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At least 19 recordsLinked to original sources
PubMed1977

Double-blind evaluation of glucagon and propantheline bromide (pro-banthine) for hypotonic duodenography.

The hypotonic effect of glucagon (2 mg) and propantheline bromide (Pro-Banthine, 30 mg) on the upper gastrointestinal tract was compared in a double-blind study in 12 healthy volunteers and 36 patients. The solvent solution for the two drugs was used as a placebo. Both drugs and placebo were administered intramuscularly. The time of onset of the hypotonic effect was similar for both drugs, with maximum effect achieved 10 min after injection. Effects of glucagon dissapeared rapidly after 30 min, while Pro-Banthine still retained 50% of its maximum effect 2 1/2 hr after injection. Side effects of Pro-banthine were related to the long duration of the hypotonic effect (4-6 hr). A significant placebo effect on the duodenal C loop was observed. Glucagon appears to be the drug of choice since its hypotonic and hypomotile effects on the gastrointestinal tract are comparable to propantheline bromide while having the advantage of shorter duration and practically no side effects.

Adult↗
PubMed1975

Side effects and skills related to driving after intramuscular administration of bupivacaine and etidocaine.

Eleven healthy subjects were injected intramuscularly with a saline placebo, 1.3 mg/kg of 0.5% plain bupivacaine, or 2.6 mg/kg of 1.0% plain etidocaine in a double-blind cross-over fashion. Before and at 1/2, 2 and 4 h after injection, side effects were recorded, and psychomotor skills related to driving were measured. Fatigue, dizziness, and sore thighs were significantly more common with etidocaine than with bupivacaine or the saline solution. Bupivacaine significantly impaired eye-hand cooridination and flicker fusion discrimination during the whole observation period. Etidocaine impaired flicker fusion discrimination only. The subjects' adaption to darkness, sensitivity to brightness, and visual discrimination ability in bright counterlight remained unaltered after each treatment. The results suggest that such psychomotor performance as driving ability is impaired for at least 2 h after a patient receives 1.3 mg/kg of plain bupivacaine or 2.6 mg/kg of plain etidocaine intramuscularly.

Acetanilides↗
PubMed1977

[Hormontal treatment of pre-tumorous diseases of the testis in rats].

Tumours and proliferates of the testes from spermatogenic epithelium were treated with estrogens, and those from the interstitial cells-with androgens and 17-hydrosyprogesterone caproate. Depression of the folliculo-stimulating function of the pituitary body with a simultaneous stimulation of the luteinizing hormones (LH) production under the effect of estrogen led to cessation of teratoma and seminoma growth, and to the resolution of the proliferates. When androgens or 17-hydroxyprogesterone caproate were used, depression of the LH led to cessation of the tumour growth, and to the resolution of proliferion of proliferates from the interstitial cells.

Animals↗
PubMedDate not supplied

Effect of intra-arterial reserpine in patients suffering from Raynaud's phenomenon.

Several papers have established the beneficial effect of Reserpine applied intra-arterially in patients suffering from Raynaud's phenomenon. In the present study this effect was investigated in 15 patients, some of whom had been submitted previously to sympathectomy, and in healthy controls. A solution of 1.25 mg Reserpine in 10 ml normal saline was injected in the course of one minute in the brachial artery. Blood pressure, pulse rate, bilateral finger venous occlusion plethysmography and fingertip temperature measurements were carried out for two hours following the injection. Later, venous occlusion plethysmographic and clinical controls were continued weekly, until the Reserpine effect had ceased. Normal subjects, patients suffering from Raynaud's phenomenon undergoing no surgical treatment and those submitted to preganglionic sympathectomy showed a conspicuous increase in digital blood flow, while in one patient, who had stellectomy the fingerflow remained unchanged. This effect remained chiefly located on the injected side. There were no blood pressure or pulse rate changes while in the lying position. Hypotension by passive orthostasis was observed two hours after the injection. The possible mechanism of Reserpine is discussed.

Adult↗
PubMed1977

The production of denervation-like changes in rat muscle by colchicine, without interference with axonal transport or muscle activity.

1. Rat extensor digitorum longus (EDL) muscles were examined after colchicine treatment of the sciatic nerve. Colchicine was applied in one of two ways: (i) a single sub-epineural injection; (ii) a chronically implanted silicone cuff. 2. After the sub-epineural injection, the entire membrane of muscle fibres became sensitive to iontophoretically applied acetylcholine and the muscle action potentials became resistant to tetrodotoxin. However, the majority of these fibres were found to be normally innervated. 3. These effects were not restricted to the EDL muscle of the colchicine injected side but were also found in the EDL muscle of the contralateral side, indicating that the action of colchicine was systemic. 4. In the treated sciatic nerve there was a partial block of axonal transport of 3H-labelled proteins, which correlated with a partial paralysis of the ipsilateral leg. However, axoplasmic transport was found to be normal in the contralateral sciatic nerve and the contralateral limb was not paralysed despite the supersensitivity of the investigated muscle on that side. 5. When colchicine was applied with a silicone cuff, denervation-like changes were confined to the ipsilateral EDL muscle. However, impulse conduction block at the level of the cuff was usually observed. 6. It is concluded that (i) colchicine can produce denervation-like changes in normally active muscle without blocking axoplasmic transport, through an action probably exerted directly on the muscle membrane, and (ii) that colchicine-cuff experiments failed to provide unambiguous evidence in support of the existence of neurotrophic influences on the muscle membrane.

Acetylcholine↗
PubMed1979

Glucose carriers at maternal and fetal sides of the trophoblast in guinea pig placenta.

Trophoblast uptake and unidirectional influx of 3H-labeled hexoses were measured relative to L-[14C]glucose (extracellular marker) using a single-circulation, paired-tracer dilution technique. Successive runs were performed in the fetal and maternal circulations of isolated dually perfused guinea pig placentas, obtained from anesthetized dams and perfused for 60--140 min. The leakiness, estimated from the percentage of the L-glucose dose that crossed the trophoblast, varied (25 +/- 3% (SE), n = 28). On the injection side the maximal sugar uptake (Umax) was measured from early venous concentration ratios, since rapid tracer backflux occurred: Umax = (1 -- 3H/14C) x 100. Umax was independent of the leakiness. In all 14 placentas studied, stereospecific saturable transport of D-glucose was demonstrated at fetal (Umax = 56 +/- 4% (SE), n = 14) and maternal (62 +/- 1% (SE), n = 14) surfaces. The mean unidirectional influxes were 3.3 and 3.5 mumol.min-1.g-1, respectively. Uptakes were inhibited by phloretin and less effectively by phlorizin. D-glucose, 3-O-methylglucose, D-mannose and D-galactose had similar Umax values, about four times that of D-fructose. Tracer backflux and transplacental flux were also equal from both sides. It is concluded that similar hexose carriers, which resemble the human erythrocyte carrier, exist at the membrane on both sides of the trophoblast. The nondestructive technique employed characterizes carriers and receptors at the blood side of cells and could be applied to the placenta or other organs in the intact animal.

Animals↗
PubMed1975

An evaluation of the use of intraventricularly administered [3H]5-hydroxytryptamine as a marker for endogenous brain 5-hydroxytryptamine.

Following the intraventricular injection of a small amount of [3H]5-hydroxytryptamine ([3H]5-HT), the amount of radioactivity in telencephalic structures on the injected side was 6--7 times larger than that in corresponding areas on the opposite side. Moreover, a multiphasic disappearance of [3H]5-HT from whole brain or midbrain was found after the intraventricular injection of the labeled amine. However, after the intraventricular injection of [3H]tryptophan, the levels of [3H]5-HT in midbrain declined in a monophasic manner. A significant portion of the labeled amine derived from intraventricularly administered [3H]5-HT was resistant to the depleting effect of Ro4-1284 or to that elicited by destruction of the midbrain raphe nuclei, both of which caused an almost complete loss of endogenous 5-HT and labeled 5-HT formed from tryptophan. It thus appears that the intraventricular injection of [3H]5-HT leads to the formation of artifactual pools which are not present if the amine is synthesized in vivo. Studies with 6-hydroxydopamine suggested, however, that uptake of [3H]5-HT into adrenergic neurons did not occur to any great extent.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1975

Biological importance of retrograde axonal transport of nerve growth factor in adrenergic neurons.

Previous studies have shown that nerve growth factor (NGF) produces a selective induction of tyrosine hydroxylase (TH) in peripheral adrenergic neurons and that NGF is transported retrogradely with a high selectivity from the adrenergic nerve terminals to the perikaryon. In order to investigate the biological importance of retrograde NGF transport, the following experiments have been performed; (a) effect of NGF on TH activity in superior cervical ganglia (SCG) after unilateral injection into the anterior eye chamber and the submaxillary gland; and (b) effect of systemic injection of NGF on TH activity in SCG after blockage of retrograde axonal transport by axotomy. After unilateral injection of NGF into the anterior eye chamber and submaxillary gland of both 8-10-day-old rats and adult mice, the increase in TH activity in the SCG was considerably larger on the injected than on the non-injected side although the adrenergic neurons supplying the two organs do not account for more than 25% of the total number of adrenergic neurons in the SCG. A direct diffusion mechanism could be excluded by the fact that unilateral local injection of [125 I] produced no significant side difference in the accumulation of radioactivity in the SCG 2 after injection whereas after 14 h there was a several-fold difference between the injected and non-injected side. Moreover, the nodose ganglia which are located very close to the SCG exhibited no statistically significant difference in the accumulation of radioactivity at any time. Forty-eight hours after subcutaneous injections of 10 mg/kg of NGF the increase in TH activity of the SCG amounted to 154% on the intact side and to 92% on the axotomized side. However, these experiments do not permit decisions about the extent the axotomy, as such, impaired the response to NGF. It is concluded that the biological effect of NGF results to a considerable extent, from the moiety which reaches the cell body by retrograde transport from the nerve terminals.

Animals↗
PubMed1978

Receptor-linked cyclic AMP systems in rat neostriatum: differential localization revealed by kainic acid injection.

Various receptor-linked cyclic AMP systems were measured in rat neostriatum 2--14 days after selective destruction of neuronal cell bodies and dendrites by micro-injection of 3 microgram of kainic acid. Basal adenylate cyclase activity was reduced by up to 56% in the injected side and the sensitivity to dopamine was abolished. Up to 84% of cyclic nucleotide phosphodiesterase activity, hydrolyzing either cyclic AMP or cyclic GMP, was destroyed by kainic acid injection. Specific binding of [3H]etorphine and [3H]spiroperidol was reduced by up to 62% in the injected side, while non-specific binding was unchanged. All of these changes were time-dependent, and were greatest 7--14 days after kainic acid treatment. On the other hand, intrastriatal kainic acid injection caused no change in the steady-state concentration of cyclic AMP in striatal slices, or in the in vivo cyclic AMP content in the striatum of rats killed by microwave irradiation. Receptor-mediated increases in cyclic AMP accumulation in striatal slices were either unchanged or markedly potentiated by kainic acid treatment. The maximum response to adenosine was unchanged, while the response to isoprenaline was increased up to 3.7-fold, the response to dopamine increased up to 6.7-fold, and the response to PGE1 increased up to 30-fold. The effect of dopamine in kainic acid-treated striatal slices was no longer blocked by fluphenazine, but was blocked by propranolol, suggesting an interaction of dopamine with a beta-adrenoceptor in kainic acid-treated slices. The results suggest differential cellular localizations of the various receptor-linked cyclic AMP systems in rat neostriatum. Some dopamine and opiate receptors, as well as most of the phosphodiesterase activity, are associated with local neuronal elements, while beta-adrenoceptor, adenosine and PGE1 alterations in cyclic AMP are not. The potentiation of the beta-adrenoceptor and PGE1 responses suggests that they may occur in glial cells. In addition, the pool of adenylate cyclase destroyed by kainic acid appears to make little contribution to normal levels of cyclic AMP in the tissue.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1976

Adenosine 3',5'-cyclic monophosphate as a possible mediator of rotational behaviour induced by dopaminergic receptor stimulation in rats lesioned unilaterally in the substantia nigra.

A possible involvement of c-AMP in the rotational behaviour induced by a stimulation of dopamine receptors in corpus striatum of rats was investigated. Rats were lesioned unilaterally in the substantia nigra with 6-hydroxydopamine. Intraventricular injection of dopamine, norepinephrine and apomorphine induced rotational behaviour towards the intact side as did dibutyryl c-AMP (dB-c-AMP). Dopamine, norepinephrine and apomorphine could activate adenylate cyclase in homogenates of caudate nucleus. The activation by dopamine was blocked by haloperidol. I.p. injected apomorphine increased c-AMP content bilaterally in caudate nucleus and caused turning towards the intact side; theophylline potentiated and haloperidol blocked the effect. In non-lesioned rats, dopamine and norepinephrine, when injected unilaterally into the caudate nucleus, elicited truning twoards the non-injected side if the rats were pretreated with reserpine and tranylcypromine. c-AMP and dB-c-AMP given similarly to rats pretreated with theophylline also produced turning towards the non-injected side regardless the pretreatment with reserpine and tranylcypromine. All these results emphasize the possibility that c-AMP acts as a second messenger in the central dopaminergic pathway in rats. The supersensitivity of the dopaminergic system which developed after denervation is also discussed.

Adenylyl Cyclases↗
PubMed1979

Evidence that a nigral gabaergic--cholinergic balance controls posture.

The intranigral injection of kainic acid (k.a.) (3.5 nM/s.n.) produced a lesion which resulted in a decreased muscarinic receptor binding capacity and in a decreased choline acetyl transferase (CAT) activity confined to the pars reticulata. The unilateral, intranigral injection of carbachol in the substantia nigra (s.n.) produced turning, ipsilateral to the injected side, of dose-related intensity, which was antagonized by scopolamine given either i.p. or intranigrally together with carbachol. The bilateral, intranigral injection of carbachol produced rigid catalepsy, highly resistant to apomorphine administration and antagonized by scopolamine. On the other hand, the catalepsy produced by intranigral picrotoxin was much more sensitive to apomorphine and was disrupted by systemic scopolamine administration. Intranigral scopolamine per se produced either contralateral turning or stereotyped movements consistently, when injected unilaterally or bilaterally, respectively. In addition, scopolamine injected bilaterally in the s.n. but not in the caudate nucleus (c.n.), at the concentration of 64 nM side, was able to antagonize the haloperidol-induced catalepsy and to prevent the tremors and the muscular rigidity produced by arecoline. This effect of scopolamine was surmountable with a higher dose of arecoline. Finally, intranigral muscimol (0.44 nM/s.n.) prevented the occurrence of the parkinsonian syndrome produced by systemic arecoline. It is concluded that the muscarinic receptors present in the s.n. pars reticulata play a role in the control of posture opposite to that of the nigral GABA receptors.

Animals↗
PubMed1979

Opposite turning effects of dainic and ibotenic acid injected in the rat substantia nigra.

Unilateral intranigral administration of kainic and ibotenic acid, two putative stimulants of glutamatergic mechanisms, elicited turning behaviour starting from doses of 10 ng. While the turning produced by kainic acid was ipsilateral, that produced by ibotenic acid was contralateral to the injected side. Previous destruction of dopaminergic neurons on the side of the intranigral injection failed to reduce the turning behaviour. Peripheral treatment with picrotoxin did not reduce the turning in response to ibotenic acid. The results might suggest the existence of excitatory and inhibitory glutamate receptors which control nigral non-dopaminergic neurons mediating turning-behaviour.

Animals↗
PubMed1978

Stimulation of dopamine synthesis in caudate nucleus by intrastriatal enkephalins and antagonism by naloxone.

The intraventricular injection of methionine-enkephalin (50 to 100 micrograms) or [d-Ala2]-methionine-enkephalinamide (1.5 to 12 micrograms), a synthetic enkephalin analog resistant to enzyme degradation, caused a marked dose-dependent increase in dihydroxyphenylacetic acid and homovanillic acid concentrations in the rat striatum. The [d-Ala2] analog increased the accumulation of dopa in the striatum after aromatic amino acid decarboxylase inhibition, indicating that it increased dopamine synthesis. At the highest doses used both enkephalins failed to modify brain serotonin metabolism. The monolateral microinjection of the [d-Ala2]] analog (3 to 6 micrograms) into the caudate nucleus increased the concentration of dihydroxyphenylacetic acid in the injected side, whereas bilateral injection increased the concentration of this compound in both caudate nuclei and caused catalepsy. The stimulant effect of the [d-Ala2] analog on dopamine synthesis in the striatum persisted after destruction of striatal postsynaptic dopamine receptors with kainic acid. The biochemical and behavioral effects of enkephalins were prevented by naloxone, a specific narcotic antagonist. The results indicate that enkephalins stimulate dopamine synthesis by an action on opioid receptors localized on dopaminergic nerve terminals.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2026

Distribution of transgene in the rodent choroid plexus after intracerebroventricular injection of adeno-associated virus.

Using adeno-associated virus to transfer genetic information to the choroid plexus has emerged as a promising route for long-term gene therapy in the brain for a variety of conditions. Overexpression of proteins has proved effective in small animal models but few attempts have been made to translate this technology to clinic, suppress the activity of a protein of interest, or further expand the limited capsid serotypes known to have choroid plexus tropism. We utilise transfer of green fluorescent protein to show choroid plexus epithelium tropism for novel AAV6 derived capsid ShH10Y445F in mouse, rat and porcine tissue explant cultures. In vivo tropism is shown in the mouse following stereotactic intracerebroventricular injection. We examined the distribution of viral transduction across the choroid plexus in all four ventricles following a single unilateral intracerebroventricular injection using both green fluorescent protein as a transgene, but also the CRISPR/Cas9 system to deliver permanent knockdown of apical water channel aquaporin-1. Quantitative immunofluorescence and SURVEYOR assay were used to statistically assess the magnitude and extent of choroid plexus knockdown across the ventricular system. We conclude that serotype ShH10Y445F targets choroid plexus epithelium in mouse, rat and pig; and when carrying the CRISPR/Cas9 system can reduce target protein expression in these cells. Transduced choroid plexus epithelial cells distribute unevenly with a bias toward the lateral ventricle on the injected side and a preferential infection of choroid plexus in the lateral over the third and fourth ventricles. Overcoming irregular distribution represents a challenge for clinical translation of this technology where clinical efficacy may require manipulation of the entire choroid plexus.

Animals↗
PubMed1976

In vivo and in vitro conjugation and metabolism of estrogens by the baboon kidney.

Labeled estrogen was injected into one of the renal arteries of baboons and urine was collected separately from each ureter via ureterostomy at various time intervals over a period of 7 h; the urinary metabolites were analyzed by DEAE-Sephadex chromatography and enzyme hydrolyses. Identification of the aglycones was made by TLC and co-crystallization upon admixture with authentic compounds. When [3H]estradiol-17beta (E2) was injected into one of the renal arteries, the major metabolites were [3H]E2-3-glucosiduronate (E2-3G) and [3H]estrone-3-glucosiduronate (E1-3G); [3H]E2-3G was excreted predominantly into the urine from the injected side during the initial 30 min after injection. Formation of [3H]E1-3G was not detectable for the first 5 min in the urine from either side. However, its excretion gradually increased and the amount was almost equal from both sides in the later hours of collection. Injection of [3H]E1 revealed ready conjugation (as E1-3G) by the kidney without significant reduction at position-17. When E2-3G, labeled with 3H at positions 6,7 and with 14C in the glucuronic moiety, was injected, it was quickly excreted in the urine of the injected side. The ratio of 3H/14C of E2-3G excreted in the urine was the same as that of the injected E2-3G. In the later periods, E1-3G, which had a slightly increased 3H/14C ratio, appeared in the urine. These results indicate that E2 and E1 are conjugated directly in the kidney to form the 3G which is excreted into the urine and that effective dehydrogenation or reduction of the steroids in vivo does not take place in the kidney. The results also show that conjugated E2 (E2-3G) is quickly excreted by the kidney of the baboon without any change in its form and that the E2-3G is dehydrogenated to E1-3G during its general circulation without significant prior removal of the glucuronic moiety. When [3H]estriol (E3) was injected, facile glucuronidation to E3-16G by the kidney was shown. Injection of an equimolar mixture of [14C]E3 and [3H]E2 showed rapid excretion of [14C]E3-16G as opposed to the slower excretion of [3H]E2-3G. These results suggested that the active sites of these conjugating enzyme systems in the kidney may be different.

Animals↗