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Miochol-E (Acetylcholine Chloride) - Summary

 
 



MIOCHOL-E SUMMARY

Miochol®-E

Miochol -E (acetylcholine chloride intraocular solution) is a parasympathomimetic preparation for intraocular use. It is packaged in a blister pack containing one vial and one ampoule. The vial contains 20 mg acetylcholine chloride and 56 mg mannitol. The accompanying ampoule contains 2 mL of a modified diluent of sodium acetate trihydrate, potassium chloride, magnesium chloride hexahydrate, calcium chloride dihydrate and sterile water for injection. The reconstituted liquid will be a sterile isotonic solution (275-330 milliosmoles/Kg) containing 20 mg acetylcholine chloride (1:100 solution) and 2.8% mannitol. The pH range is 5.0-8.2. Mannitol is used in the process of lyophilizing acetylcholine chloride, and is not considered an active ingredient.

Miochol-E (acetylcholine) is indicated for the following:

To obtain miosis of the iris in seconds after delivery of the lens in cataract surgery, in penetrating keratoplasty, iridectomy and other anterior segment surgery where rapid miosis may be required.


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NEWS HIGHLIGHTS

Published Studies Related to Miochol-E (Acetylcholine)

Dianicline, a novel alpha4beta2 nicotinic acetylcholine receptor partial agonist, for smoking cessation: a randomized placebo-controlled clinical trial. [2011.01]
INTRODUCTION: Dianicline is a alpha4beta2 nicotinic acetylcholine receptor partial agonist, a class of drugs that includes varenicline and cytisine. Varenicline is efficacious for smoking cessation, while cytisine has not been studied systematically. The efficacy of dianicline has not been previously tested in an adequately powered study... CONCLUSIONS: Dianicline did not increase cigarette smoking abstinence rates beyond the initial phase of treatment. However, self-reported craving and nicotine withdrawal symptoms were reduced.

Nicotinic acetylcholine receptor gene expression is altered in burn patients. [2010.05.01]
INTRODUCTION: Burn patients have been observed to be more susceptible to the hyperkalemic effect of the depolarizing muscle relaxant succinylcholine. Changes in nicotinic acetylcholine receptor (nAChR) subunit composition may alter electrophysiologic, pharmacologic, and metabolic characteristics of the receptor inducing hyperkalemia on exposure to succinylcholine. No studies have been performed that show the upregulation and/or alteration of nAChR subunit composition in human burn patients. The scarcity of studies performed on humans with burn injury is mainly attributable to the technical and ethical difficulties in obtaining muscle biopsies at different time frames of illness in these acutely injured patients. nAChRs are expressed in oral keratinocytes and are upregulated or altered in smokers. However, no studies have addressed the expression of nAChRs in the oral mucosa of burn patients... CONCLUSION: Thermal injury may infer a systemic effect because upregulation/alteration of nAChRs occurs in nonmuscle tissues distant from the site of injury. The effect of thermal injury on nAChR gene subunits can be studied using a minimally invasive method (buccal mucosal scraping) and a highly sensitive technology (real-time reverse transcriptase polymerase chain reaction) obviating the need for more invasive methods.

Acetylcholine-esterase inhibitor pyridostigmine decreases T cell overactivation in patients infected by HIV. [2009.08]
HIV infection is characterized by persistent immune activation, increased production of proinflammatory cytokines, and rapid T cell turnover...

Quantification of eccrine sweat glands with acetylcholine sweat-spot test and anatomical redistribution of sweating after T2-T3 thoracoscopic sympathicolysis. [2009.02]
BACKGROUND: In this study, patients treated by thoracoscopic sympathicolysis for palmar hyperhidrosis were evaluated to determine the number and response of sweat glands to intradermal acetylcholine stimulus... CONCLUSION: It is well-known that Cannon's law of denervation (1939) is not applicable to the sweat glands, that is, there is no hyperactivation following intradermal acetylcholine stimulation. However, some response, which increased over the first 6 months following surgery, was observed in our study. Nevertheless, this activation is subsequently self-limiting, resulting in no gland atrophy, and reinnervation occurs without patient awareness.

Nicotinic acetylcholine receptor beta2 subunit gene implicated in a systems-based candidate gene study of smoking cessation. [2008.09.15]
Although the efficacy of pharmacotherapy for tobacco dependence has been previously demonstrated, there is substantial variability among individuals in treatment response. We performed a systems-based candidate gene study of 1295 single nucleotide polymorphisms (SNPs) in 58 genes within the neuronal nicotinic receptor and dopamine systems to investigate their role in smoking cessation in a bupropion placebo-controlled randomized clinical trial.

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Clinical Trials Related to Miochol-E (Acetylcholine)

Clonidine-Induced Spinal Acetylcholine Release: Normal Volunteers vs. Neuropathic Pain [Recruiting]
The purpose of this study is to compare the amount of acetylcholine release after a single injection of clonidine in normal volunteers and individuals with neuropathic pain.

Adenosine Receptors Influence Ischemia-Reperfusion Injury [Suspended]
Ischemic preconditioning is defined as the development of tolerance to ischemia-reperfusion injury by a previous short bout of ischemia resulting in a marked reduction in infarct size. This mechanism can be mimicked by several pharmacological substances such as acetylcholine and adenosine.

To detect ischemia-reperfusion injury in humans in vivo Kharbanda et al. developed a method in which endothelial dysfunction represents the effects of ischemic preconditioning. This method, however, uses acetylcholine to measure endothelial function before and after forearm ischemia. We, the investigators at Radboud University, hypothesize that the use of acetylcholine in this model reduces ischemia-reperfusion injury. Therefore, we will compare this protocol with a protocol in which endothelial function is only measured after ischemia. We expect an increase in ischemia-reperfusion injury when endothelial function is only measured after the forearm ischemia.

After determining the optimal method to measure ischemia-reperfusion injury of the vascular endothelium we will determine the effect of acute and chronic caffeine, an adenosine receptor antagonist, on ischemic preconditioning. With this study we expect to find that adenosine mimics ischemic preconditioning of the vascular endothelium. Moreover, we expect to find that acute caffeine intake reduces ischemia-reperfusion injury whereas chronic caffeine intake does not. This study will increase our knowledge about the mechanism of ischemic preconditioning and may also provide leads to exploit this endogenous protective mechanism in a clinical setting.

Storage Lesion in Banked Blood Due to Disruption of Nitric Oxide (NO) Homeostasis [Recruiting]
The purpose of this study is to explore the impact of aged blood on endothelial function by measuring forearm blood flow during intra-arterial acetylcholine infusion in normal healthy human volunteers after infusion of autologous blood stored for 5-10 days or 35-42 days. Our hypothesis is that 1) the vasodilatory response to the infusion of acetylcholine will be reduced in the 35-42 day group compared with the 5-10 day group, because of scavenging of the NO released from the endothelium by the hemolytic process in the aged blood, 2) that the infusion of aged stored blood will produce vasoconstriction, measured by reduced forearm blood flow during infusion of the 35-42 day compared with the 5-10 day old blood, and that 3) there will be increases in venous levels of cell free plasma hemoglobin, red cell microparticles, red cell membrane damage, arginase levels and activity, decreased arginine levels, markers of oxidative stress (carbamylated proteins and nitrated tyrosine residues), and increases in plasma in vitro NO consumption during the infusion of 35-42 day old compared to 5-10 day old blood.

Endothelial Injury and Development of Coronary Intimal Thickening After Heart Transplantation [Recruiting]
Coronary allograft vasculopathy (CAV) is the leading cause of late graft failure and second leading cause of late mortality after heart transplantation. CAV has been associated with a variety of traditional risk factors for atherosclerosis; however, immune mediated injury from development of de-novo donor-specific antibodies after transplantation also likely plays an important role. Similar to the progression of traditional atherosclerosis, it is likely that endothelial dysfunction is the precursor to the development of intimal thickening and CAV. The investigators hypothesize that coronary allograft vasculopathy after heart transplantation as defined by progressive neointimal hyperplasia is preceded by endothelial dysfunction, which in turn is at least partly mediated by donor specific antibodies. The investigators are proposing a prospective study in humans to test the above hypothesis and further mechanistically understand how CAV progresses. In this study the investigators will test for coronary endothelial function by infusing acetylcholine into the coronary artery and measure intimal hyperplasia by optical coherence tomography (OCT) and compare findings in patients with and without donor specific antibodies.

Acetylcholine and Postoperative Cognitive Change in Aged Patients [Recruiting]

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Page last updated: 2011-12-09

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