Phenylephrine 5.4mg / Tropicamide 0.28mg ophthalmic inserts preservative free

AimTo compare the efficacy of different administration regimens of compound tropicamide eyedrops (CTE) for pupil dilation for children with dark iris.MethodsA prospective, comparative, randomized interventional study was conducted. Children in Group 1 received CTE 3 times with a 3min interval between each application. Children in Group 2 received CTE 4 times with a 5min interval between each application. We measured their pupil diameters at baseline (pre-drug instillation) and 30min and 60min post-drug instillation and assessed the pupillary light reflex at 60min post-drug instillation.ResultsIn total, 194 eyes of 101 children were enrolled. The changes of pupil diameter at 30min and 60min post-drug instillation were 1.2±0.6 mm and 2.3±1.0 mm in Group 1, and 2.3±0.9 mm and 3.7±1.0 mm in Group 2, respectively. Group 2 showed a larger change in pupil size than Group 1 at 30min (PPConclusionIncreasing the frequency of compound tropicamide and lengthening the interval between eye drop applications can produce stronger mydriatic effects.

Abstract licence: CC BY-NC-ND

PurposeTo assess retinal and choroidal changes following rapid mydriasis in healthy adults.MethodsSeventy-one volunteers (71 right eyes) participated in a prospective randomised controlled trial. They were divided into two groups: tropicamide (n=36) and a mixture (tropicamide:phenylephrine=1:1, n=35) groups. Ophthalmic examinations included visual acuity, intraocular pressure and axial length measurements. Ultra-widefield swept-source optical coherence tomography angiography was used to assess retinal and choroidal parameters before and after mydriasis. This technique covers a 24×20 mm² area, allowing for non-invasive, simultaneous structural and haemodynamic assessment of retinal and choroidal regions.ResultsBoth central (tropicamide: 33.3%; mixture: 22.22%) and mid-peripheral (tropicamide: 28.47%; mixture: 36.81%) retinas thickened slightly postmydriasis (p>0.05, FDR corrected).ConclusionsRapid mydriasis causes slight retinal thickening, the slight change in the outer layer, particularly in the temporal and inferior regions. There were no significant changes in the choroid parameters following mydriasis, except for choroidal stroma volume. The limitation of this study was the small sample size and the absence of a control group.

Abstract licence: CC BY-NC

BackgroundTo assess the effect of cycloplegia on keratometry and horizontal white to white (WTW) measurements in presbyopic patients with type 2 diabetes.MethodsThe post-hoc analysis included 88 eyes from 88 patients with type 2 diabetes aged >40 years. Flat keratometry (Kf), steep keratometry (Ks), mean keratometry (Km), corneal astigmatism (CA), and WTW were measured using the RC-5000 auto kerato-refractometer (Tomey Inc., Nagoya, Japan), before and thirty minutes after the instillation of two drops (administered five minutes apart) of either 0.5% (46 patients) or 1% tropicamide (42 patients).ResultsThe mean changes in Kf, Ks, Km, CA, and WTW were - 0.01 ± 0.26 D, -0.05 ± 0.23 D, -0.03 ± 0.19 D, -0.04 ± 0.31 D, and 0.05 ± 0.24 mm, respectively, in the 0.5% tropicamide group. These values were - 0.07 ± 0.28 D, 0.01 ± 0.23 D, -0.03 ± 0.21 D, 0.08 ± 0.29 D, and 0.04 ± 0.15 mm, respectively, in the 1% tropicamide group. The changes following cycloplegia were not statistically significant (P ˃ 0.05).ConclusionsPost-cycloplegia keratometry and WTW measurements were comparable to pre-cycloplegia values in presbyopic patients with type 2 diabetes, suggesting that these measurements can be reliably obtained after cycloplegia.Trial registrationIRCT.ir, registration number: IRCT20200829048553N1, 2021-05-31.Clinicaltrialsgov, ID: NCT04932213, 2021-06-21.

Abstract licence: CC BY

We examined the activation of the p38 mitogen-activated protein kinase (p38-MAPK) pathway by the G protein–coupled receptor agonists, endothelin-1 and phenylephrine in primary cultures of cardiac myocytes from neonatal rat hearts. Both agonists increased the phosphorylation (activation) of p38-MAPK by ∼12-fold. A p38-MAPK substrate, MAPK-activated protein kinase 2 (MAPKAPK2), was activated approximately fourfold and 10 μM SB203580, a p38-MAPK inhibitor, abolished this activation. Phosphorylation of the MAPKAPK2 substrate, heat shock protein 25/27, was also increased. Using selective inhibitors, activation of the p38-MAPK pathway by endothelin-1 was shown to involve protein kinase C but not Gi/Go nor the extracellularly responsive kinase (ERK) pathway. SB203580 failed to inhibit the morphological changes associated with cardiac myocyte hypertrophy induced by endothelin-1 or phenylephrine between 4 and 24 h. However, it decreased the myofibrillar organization and cell profile at 48 h. In contrast, inhibition of the ERK cascade with PD98059 prevented the increase in myofibrillar organization but not cell profile. These data are not consistent with a role for the p38-MAPK pathway in the immediate induction of the morphological changes of hypertrophy but suggest that it may be necessary over a longer period to maintain the response.

Abstract licence: CC BY-NC-SA