Intravenous administration of clonidine reduces intraocular pressure and alters ocular blood flow

Weigert, Günther; Resch, Hemma; Luksch, Alexandra; Reitsamer, Herbert A.; Fuchsjäger-Mayrl, Gabriele; Schmetterer, Leopold; Garhöfer, Gerhard

doi:10.1136/bjo.2007.116574

Cited by 18 publications

(8 citation statements)

References 28 publications

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“…before induction as a premedicant blunted the rise in IOP caused by suxamethonium, laryngoscopy and endotracheal intubation. Our study correlates with the studies done by G Weigert (2007) 12 , Mowafi (2008) 7 and Pal CK (2011) 8 , as in all of their studies there is a reduction in IOP in dexmedetomidine and clonidine Groups at various time intervals.…”

Section: Discussionsupporting

confidence: 76%

A Comparative Study of Dexmedetomidine and Clonidine as Premedicant on Intraocular Pressure and Haemodynamic Changes in Non-Ophthalmic Surgeries

Yadav¹,

Pareek²,

Sharma³

2016

jemds

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Section: Discussionsupporting

confidence: 76%

A Comparative Study of Dexmedetomidine and Clonidine as Premedicant on Intraocular Pressure and Haemodynamic Changes in Non-Ophthalmic Surgeries

Yadav¹,

Pareek²,

Sharma³

2016

jemds

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“…Compared with Clo, systemic BMD administration does not affect IOP, 31, 34 suggesting that BMD's neuroprotective effect is IOP independent. This observation is supported by the LoGTs study, 13 where BMD was effective in preserving visual field independent of IOP reduction in adults with low-pressure glaucoma.…”

Section: Discussionmentioning

confidence: 89%

“…Systemic Clo treatment lowered IOP at 1, 2 and 3 weeks compared with the untreated OHT group (all P <0.01), whereas systemic BMD had no effect on IOP (Figure 2a), as expected. 31 …”

Section: Resultsmentioning

confidence: 99%

Non-amyloidogenic effects of α2 adrenergic agonists: implications for brimonidine-mediated neuroprotection

Nizari¹,

Guo²,

Davis³

et al. 2016

Cell Death Dis

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The amyloid beta (Aβ) pathway is strongly implicated in neurodegenerative conditions such as Alzheimer's disease and more recently, glaucoma. Here, we identify the α2 adrenergic receptor agonists (α2ARA) used to lower intraocular pressure can prevent retinal ganglion cell (RGC) death via the non-amyloidogenic Aβ-pathway. Neuroprotective effects were confirmed in vivo and in vitro in different glaucoma-related models using α2ARAs brimonidine (BMD), clonidine (Clo) and dexmedetomidine. α2ARA treatment significantly reduced RGC apoptosis in experimental-glaucoma models by 97.7% and 92.8% (BMD, P<0.01) and 98% and 92.3% (Clo, P<0.01)) at 3 and 8 weeks, respectively. A reduction was seen in an experimental Aβ-induced neurotoxicity model (67% BMD and 88.6% Clo, both P<0.01, respectively), and in vitro, where α2ARAs significantly (P<0.05) prevented cell death, under both hypoxic (CoCl2) and stress (UV) conditions. In experimental-glaucoma, BMD induced ninefold and 25-fold and 36-fold and fourfold reductions in Aβ and amyloid precursor protein (APP) levels at 3 and 8 weeks, respectively, in the RGC layer, with similar results with Clo, and in vitro with all three α2ARAs. BMD significantly increased soluble APPα (sAPPα) levels at 3 and 8 weeks (2.1 and 1.6-fold) in vivo and in vitro with the CoCl2 and UV-light insults. Furthermore, treatment of UV-insulted cells with an sAPPα antibody significantly reduced cell viability compared with BMD-treated control (52%), co-treatment (33%) and untreated control (27%). Finally, we show that α2ARAs modulate levels of laminin and MMP-9 in RGCs, potentially linked to changes in Aβ through APP processing. Together, these results provide new evidence that α2ARAs are neuroprotective through their effects on the Aβ pathway and sAPPα, which to our knowledge, is the first description. Studies have identified the need for α-secretase activators and sAPPα-mimetics in neurodegeneration; α2ARAs, already clinically available, present a promising therapy, with applications not only to reducing RGC death in glaucoma but also other neurodegenerative processes involving Aβ.

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“…Clonidine, another alpha 2 agonist, also decreases IOP following systemic[ 1 17 ] as well as topical administration. [ 18 ] It causes an increase in vascular resistance and thereby reduces retinal blood flow.…”

Section: Discussionmentioning

confidence: 99%

“…Though many newer short-acting muscle relaxants have been introduced into the anesthetic practice, none of these agents could be projected as a replacement to succinylcholine in emergency situations. Hence, premedication with alpha 2 agonists such as dexmedetomidine and clonidine which are known to reduce IOP[ 1 2 ] could help us to combat the ocular adverse effects of succinylcholine.…”

Section: Introductionmentioning

confidence: 99%

Efficacy of alpha ₂ agonists in obtunding rise in intraocular pressure after succinylcholine and that following laryngoscopy and intubation

2015

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Context:Elevation of intraocular pressure (IOP) is an inherent and inadvertent association with the use of succinylcholine and alpha2 agonists can be used to obtund this effect.Aims:The study was aimed to assess the efficacy of intravenous dexmedetomidine and clonidine premedication in attenuating rise in IOP during laryngoscopy and intubation following administration of succinylcholine.Settings and Design:This prospective, observational study was conducted in 40 patients aged 20–60 years undergoing non ophthalmic surgical procedures.Subjects and Methods:For patients in Group D, dexmedetomidine 0.4 mcg/kg and in Group C clonidine 1 μg/kg over 10 min was administered before induction. All patients were induced with propofol. Laryngoscopy and intubation were performed 1 min after administration of succinylcholine 2 mg/kg.Statistical Analysis Used:Mann–Whitney, Chi-square and Wilcoxon tests.Results:Mean baseline IOP of both groups were comparable (15.4 ± 2.6 vs. 14.7 ± 2.3). Following premedication and induction, IOP decreased in both groups and the reduction was significantly more in Group D. Following administration of succinylcholine and 1 min after intubation IOP raised and exceeded the baseline value in Group C (16.0 ± 1.6 and 18.6 ± 2.2). Though there was an increase in IOP in Group D (12.0 ± 1.9 and 14.0 ± 2.1), it did not reach up to baseline values. Then there was a gradual reduction in IOP in both groups at 3, 5, and 10 min and Group D continued to have a significantly low IOP than Group C up to 10 min.Conclusions:Dexmedetomidine 0.4 μg/kg resulted in a reduction of IOP and blunted the increase in IOP, which followed administration of succinylcholine, laryngoscopy, and intubation. Though clonidine 1 μg/kg reduced IOP, it did not prevent rise in IOP following succinylcholine, laryngoscopy, and intubation.

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Intravenous administration of clonidine reduces intraocular pressure and alters ocular blood flow

Abstract: The short-time increase in choroidal and optic nerve head blood flow indicates a transient vasodilatory effect of clonidine due to an unknown mechanism. The decrease in retinal blood flow indicates clonidine-induced vasoconstriction in the retinal microvasculature.

Cited by 18 publications

References 28 publications

A Comparative Study of Dexmedetomidine and Clonidine as Premedicant on Intraocular Pressure and Haemodynamic Changes in Non-Ophthalmic Surgeries

A Comparative Study of Dexmedetomidine and Clonidine as Premedicant on Intraocular Pressure and Haemodynamic Changes in Non-Ophthalmic Surgeries

Non-amyloidogenic effects of α2 adrenergic agonists: implications for brimonidine-mediated neuroprotection

Efficacy of alpha ₂ agonists in obtunding rise in intraocular pressure after succinylcholine and that following laryngoscopy and intubation

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Intravenous administration of clonidine reduces intraocular pressure and alters ocular blood flow

Abstract: The short-time increase in choroidal and optic nerve head blood flow indicates a transient vasodilatory effect of clonidine due to an unknown mechanism. The decrease in retinal blood flow indicates clonidine-induced vasoconstriction in the retinal microvasculature.

Cited by 18 publications

References 28 publications

A Comparative Study of Dexmedetomidine and Clonidine as Premedicant on Intraocular Pressure and Haemodynamic Changes in Non-Ophthalmic Surgeries

A Comparative Study of Dexmedetomidine and Clonidine as Premedicant on Intraocular Pressure and Haemodynamic Changes in Non-Ophthalmic Surgeries

Non-amyloidogenic effects of α2 adrenergic agonists: implications for brimonidine-mediated neuroprotection

Efficacy of alpha 2 agonists in obtunding rise in intraocular pressure after succinylcholine and that following laryngoscopy and intubation

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Efficacy of alpha ₂ agonists in obtunding rise in intraocular pressure after succinylcholine and that following laryngoscopy and intubation