Dapiprazole hydrochloride

Efficacy of dapiprazole

A study was performed to evaluate the clinical usefulness of dapiprazole in a private clinical setting. This study was unmasked, but used one eye of each subject as a control. Thirty consecutive subjects were given dapiprazole as directed by the manufacturer. The administration of dapiprazole followed bilateral dilation for routine fundus examination. Subjects were dilated using one drop each of proparacaine 0.5%, tropicamide 1.0%, and phenylephrine 2.5%. Pupil diameter, amplitude of accommodation, and conjunctival injection were evaluated. Each of these three variables was measured (1) before instillation of the diagnostic agents, (2) before the instillation of diapiprazole, and (3) at 30, 60, 120, and 180 min after the final instillation of dapiprazole. The average pupillary recovery time for dapiprazole-treated eyes was similar to previously published data. Accommodation also showed significant recovery, with comfortable reading ability returning after approximately 30 min. The design of our study did not permit us to determine what portion of accommodation recovery was attributable to alpha ciliary muscle effect and what portion resulted from the increased depth of field that was due to the pupillary constriction. All of our subjects exhibited conjunctival hyperemia after the administration of dapiprazole. This side effect persisted through the entire 180-min observation period that followed dapiprazole administration.

Dapiprazole's effect upon accommodative recovery: is it due entirely to changes in depth of field?

We conducted a study to evaluate the ability of dapiprazole 0.5% ophthalmic solution to reverse accommodative loss brought about by mydriatic drugs having mild cycloplegic effects. To accomplish this, we analyzed data from several earlier randomized, masked clinical studies. Our composite data include over 90 subjects dilated with tropicamide. Tropicamide was used alone in 1% concentration, as well as in combination with phenylephrine, 2.5% and in the proprietary preparation, Paremyd (Allergan Pharmaceuticals). Accommodative amplitude and pupillary diameter were measured before instilling dilating drops and then again one-half hour later, immediately before instilling either dapiprazole or a placebo. Accommodative amplitude and pupil diameter measurements were then repeated four more times, on both the treatment and control eyes and at 30, 60, 120, and 180 min after instillation of the last drop of dapiprazole or placebo. We found accelerated "accommodative" recovery with dapiprazole for each of the three tropicamide-containing drugs used in our study. This is not surprising because some recovery of accommodative amplitude after dapiprazole's administration is expected. This is because dapiprazole accelerates pupillary recovery and a narrowing of the pupil gives rise to an increase in ocular depth of field. Rate of accommodative recovery with dapiprazole was found not to be significantly different for all three tropicamide-containing preparations tested (p > 0.05). Does dapiprazole produce improvement in amplitude of accommodation beyond that attributable to increased depth of field?(ABSTRACT TRUNCATED AT 250 WORDS)

Dapiprazole clinical efficiency for counteracting tropicamide 1%

We evaluated the clinical usefulness of dapiprazole in reversing the effects of tropicamide 1.0%. Our study was random, masked with placebo, and used one eye of each subject as a control. Thirty subjects were given dapiprazole as directed by the manufacturer 30 min after being dilated by one drop each of proparacaine 0.5%, tropicamide 1.0%, and then 5 min later another drop of tropicamide 1.0%. Pupil diameter, amplitude of accommodation, conjunctival injection, and intraocular pressure were evaluated. Each of these variables was measured: (1) before instillation of the diagnostic agents; (2) before the instillation of dapiprazole; and (3) at 30, 60, 120, and 180 min after the final instillation of dapiprazole. The average pupillary recovery time for dapiprazole-treated eyes was significantly less than for nontreated eyes. Accommodation also showed faster recovery. Comfortable reading ability returned after approximately 43 min with dapiprazole vs. 66 min without dapiprazole. All of our subjects exhibited conjunctival hyperemia after the administration of dapiprazole. This persisted throughout the 180 min observation period after its administration.

Effects of intraocular dapiprazole in the rabbit eye

Dapiprazole produces miosis by blocking the alpha 1 receptors in the radial muscle of the iris; its intraocular effect has not yet been investigated. In this preliminary experimental animal study, we investigated the intracameral use of 0.2 ml of 0.005%, 0.0075%, 0.01%, and 0.05% dapiprazole to reverse mydriasis by 10% phenylephrine plus 0.5% tropicamide. With the 0.05% dapiprazole concentration, the values (mean +/- S.E.) of pupillary diameter were as follows: prior to the experiment, 5.3 +/- 0.31 mm; after mydriatics, 8.7 +/- 0.22 mm; after intraocular dapiprazole, 5.6 mm +/- 0.29. The results showed a dose-related miotic effect of dapiprazole. No difference in the toxicity parameters (inflammatory score, corneal thickness, endothelial cell counting, aqueous humor protein concentration, and intraocular pressure) was found between dapiprazole-treated eyes and saline-solution-treated eyes. Intraocular 0.01% and 0.05% dapiprazole is an effective miotic agent that may be helpful during surgery when the reversal of sympathomimetic mydriasis is needed.

Effects of peripheral sympathetic blockade with dapiprazole on the fear-inhibited light reflex

Fear (e.g. associated with the threat of an electric shock) causes an increase in initial pupil diameter (IPD) and a decrease in the amplitude of the light reflex response. There is evidence for dissociation between the two responses to threat: only the reduction in light reflex response amplitude is sensitive to the anxiolytic drug diazepam. We examined the effects of peripheral sympathetic blockade with the alpha(1)-adrenoceptor antagonist dapiprazole on both responses to threat on the basis of the hypothesis that only the response of the IPD will be affected, whereas the response of the light reflex will remain unaffected. Twelve healthy volunteers (Experiment 1) and eight healthy volunteers with smaller pupils (Experiment 2) participated in one experimental session. Dapiprazole 0.5% (two drops of 20 microl, three times) was instilled in the subjects' right or left eye while the contralateral eye was treated with placebo eye drops (artificial tear, two drops of 20 microl, three times) according to a single-blind balanced design. Pupil diameter was monitored by infrared binocular television pupillometry. At the point of maximum dapiprazole-evoked miosis, the light reflex was elicited three times in each of three Safe blocks (no possibility of electric shock), alternating with three Threat blocks (possibility of electric shock). At the end of each Safe and Threat block, subjects rated their mood and feelings on the Visual Analogue Scales. In Experiment 1, dapiprazole caused significant miosis. Threat increased subjectively rated anxiety and inhibited the light reflex. The inhibition of the light reflex was unaffected by dapiprazole. The threat-induced increase in IPD was also unaffected by dapiprazole, probably due to a ceiling effect curtailing the threat-induced increase in IPD. In the smaller pupil group in Experiment 2, where the possible contribution of a ceiling effect was minimized, dapiprazole suppressed the threat-induced increase in IPD. The inhibition of the light reflex by threat is likely to reflect central parasympathetic inhibition and is unlikely to involve the peripheral sympathetic innervation of the iris. The threat-induced increase in IPD is likely to reflect mainly central sympathetic excitation. The different central autonomic mechanisms underlying the two pupillary responses to threat may explain the dissociation between the separate effects of threat on IPD and light reflex amplitude.