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At least 19 recordsLinked to original sources

[Correction of the symptoms of late substance withdrawal syndrome by intra-conjunctival administration of 5% homatropine solution (preliminary report)].

The "late" or post-acute alcohol withdrawal syndrome (PAWs) is characterized by recurring waves of psychosomatic disturbances, and return for alcohol for the relief of these symptoms is a commonplace in many of abstinent alcoholics. However, the exact mechanism(s) is not fully known and there is no established any rapid treatment. We now have some data which seem to confirm our original and successful experience with local homatropine in clearly defined cases of the PAW syndrome. 28 alcoholic inpatients suffering from severe signs of the post-acute alcohol withdrawal (PAW) syndrome were randomly administered either homatropine hydrobromide or placebo eyedrops. Administration of topical homatropine (two 0.5% drops were given twice being spaced 15 minutes apart), unlike that of placebo had, within 60 minutes, caused a significant and then usually maintained clinical improvement, as evidenced by decreases of intensity of the PAW symptoms (irritability, depressed mood, anxiety, somatic and vegetative disorders (p less than or equal to 0.01), as well as a considerable reduction of the self-rated "desire for drink" phenomenon (less than or equal to 0.01). Post-homatropine responses observed so far seem to be initiated by the reflexory-induced haemodynamic and thermoregulatory changes with a transient but still significant fall in the systolic blood pressure, pulse rate, and oral temperature. Of importance may be the fact that in majority of patients, the PAW symptoms decreased and well-being increased parallel with the fall in prolactin levels (p less than or equal to 0.01): this has usually been noted at 60 minutes after the first homatropine dosing and might indicate a possible involvement of, at least, the cholinergic-serotonergic pathways.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Transcutaneous electrical stimulation applied to the infratrochlear nerve induces a homatropine-resistant miosis in humans.

1. Both high- and low-intensity transcutaneous electrical stimuli were applied to the emergence of the infratrochlear nerve in 18 healthy subjects. The effect on the size of the homolateral pupil was investigated. The width of the pupil was also measured when high-intensity transcutaneous electrical stimulation was applied to the contralateral side. 2. The high-intensity pulse resulted in constriction of the pupil when the stimulation was homolateral. The miosis was slow in onset (120 s latency) and long-lasting (80 s). No pupillary changes were detected after either ipsilateral low-intensity or contralateral high-intensity stimuli. 3. In 11 healthy subjects, the pupillary response to transcutaneous electrical stimulation was evaluated during iris parasympathetic blockade induced by homatropine eyedrops. The disappearance of the light reflex due to homatropine was considered an index of the parasympathetic blockade. Afterwards, a high-intensity pulse was transcutaneously delivered to the emergence of the infratrochlear nerve and the ipsilateral pupil size was measured. 4. A reduction in the pupillary size followed the electrical stimulation, still under the effect of homatropine which abolished the light reflex. The time course of this pupillary constriction was similar to that seen without the influence of homatropine. 5. The findings suggest that homolateral miosis, observed after unilateral high-intensity stimulation of the infratrochlear nerve, does not stem from cholinergic activation. It has been suggested that miosis induced by transcutaneous electrical stimulation may be due to an antidromic activation of the iris sensory fibres.

Adult↗

Status of cyclopentolate as a cycloplegic in children: a comparison with atropine and homatropine.

We compared the cycloplegic effects of cyclopentolate, homatropine and atropine by the retinoscopy findings and residual accommodation left following their use in the same individual. The mean residual accommodation measured after the use of cyclopentolate, homatropine and atropine was 1.48 +/- 0.33 D, 2.32 +/- 0.37 D and 1.10 D +/- 0.28 D, respectively, and the mean difference in retinoscopy readings between cyclopentolate and homatropine, homatropine and atropine, and atropine and cyclopentolate was 0.46 +/- 0.21, 0.71 +/- 0.23 and 0.26 +/- 0.14, respectively. We further observed that a tonus allowance of about +0.75 D would suffice for cyclopentolate. The merits for recommending cyclopentolate as a routine cycloplegic in children are discussed.

Accommodation, Ocular↗

Ultrasonic study to see the effect of topical pilocarpine and homatropine on anterior chamber depth in phakic cases.

Pilocarpine and Homatropine are the drugs having known effect on the depth of anterior chamber. The purpose of this study was to demonstrate the time of onset, peak effect and its duration of action as well as shallowing/deepening of the anterior chamber, after single instillation of pilocarpine 2% or homatropine bromide 2%, topically in one eye. Also we tried to see if there is any effect on the contralateral eye, due to systemic absorption of pilocarpine, homatropine after topical instillation of the drug in one eye. Pilocarpine causes a measurable shallowing of the anterior chamber with onset of effect with in 20 minutes and a peak in 60 minutes, the average narrowing being 0.26 mm. (range 0.20-0.29 mm.). Homatropine has a measurable deepening effect on the anterior chamber, due to axial flattening of the lens because of cycloplegia, with a range of 0.33 to 0.36 mm. In 70% of the cases the effect passes away with in 24 hours., but in 30% it comes to normal in 48 hours.

Adult↗

Morphine eye-drops reduce homatropine induced mydriasis in man.

In 7 healthy volunteers 4% morphine eye-drops, when administered to one eye, caused a miosis limited to that eye. In 7 other healthy volunteers morphine was administered into one eye after bilateral instillation of 0.5% homatropine ophthalmic drops; the eye treated with morphine and homatropine showed a mydriasis less intense than the other eye treated only with homatropine. It is suggested that topical morphine locally affects sympathetic function by inhibiting noradrenaline release into the iris neuromuscular junction.

Female↗

[Neurological manifestations in the intoxication of infants by dimethicone combined with homatropine: report of 6 cases].

OBJECTIVE: to alert that use of dimethicone plus homatropine in infants up to two months, may cause episodes of transitory extrapyramidal disturbances. METHOD: report 6 infants up to two months old, in daily use of dimethicone plus homatropine, that presented typical symptoms of the basal ganglia dysfunction, characterized by repeated crisis of short duration with tonic back shift of the head (opisthotonos), deviation of the eyes upward with looking fixed and terror expression, maintained in extending hypertonia posture of the 4 members and cry and/or guttural sounds emission. RESULTS: the extrapyramidal symptoms disappeared (and did not return) after interruption of dimethicone plus homatropine. Abnormalities were not verified in neurological examination, EEG and blood tests. CONCLUSIONS: the associated dimethicone/homatropine can produce in infants with less than 2 months, basal ganglia disturbances. The differentiation of these symptoms with the widespread epileptic crisis is essential, in order to avoid the erroneous use of antiepileptic drugs.

Basal Ganglia Diseases↗

Chiral resolution of atropine, homatropine and eight synthetic tropinyl and piperidinyl esters by capillary zone electrophoresis with cyclodextrin additives.

Chiral resolution of atropine, homatropine and eight synthetic tropinyl and piperidinyl esters were studied by capillary zone electrophoresis with cyclodextrin additives. Atropine and eight synthetic derivatives were successfully resolved by heptakis-(2,3,6-tri-O-methyl)-beta-cyclodextrin (TM-beta-CD) at concentrations ranging from 10 to 40 mM. Homatropine was baseline resolved by 10 mM beta-cyclodextrin and hydroxypropyl-beta-cyclodextrin (HP-beta-CD), respectively. The developed method was employed for the determination of atropine enantiomers in human serum.

Atropine↗

Analysis of homatropine methylbromide dosage forms.

A stability-indicating method of analysis of homatropine methylbromide in pharmaceutical formulations was developed. This method is based on the formation of a picric acid-quaternary ammonium complex, which is adsorbed on acid-washed diatomaceous earth in alkaline media followed by on-column chloroform extraction. The picrate complex is measured spectrophotometrically at 365 nm. The method was selective for homatropine methylbromide in that there was no interference from its major hydrolytic decomposition products, tropinium methylbromide and mandelic acid.

Methods↗

Modification by hexamethonium of the muscarinic receptors blocking activity of pancuronium and homatropine in isolated tissues of the guinea-pig.

In the guinea-pig left atrium, hexamethonium (C6) (0.1-3 mM) caused a parallel rightward shift of concentration-response curves for the negative inotropic response to carbachol (CCh) and oxotremorine (Oxo), the dose ratios obtained with the latter agonist being significantly greater than those for CCh at all concentrations of C6 investigated. In the presence of C6, the muscarinic receptor blocking activity of homatropine (20 microM) or of pancuronium (0.3-2.7 microM) appears to be reduced but if the effect of hexamethonium on concentration-response curves to the agonists is taken into consideration, the dose ratios produced by the combination of C6 with either homatropine or pancuronium were essentially as predicted for the combination of 2 competitive antagonists. The difference in the affinity of pancuronium for cardiac muscarinic receptors and ileal muscarinic receptors was also reduced in the presence of hexamethonium (0.3 mM).

Animals↗

Repeated delirium from homatropine eye-drops. A case report.

The administration of homatropine eye-drops precipitated several episodes of delirium in a 69-year-old woman. The unusual susceptibility of this patient to the central anticholinergic effect of homatropine is perhaps related to a preexisting mild cognitive defect possibly related to a cholinergic neurotransmitter deficit.

Aged↗

Separation of optical isomers of scopolamine, cocaine, homatropine, and atropine.

Different drug stereoisomers can have different physiological and therapeutic effects. Difficulties in separating optical isomers often make it impractical to market stereochemically pure products or to monitor isomeric contamination. This is not thought to be a problem with drugs isolated from biological sources (the alkaloids, for example). However, small amounts of isomeric impurities also exist in many biological systems. More importantly the isolation and purification process can cause partial or complete racimization in some cases. Great care must be taken in the handling of some drugs and an efficient, sensitive means to monitor racimization is important. Liquid chromatographic separation on a chiral beta-cyclodextrin bonded phase can be an effective technique in many cases. Its use in separating optical isomers of dl-scopolamine, dl-hyoscyamine, dl-homatropine, and dl-cocaine is discussed.

Atropine↗

Development and validation of a capillary zone electrophoresis method for the determination of atropine, homatropine and scopolamine in ophthalmic solutions.

A capillary zone electrophoresis method is described for the simultaneous determination of atropine, homatropine and scopolamine. Successful results were obtained after optimization of the electrophoretic parameters such as buffer composition and pH. The best separation was achieved using a 100 mM Tris-phosphate running buffer at pH 7. The validation data proved that the method had the requisite selectivity, sensitivity, reproducibility and linearity to be used for the assay of these compounds in pharmaceutical formulations. Dosage of the separate drugs in ophthalmic preparations is also presented.

Atropine↗

Systemic toxicity from ocular homatropine.

Toxidromes are well known to emergency physicians. An unclear or incomplete history and subtle findings on physical examination make the diagnosis of poisonings challenging. This article reports a patient who had an acute onset of visual hallucinations, pressured speech, and mania. Although she denied taking any medications, she was ultimately diagnosed as having anticholinergic toxicity. On further questioning of family members, it was discovered that she was being treated for anterior uveitis with 5% homatropine. This case illustrates the potential role of ocular medications in systemic toxicity. Patients often do not consider eyedrops to be medications, and their use may be overlooked in the medical history. It also is important to educate patients and medical staff in methods to minimize systemic toxicity when using ocular medication.

Acute Disease↗

Rectal absorption of homatropine [14C]methylbromide in the rat.

Homatropine[14C]methylbromide (HMB-14C) was administered to rats by intramuscular injection, oral gavage and rectal suppository. Plasma concentration of 14C were measured over the subsequent 12 h. Peak plasma concentrations were higher and achieved more rapidly after rectal administration than by the other routes whether HMB-14C was administered in a water-soluble suppository base or in aqueous solution. Twelve h after the suppositories were inserted and retained 28% of the 14C had been excreted in the urine while 56% remained in the large intestine. Unlabelled HMB, given in rectal suppositories to anaesthetized rats, caused prompt blockade of the effects of vagal stimulation on pulse rate and of intravenous acetylcholine on blood pressure. These results confirm the rapid rectal absorption of the drug.

Absorption↗

An evaluation of the effectiveness of intramuscular atropine or homatropine eyedrops in preventing the effects of physostigmine eyedrops on human vision.

An intramuscular injection of 2 mg atropine sulphate was given at either 8 or 120 min prior to instillation of 0.25% physostigmine sulphate eyedrops. In this way, the maximum accommodative change and the concomitant reduction in contrast sensitivity caused by physostigmine coincided with, respectively, the peak plasma atropine concentration or the fully developed mydriasis and reduction of near-point accommodation caused by atropine. Atropine at both times did not affect the miosis, the reduction in near-point, the increase in accommodation or the reduction in contrast sensitivity caused by physostigmine. Contrast sensitivity to a phase-reversed grating pattern was actually diminished by atropine, though this was not statistically significant. By contrast, 2% homatropine hydrobromide eyedrops did effectively antagonize physostigmine's actions. This indicates that the rate of delivery of atropine from the intramuscular injection was insufficient to compete against the ocular effects of physostigmine.

Accommodation, Ocular↗