newly synthesized 3 H-acetylcholine from rat cerebral cortex slices in vitro.

1. Slices of rat cerebral cortex after treatment with the irreversible cholinesterase inhibitor soman, were incubated for 5 min in a Krebs-Henseleit solution containing 25 mM KCl and (3)H-choline. Subsequently incubation was continued in a medium containing non-radioactive choline and this medium was replaced at 5 min intervals. The amounts of labelled and total acetylcholine (ACh) released into the medium and extracted from the slices were determined at intervals.2. After the initial 5 min contact with (3)H-choline, 44% of the newly synthesized ACh contained a choline moiety originating from the choline in the medium. During the initial 5 min and the subsequent incubation part of the labelled ACh was released. While the rate of total ACh release remained constant, that of the release of labelled ACh was highest in the 5 min period following the initial incubation with (3)H-choline and then declined exponentially.3. The ratio of labelled ACh/total ACh in the ACh released during the initial 5 min incubation with (3)H-choline and during the subsequent 5 min was about three times as high as that in the ACh extracted from the slices at the end of these incubation periods.4. The ratio of labelled ACh/total ACh in superficial layers of the slices was not higher than that in the total slices.5. The rates of release of labelled and unlabelled ACh decreased when calcium was omitted from the incubation medium and were restored when the calcium was added. This suggests that both labelled and unlabelled ACh were released from nerve endings. The efflux of (3)H-choline was not calcium dependent.6. It is concluded that labelled ACh newly synthesized from externally applied (3)H-choline does not exchange immediately with all other ACh in the tissue and has a greater chance of being released than unlabelled ACh.

Acetylcholine↗
PubMedDate not supplied

Changes in rat brain norepinephrine levels and turnover after olfactory bulbectomy.

After bilateral olfactory bulbectomy in rats a significant increase of norepinephrine (NE) level in the hypothalamus was found. However, no difference was observed between hypothalamic NE turnover of bulbectomized and sham operated animals in the amygdaloid cortex the NE level was not affected by bulbectomy. In this area, however, the NE turnover appeared to be decreased after bulbectomy. The latter finding may be related to the deficits in passive avoidance behaviour as found in bulbectomized rats.

Amygdala↗