Improved determination of acetylcholinesterase activity in human whole blood

Worek, Franz; Mast, Ulrike; Kiderlen, Daniela; Diepold, Christine; Eyer, Peter

doi:10.1016/s0009-8981(99)00144-8

Cited by 488 publications

(304 citation statements)

References 38 publications

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“…Plasma was separated from an EDTA blood sample and frozen at -20°C. BuChE activity was assayed as described (30,31). The median (IQR) BuChE activity in this population is 4,500 (3,200) mU/mL (Eyer, unpublished).…”

Section: Hypotension In Severe Dimethoate Self-poisoning 881mentioning

confidence: 99%

Hypotension in severe dimethoate self-poisoning

Davies

Roberts

Eyer³

et al. 2008

Clinical Toxicology

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Introduction. Acute self-poisoning with the organophosphorus (OP) pesticide dimethoate has a human case fatality three-fold higher than poisoning with chlorpyrifos despite similar animal toxicity. The typical clinical presentation of severe dimethoate poisoning is quite distinct from that of chlorpyrifos and other OP pesticides: many patients present with hypotension that progresses to shock and death within 12-48 h post-ingestion. The pathophysiology of this syndrome is not clear. Case reports. We present here three patients with proven severe dimethoate poisoning. Clinically, all had inappropriate peripheral vasodilatation and profound hypotension on presentation, which progressed despite treatment with atropine, i.v. fluids, pralidoxime chloride, and inotropes. All died 2.5-32 h post-admission. Continuous cardiac monitoring and quantification of troponin T provided little evidence for a primary cardiotoxic effect of dimethoate. Conclusion. Severe dimethoate self-poisoning causes a syndrome characterized by marked hypotension with progression to distributive shock and death despite standard treatments. A lack of cardiotoxicity until just before death suggests that the mechanism is of OP-induced low systemic vascular resistance (SVR). Further invasive studies of cardiac function and SVR, and post-mortem histology, are required to better describe this syndrome and to establish the role of vasopressors and high-dose atropine in therapy.

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Section: Hypotension In Severe Dimethoate Self-poisoning 881mentioning

confidence: 99%

Hypotension in severe dimethoate self-poisoning

Davies

Roberts

Eyer³

et al. 2008

Clinical Toxicology

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“…The results showed that the novel substrates were AChEselective in human blood cholinesterases and were scarcely hydrolyzed by BChE and other esterases in the rat brain tissue and the monkey blood. This suggests that the AChEspecific activity in highly diluted human whole blood can be sufficiently measured with the novel substrates within 10 min because AChE activity in a 316-fold diluted human whole blood measured with ATCh (16-19 U/l at 37°C at 436 nm (eϭ10600 M Ϫ1 cm Ϫ1 ) 8) was much higher than that used in the present study (2.7 U/l in Table 1, and 2.3 U/l in Table 3). …”

Section: Discussionmentioning

confidence: 99%

“…Subsequent procedures were identical to those described above, whereas the absorbance was measured at 436 nm (eϭ10600 M Ϫ1 cm Ϫ1 ) to avoid the high absorption of hemoglobin. 8) The blood samples were finally diluted 936-fold in cuvettes. The specificity of AChE towards compounds was measured by the addition of the specific AChE inhibitor BW284c51 (1 mM in each cuvette).…”

Section: Hydrolysis Rates Of Matp and Matp؉ ؉ In Monkeymentioning

confidence: 99%

Piperidine-4-methanthiol Ester Derivatives for a Selective Acetylcholinesterase Assay

Kikuchi

Okamura

Fukushi

et al. 2010

Biological & Pharmaceutical Bulletin

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“…Measurement of AChE Activity The measurement of AChE activity of whole blood cells with or without AChE inhibitor was carried out according to the method previously reported by Worek et al 16) Briefly, whole blood dilutions were prepared from freshly heparinized blood samples by adding 100 ml to 10 ml ice-cold diluting reagent (0.1 mM phosphate buffer with 0.03% TritonX-100, pH 7.4). After careful mixing, the samples were frozen immediately (Ϫ30°C) and kept until the analysis.…”

Section: Methodsmentioning

confidence: 99%

Demonstration of Muscarinic and Nicotinic Receptor Binding Activities of Distigmine to Treat Detrusor Underactivity

Harada

Fushimi

Kato

et al. 2010

Biological & Pharmaceutical Bulletin

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Impaired bladder emptying can be caused by chronic conditions such as bladder outlet obstruction in men with benign prostatic hyperplasia and impaired detrusor contractility in patients of either sex. 1) Detrusor underactivity is defined as a contraction of reduced strength and/or duration resulting in prolonged bladder emptying within a normal time span. 2) Some of the established causes of detrusor underactivity include neurogenic, myogenic, aging, and medication side effects.3) The medical treatment for detrusor underactivity aims to enhance detrusor contractility and to reduce urethral outlet resistance thereby improving voiding. Standard pharmacotherapy includes the use of a-adrenoceptor antagonists to reduce outlet resistance, muscarinic agonists, and acetylcholinesterase (AChE) inhibitors.Pharmacotherapy using cholinomimetic drugs such as muscarinic agonists and AChE inhibitors has been used to treat impaired bladder emptying 4,5) since these drugs improve detrusor contractility by activating the parasympathetic cholinergic system. AChE inhibitors are considered to increase detrusor contractility by inactivating cholinesterase, thus maintaining cholinergic stimulation. Alternatively, the potential interaction of AChE inhibitors with cholinergic receptors has been also implicated in the therapeutic and/or side-effects associated with this class of compounds. 6,7) It was previously shown that neostigmine interacts directly with muscarinic and nicotinic receptor sites. [6][7][8] Distigmine bromide (distigmine) (Fig. 1), a reversible and long-acting carbamate cholinesterase inhibitor, has been clinically used to treat patients with voiding dysfunction associated with impaired detrusor contractility. 9-11) Bougas et al. 9) reported that treatment with distigmine resulted in a statistically significant reduction in residual volume and percentage residual volume, obviating the need for intermittent selfcatheterization in patients with detrusor underactivity. In addition, the maximum flow rate and detrusor pressure at maximum flow increased. These results suggested that distigmine has clinical efficacy in patients with detrusor underactivity. 9) Horinouchi et al. 12) revealed that distigmine significantly potentiated acetylcholine (ACh)-induced contractions of the The present study was undertaken to examine whether distigmine, a therapeutic agent used to treat detrusor underactivity, binds directly to muscarinic and nicotinic receptors. We used radioreceptor binding assays and compared the effects of distigmine with those of neostigmine and donepedil. The inhibitory effect of distigmine on the blood acetylcholinesterase (AChE) activity was significantly weaker than that of neostigmine.

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Improved determination of acetylcholinesterase activity in human whole blood

Cited by 488 publications

References 38 publications

Hypotension in severe dimethoate self-poisoning

Hypotension in severe dimethoate self-poisoning

Piperidine-4-methanthiol Ester Derivatives for a Selective Acetylcholinesterase Assay

Demonstration of Muscarinic and Nicotinic Receptor Binding Activities of Distigmine to Treat Detrusor Underactivity

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