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At least 127 records · Page 7Linked to original sources
PubMed1964

OBSERVATIONS ON THE MODE OF ACTION OF SOME CENTRAL DEPRESSANT DRUGS ON TRANSMISSION THROUGH THE CAT SUPERIOR CERVICAL GANGLION.

Methylpentynol, paraldehyde, amylobarbitone and procainamide blocked transmission through the cat superior cervical ganglion, and antagonized the ganglion-stimulating actions of acetylcholine and carbachol injected intra-arterially to the ganglion. Comparison with the effects of tetraethylammonium indicated that the impaired response to acetylcholine could not wholly account for the failure of transmission, which suggested that an impaired release of transmitter substance was a contributory factor. Methylpentynol, paraldehyde and procainamide also blocked the ganglion-stimulating action of potassium chloride. In contrast, amylobarbitone and pentobarbitone did not block the stimulating action of potassium chloride, but antagonized specifically the actions of acetylcholine and carbachol. The anti-acetylcholine activities of the two barbiturate drugs at this site accord with their relative ganglion-blocking activities. It is concluded that the ganglion-blocking action of methylpentynol, paraldehyde and procainamide arises from a nonspecific depression of both presynaptic and postsynaptic elements in the ganglion, but that barbiturate compounds act more specifically on the acetylcholine receptor.

Acetylcholine↗
PubMed1964

EFFECTS OF CENTRAL DEPRESSANT DRUGS UPON ACETYLCHOLINE RELEASE.

Several central depressant and other drugs have been examined for their effects upon acetylcholine release from the stimulated, perfused cat superior cervical ganglion and rat isolated phrenic nerve-diaphragm preparations. The acetylcholine released was assayed biologically. Amylobarbitone sodium, chloral hydrate, trichloroethanol, methylpentynol, methylpentynol carbamate, paraldehyde, procaine hydrochloride and troxidone reduced the presynaptic release of acetylcholine from the ganglion. They also exhibited a postsynaptic blocking action, this component of depressant activity being particularly prominent with paraldehyde and troxidone. Closely analogous findings were obtained at the neuromuscular junction with methylpentynol and its carbamate, paraldehyde, procaine hydrochloride, trichloroethanol and troxidone. At both sites the drug-induced depression, both of transmission and of acetylcholine output, was reversible. Whereas hexamethonium regularly blocked ganglionic transmission with no effect upon acetylcholine release, tetraethylammonium not only completely blocked ganglionic transmission but concomitantly augmented acetylcholine output. These results are discussed in relation to the electrophysiological and metabolic events associated with neuro-effector transmission.

Acetylcholine↗
PubMed1970

Effects of some drugs on the responses of the rat isolated, innervated urinary bladder to indirect electrical stimulation.

1. The effects of some drugs known to inhibit transmission in the superior cervical ganglion and at the neuromuscular junction were investigated on the cholinergic nerve-smooth muscle junction, using the rat isolated innervated urinary bladder preparation.2. HC-3 and Win 4981 inhibited the indirectly evoked contractions; the block was typically slow in onset, depended on the rate of stimulation and was partially reversed by choline. The moderate coincident inhibition of acetylcholine-responses disappeared after washing the tissue, while the block of the neuronally evoked contractions persisted.3. Morphine, methylpentynol carbamate, chloral hydrate and strychnine inhibited indirectly evoked contractions without inhibiting the responses to acetylcholine. Paraldehyde inhibited both types of response.4. Hexamethonium, mecamylamine and tubocurarine had no effect on either type of response. Tetraethylammonium augmented both types of response; the augmentation due to lower concentration was followed by a moderate block of the neuronally evoked contractions.5. Small concentrations of procaine markedly inhibited responses to acetylcholine and produced a partial block of the neuronally evoked contractions.6. None of the drugs affected conduction in the isolated phrenic nerve.7. All the drugs other than paraldehyde and procaine appeared to act at the nerve terminals. The results are generally consistent with the view that HC-3 and Win 4981 act by limiting transport of choline across nerve membrane and that the other drugs act by inhibiting the release of acetylcholine. A reduction in sensitivity of the effector cell membrane may account, wholly or in part, for the action of paraldehyde and procaine.

Animals↗
PubMed1986

A scanning electron microscopy and histological study on the effects of the mutant eyeless (e/e) gene upon the hypothalamus in the Mexican axolotl Ambystoma mexicanum Shaw.

A scanning electron microscopy, histological, and immunochemical investigation examined the effects of the mutant gene (e) upon hypothalamic development in the Mexican axolotl. The adult eyeless mutant is sterile. Previous studies indicated that this reproductive defect was due to the mutation's effect upon the hypothalamus. The present study demonstrated the pleiotropic effects of the eyeless gene upon development of the hypothalamus. Scanning electron microscopy studies looked at the early ontogeny of the hypothalamohypophyseal system. The major morphological difference observed in the hypothalamus of normals compared to eyeless mutants was the reduced nature or complete lack of a preoptic recess in eyeless mutants. Early embryonic tissue movements also differed when normal siblings were compared to eyeless mutant axolotls. Histological examination looking for paraldehyde-fuchsin-positive secretory neurons revealed a paired nucleus preopticus in both normals and eyeless mutants, but this region lacked the emanating paraldehyde-fuchsin-positive fiber tracts in eyeless mutants. The neurohypophysis of the eyeless mutants was atrophied and contained far less paraldehyde-fuchsin-positive material when compared to normal axolotls. Immunochemical studies were done to look at the distribution of immunoreactive luteinizing-hormone-releasing hormone (ir-LHRH) in brains of eyed and eyeless mutant axolotls of different stages. This study detected deficiencies in ir-LHRH in the anterior hypothalamus of eyeless mutants. In general in the eyeless mutant axolotl, the observed anterior hypothalamic deficiencies are comparable to those observed in anurans which have had their optic vesicles removed. These observations suggest a possible utility of the eyeless mutant axolotl for studies concerned with endocrine development in the absence of hypothalamic modulation.

Ambystoma↗
PubMed1994

Immunogold detection of two neurohormones: the locust ovary maturing parsin and neuroparsin.

The cellular localization of two neurohormones of the locust pars intercerebralis-corpora cardiaca system: the ovary maturing parsin and neuroparsin, was investigated using electron microscopic immunocytochemistry (post-embedding immunogold labelling). The ovary maturing parsin and neuroparsin containing cells were first identified in semithin sections treated by combined histochemical- and immunostaining. The neuroparsin cells were paraldehyde fuchsin positive (A-type cells) and the ovary maturing parsin cells were paraldehyde fuchsin negative when semithin sections were stained with paraldehyde fuchsin and immunostained with anti-ovary maturing parsin serum. The ovary maturing parsin and neuroparsin producing cells were identified on immunogold labelled ultrathin sections adjacent to double stained semithin sections. Ovary maturing parsin cells have larger more numerous vesicles of greater electron density than neuroparsin cells. The neuroparsin cells contained more lysosomal structures than the ovary maturing parsin cells suggesting different neurosecretory dynamics. Thus, immunogold labelling with antisera specific for each neurohormone demonstrates the individual nature of these two neurosecretory cells in the pars intercerebralis of the Locust.

Animals↗
PubMed2004

Emergency drug availability on general paediatric units.

Following an incident where intravenous lorazepam was not available on a general paediatric ward we undertook a national survey of emergency drug availability on general paediatric units in the United Kingdom. Drugs chosen were those recommended in the Advanced Paediatric Life Support manual and the British National Formulary for the management of the most common paediatric emergencies. Twelve drugs were chosen covering emergencies in the following systems: cardiovascular (adrenaline (epinephrine), atropine and adenosine); neurological (flumazenil, lorazepam, paraldehyde, phenytoin and mannitol); metabolic (Hypostop Gel and glucagon); analgesia related (naloxone); and respiratory (aminophylline). A thirteenth drug, intravenous salbutamol was included in a reminder letter sent to non-responding units. Questionnaires were sent to 274 units. Replies were received from 242 (88.3%), of whom 20 did not have a general paediatric ward, leaving 222 units (81.0%). Drug availability varied for the different drugs: adrenaline (available on 100% of units), atropine (98.2%), naloxone (96.4%), phenytoin (95.9%), aminophylline (93.2%), paraldehyde (92.3%), mannitol (87.8%), lorazepam (86.9%), glucagon (86.5%), Hypostop Gel (80.6%), adenosine (72.1%) and flumazenil (66.7%). Six of the drugs were classified as first line agents (adrenaline, atropine, adenosine, lorazepam, paraldehyde and aminophylline). Over one in 10 units did not stock two or more of these first line drugs. Consideration needs to be given to the compiling of a consensus based list of drugs that ought to be stocked on all general paediatric units.

Cardiopulmonary Resuscitation↗
PubMed2006

Induction of apoptosis with tobacco smoke and related products in A549 lung epithelial cells in vitro.

BACKGROUND: This study has investigated the ability of tobacco smoke, and ingredients of tobacco smoke, to induce apoptosis in the airway epithelial cell line A549. METHOD: A549 cells were treated with 80 microg/ml Tobacco smoke condensate (TSC), 10 mM Nicotine, 10 microM paraldehyde, 10 microM hydrogen peroxide, 1 microM Taxol (Paclitaxel), 100%, 50% and 25% cigarette smoke extract (CSE). Following 4-48 h incubation apoptosis was measured morphologically following staining of cells with DAPI. TUNEL staining was also used to assess DNA damage after 24 and 48 h incubation. In addition, loss of mitochondrial cytochrome C and activation of Bax-alpha, early events in the apoptotic process, were measured after 4 h of incubation. RESULTS: Incubation of A549 cells with vehicle, Taxol, TSC, nicotine, paraldehyde, hydrogen peroxide and CSE caused a time-dependent detachment of the cells from the flask between 6 and 48 h. DAPI staining revealed that the cells remaining adhered to the flask appeared healthy whereas some of those that had detached appeared to be either apoptotic or indeterminate. Treatment with Taxol, TSC, nicotine, paraldehyde, hydrogen peroxide and CSE caused a significant increase in the number of apoptotic cells. Similarly, treatment with Taxol, TSC, nicotine, hydrogen peroxide and CSE caused a significant increase in the number of apoptotic cells among the cells that had detached from the culture plate. After 4 h of incubation, Taxol, TSC, hydrogen peroxide and CSE caused a significant reduction in mitochondrial cytochrome C and an increase in cytosolic cytochrome C. At the same time point, hydrogen peroxide and CSE significantly increased the concentration of Bax-alpha in the mitochondria. CONCLUSION: Tobacco smoke initiates apoptosis in A549 airway epithelial cells as a result of mitochondrial damage and that this results in a cell detachment and full apoptosis. This effect appears to result from factors in tobacco smoke other than nicotine and may result from free radical activity. However, additional stable factors may also be involved since the free radical content of TSC is likely to be low.

Journal Article↗