The Influence of Cyclogyl® and Neosynephrine® on Tonographic Studies of Miotic Control in Open-Angle Glaucoma

Schimek, Robert A.; Lieberman, Warren J.

doi:10.1016/0002-9394(61)91813-x

Cited by 32 publications

(11 citation statements)

References 5 publications

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“…Other key factors that may be considered include blockage of the pumping action of the ciliary muscle 25 , change in the secretion rate of the aqueous humor, or a change in the scleral rigidity. 26 Several limitations of this study may have affected our results. First, the number of subjects in both groups was relatively small, limiting our ability to identify small changes in the very variable ASM parameters.…”

Section: Discussionmentioning

confidence: 91%

“…As these veins have smooth muscle and adrenergic innervation, 23 it is possible that tropicamide interferes with the smooth muscle activity in the blood vessel walls which in turn could influence IOP, but would not be detected by HRUS. Other key factors that may be considered include blockage of the pumping action of the ciliary muscle 25 , change in the secretion rate of the aqueous humor, or a change in the scleral rigidity 26 …”

Section: Discussionmentioning

confidence: 99%

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Effects of unilateral topical administration of 0.5% tropicamide on anterior segment morphology and intraocular pressure in normal cats and cats with primary congenital glaucoma

Gomes

Bentley

Lin

et al. 2011

Veterinary Ophthalmology

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Objective To determine the effects of topical 0.5% tropicamide on anterior segment morphology (ASM) and intraocular pressure (IOP) in normal and glaucomatous cats. Animals used Normal cats and cats with inherited primary congenital glaucoma (PCG). Procedures Control IOP curves were performed in untreated normal and PCG cats. In the first experiment, tropicamide was applied OD in eight normal and nine PCG cats. IOP and pupillary diameter (PD) were measured at 0, 30, and 60 min, then hourly until 8 h post-treatment. In a second experiment, six normal and seven PCG cats received tropicamide OD. High-resolution ultrasound images were obtained at 0, 1, 5, and 10 h post-treatment to measure ASM changes. IOP and PD were measured OD at 0, 1, 2, 3, 5, 7, and 9 h. Results In untreated normal cats IOP OU decreased throughout the day. In PCG cats IOP OU had wide fluctuations over time. In normal cats IOP response varied in the treated eye but did not change significantly in untreated eyes. IOP significantly increased from baseline in both eyes of all treated PCG cats. Increases in IOP were associated with some ASM changes. Cats with PCG had a significantly smaller angle recess areas, diminished ciliary clefts and decreased iris-lens contact. ASM changes were not strongly correlated with IOP in all cats. Conclusions The ASM of PCG cats is markedly different from normal cats, and clinically significant increases in IOP OU occur in cats with PCG after tropicamide treatment. The mechanism for this increase remains unclear.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Effects of unilateral topical administration of 0.5% tropicamide on anterior segment morphology and intraocular pressure in normal cats and cats with primary congenital glaucoma

Gomes

Bentley

Lin

et al. 2011

Veterinary Ophthalmology

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“…Several previous studies have indicated a role for FFA in controlling EGP (9,13,26,52,55,60). The "single gateway hypothesis" was originally put forward to integrate observations on change in plasma hormones and FFA, suggesting that peripheral action of hormones exerted effects on the liver primarily by modulating plasma FFA concentrations (6).…”

Section: Discussionmentioning

confidence: 99%

Regulation of endogenous glucose production after a mixed meal in type 2 diabetes

Singhal

Caumo

Carey

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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The extent and time course of suppression of endogenous glucose production (EGP) in type 2 diabetes after a mixed meal have been determined using a new tracer methodology. Groups of age-, sex-, and weight-matched normal controls (n = 8) and diet-controlled type 2 diabetic subjects (n = 8) were studied after ingesting a standard mixed meal (550 kcal; 67% carbohydrate, 19% fat, 14% protein). There was an early insulin increment in both groups such that, by 20 min, plasma insulin levels were 266 +/- 54 and 190 +/- 53 pmol/l, respectively. EGP was similar basally [2.55 +/- 0.12 mg x kg(-1) x min(-1) in control subjects vs. 2.92 +/- 0.16 mg x kg(-1) x min(-1) in the patients (P = 0.09)]. After glucose ingestion, EGP declined rapidly in both groups to approximately 50% of basal within 30 min of the meal. Despite the initial rapid decrease, the EGP was significantly greater in the diabetic group at 60 min (1.75 +/- 0.12 vs. 1.05 +/- 0.14 mg x kg(-1) x min(-1); P < 0.01) and did not reach nadir until 210 min (0.96 +/- 0.17 mg x kg(-1) x min(-1)). Between 60 and 240 min, EGP was 47% higher in the diabetic group (0.89 +/- 0.09 vs. 1.31 +/- 0.13 mg x kg(-1) x min(-1), P < 0.02). These data quantitate the initial rapid suppression of EGP after a mixed meal in type 2 diabetes and the contribution of continuing excess glucose production to subsequent hyperglycemia.

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“…6Y8 It is interesting to note that the sympathomimetics do not provoke IOP elevation in healthy eyes 9,10 and in those suspected to have open-angle glaucoma. 11,12 However, a marked IOP elevation can be observed in eyes with open-angle glaucoma following the topical use of parasympatholytics. 8,10,13Y16 Leydhecker 7 explained the IOP rise by the vascular action of the mydriatic or cycloplegic drug.…”

Section: Parasympatholytics and Ocular Hypertensionmentioning

confidence: 99%

Drug-Induced Ocular Hypertension and Angle-Closure Glaucoma

Badhu

Bhattarai²,

Sangraula³

2013

Asia-Pacific Journal of Ophthalmology

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The objective of this study was to review the available literature on the drugs causing ocular hypertension and glaucoma. Electronic literature search was carried out using the Web sites www.pubmed.gov and www.google.com published through the year 2011. The search words were "drug induced ocular hypertension" and "drug induced glaucoma" used in combination. The articles published or translated into English were studied. Quite a significant number of drugs commonly prescribed by various physicians of different specialties can induce ocular hypertension or glaucoma. A brief account of various drugs that can induce ocular hypertension has been given in this article. Those drugs are parasympatholytics; steroids; anticholinergics, adrenergics, and antidepressants; cholinomimetics; antineoplastic agents; antipsychotic and antiparkinsonism agents; H1 and H2 receptor blockers; botulinum toxin, cardiac agents, and anticoagulants; silicone oil; sulfa drugs; and anesthetic agents. Rational use of these drugs and knowledge of their potential adverse effects can help prevent the devastating complications resulting in loss of vision and compromised quality of life.

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The Influence of Cyclogyl® and Neosynephrine® on Tonographic Studies of Miotic Control in Open-Angle Glaucoma

Cited by 32 publications

References 5 publications

Effects of unilateral topical administration of 0.5% tropicamide on anterior segment morphology and intraocular pressure in normal cats and cats with primary congenital glaucoma

Effects of unilateral topical administration of 0.5% tropicamide on anterior segment morphology and intraocular pressure in normal cats and cats with primary congenital glaucoma

Regulation of endogenous glucose production after a mixed meal in type 2 diabetes

Drug-Induced Ocular Hypertension and Angle-Closure Glaucoma

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