Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of cholinesterase activity in M. demissus hearts was demonstrated by light- and electron-microscopic histochemistry and by enzymic assay. The enzyme proved to be acetylcholinesterase (AChE) since acetylthiocholine was the preferred substrate, and eserine or BW284C5I inhibited the enzyme activity, while isoOMPA was without effect. The AChE was localized and uniformly distributed along the cell surface membranes of the cardiac muscle cells. A fraction 8-fold enriched in AChE was isolated from pooled ventricles by a combination of differential and sucrose density gradient centrifugation. This sarcolemmal fraction contained little mitochondrial contamination as determined by electron microscopy and by succinate cytochrome c reductase activity. In addition, this fraction stained uniformly for AChE, indicating that it was free of other membrane types (for example sarcoplasmic reticulum which did not stain for AChE). Therefore, this fraction contained purified cell surface membrane free of contamination by other membranous organelles.
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PMID:Acetylcholinesterase: a useful marker for the isolation of sarcolemma from the bivalve (Modiolus demissus demissus) myocardium. 74 38

Specimens of human fetal hearts from the 9th to the 27th week of intrauterine life were processed by the technique of Karnowski and Roots as modified by Lewis for the demonstration of acetylcholinesterase-positive nerve fibers by light microscopy. Cholinergic innervation was present in both atria and ventricles even in the 9th week of intrauterine life. In the ventricles the number of cholinergic fibers augmented with increasing age; they spread in the ventricular wall surrounding the vascular network including capillaries, or following their course in the close proximity of cardiac muscle fibers. Electron microscopy of heart specimens in the 27th week of intrauterine life showed that ventricular cholinergic nerve terminals were present in the subendothelial space of arteries; other cholinergic fibers were in a close apposition with ventricular myocardial cells with an intervening space of about 300 nm. These data provided evidence that the development of cholinergic innervation in both atria and ventricles of human heart began early during the intrauterine life.
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PMID:Cholinergic innervation of the ventricular myocardium in the human fetal heart. 253 63

Experiments were performed to determine the cellular associations of the molecular forms of acetylcholinesterase (AChE) in adult rat heart. For this purpose, a cardiac muscle and a non-muscle fraction were isolated from rat heart ventricles after perfusion with collagenase and hyaluronidase, extracts of these fractions were subjected to ultracentrifugation on linear density gradients of sucrose (5-20%), and fractions of these gradients were analyzed for AChE activity. The results show that only globular AChE molecular forms were present in isolated cardiac muscle cells. Globular AChE forms were also present in the non-muscle cells fraction but in different proportions. The proportions of globular AChE forms plus the high specific activity of choline acetyltransferase in the non-muscle cell fraction suggest that this fraction contains cholinergic nerve fragments. The results of this study also show that asymmetric AChE is released during the perfusion of heart with the digestive enzymes, which suggests that asymmetric AChE is bound to the extracellular matrix of heart.
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PMID:Acetylcholinesterase molecular forms in muscle and non-muscle cells of rat heart. 258 21

Although acetylcholine is known to be involved in the genesis of skeletal muscle disturbance, its effect on cardiac muscle has been scarcely studied. In the present paper, using pyridostigmine, a cholinesterase inhibitor, the possible role of acetylcholine in the genesis of cardiomyopathy was investigated. In a mortality study, it was shown that pyridostigmine (100 mg/kg) caused death of 9/10 rats within 8 h, and that the lethality of such a dose could be significantly diminished by the subsequent administration of a total dose of 4 mg/kg atropine. In all other experiments, rats were divided into three groups; the control, untreated group; the pyridostigmine + atropine group in which atropine (2 mg/kg) was administered 5 min after pyridostigmine (60 mg/kg) administration; and the pyridostigmine group in which pyridostigmine (60 mg/kg) was administered orally. Rats were killed 3 h after pyridostigmine administration, and hearts were isolated. Heart mitochondrial electron transport activity (NADH-cytochrome c reductase, succinate-cytochrome c reductase, and cytochrome c oxidase) were measured enzymatically, and mitochondrial respiratory rates and control indices were measured polarographically. Structural changes in cardiac muscles of each group were observed by electron microscopy of cardiac sections. Acetylcholine levels of left ventricle were measured by high performance liquid chromatography. Activities of NADH-cytochrome c reductase and succinate-cytochrome c reductase were not affected by pyridostigmine administration; however, cytochrome c oxidase activity was significantly reduced in the pyridostigmine group. Atropine markedly lessened this reduction in activity. A protective effect of atropine was also observed morphologically. A protective effect of atropine was also observed morphologically. In the pyridostigmine group and the pyridostigmine + atropine group, left ventricular acetylcholine levels were increased significantly compared with the control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of acetylcholine in pyridostigmine-induced myocardial injury: possible involvement of parasympathetic nervous system in the genesis of cardiomyopathy. 273 Mar 38

In the blood of rabbits and rats poisoned with Intration, after 1, 3, 6 and 10 days of the experiment activities of AChE and ChE as well as those of beta-GR, AcP, AP and KT were checked. In addition, in the cardiac muscle, kidneys and liver, marker lysosomal hydrolases, i.e. beta-GR and AcP were determined. A long-standing reduction in the activities of AChE and ChE and increase in the activities in the concentrations of nonphysiologically great lysosomal hydrolases and AP were noted. A correlation between the inhibition of cholinesterase and organic lesions was found. Lysosomal enzymes share the responsibility for the necrotic process or rabbits' and rats' cardiac muscles. The use of oximes (PAM and Toxobidine) considerably contributed to reactivation of AChE and ChE and to normalization of the test marker enzymes.
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PMID:[Organ changes in rabbits and rats in phosphothioaliphatic acid poisoning. I. Effect of inhibition of cholinesterase and various marker lysosomal hydrolases on organ changes in rabbits and rats in phosphothioaliphatic acid poisoning]. 279 31

This study has been carried out by measuring the cholinesterase (ChE) activity in blood serum and in some organs (brain, liver, spleen, kidney, small intestine, lung, and cardiac muscle) of rats before and at different time intervals after infusion of 65 dextran 70, and 5% gelatin 40 solutions (1 ml/100 g body weight). The controls received infusions of the diluent of the gelatin preparation. The data obtained showed that the infusion of the diluent in rats has no effect on ChE activity neither in blood serum nor in other organs at any time intervals after infusion. In case of dextran and gelatin, a significant increase in ChE activity in blood serum and the tested organs was observed at different time intervals after infusion. The increase in case of dextran was more marked than in case of gelatin. These measurements returned to base-line values during 72 h after infusion. Furthermore, the study failed to disclose any untoward reactions, either immediate or delayed, which could be attributed to the infusion solutions.
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PMID:Effect of dextran gelatin on cholinesterase of rats. 618 11

Histochemical reactions which demonstrate cholinesterase reactions in tissues were used for slides of serial frozen sections of hearts of pigs, dogs, and rats to determine whether there are special types of modified muscle cells in continuous pathways from the SA (sinoatrial) to the AV (atrioventricular) node. There were positive reactions for acetylcholinesterase with less reaction for butyryl cholinesterase in ganglion cells and nerve fibers. No continuous pathways of cholinesterase-reacting cardiac muscle fibers from the SA to the AV node were identified although the muscle fibers were in intimate relation with the nerve fibers. No cells of Purkinje type were demonstrated in the atria.
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PMID:A restudy of cardiac conduction pathways by techniques for visualization of cholinesterase reaction. 703 Jan 46

The levels and molecular forms of acetylcholinesterase (AChE, EC 3.1.1.7) and pseudocholinesterase (psiChE, EC 3.1.1.8) were examined in various skeletal muscles, cardiac muscles, and neural tissues from normal and dystrophic chickens. The relative amount of the heavy (Hc) form of AChE in mixed-fibre-type twitch muscles varies in proportion to the percentage of glycolytic fast-twitch fibres. Conversely, muscles with higher levels of oxidative fibres (i.e., slow-tonic oxidative-glycolytic fast-twitch, or oxidative slow-twitch) have higher proportions of the light (L) form of AChE. The effects of dystrophy on AChE and psiChE are more severe in muscles richer in glycolytic fast-twitch fibres (e.g., pectoral or posterior latissimus dorsi, PLD); there is no alteration of AChE or psiChE in a slow-tonic muscle. In the pectoral of PLD muscles from older dystrophic chickens, however, the AChE forms revert to a normal distribution while the pesChE pattern remains abnormal. Muscle psiChE is sensitive to collagenase in a similar way as is AChE, thus apparently having a similar tailed structure. Unlike skeletal muscle, cardiac muscle has very high levels of psiChE, present mainly as the L form; AChE is present mainly as the medium (M) form, with smaller amounts of L and Hc. The latter pattern of AChE forms resembles that seen in several neural tissues examined. No alterations in AChE or psiChE were found in cardiac or neural tissues from dystrophic chickens.
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PMID:Comparison of the molecular forms of the cholinesterases in tissues of normal and dystrophic chickens. 706 26

Histochemical methods were used to demonstrate acetylcholinesterase in the wall of cardiac blood vessels in the baboon, dog and vervet monkey. To remove cholinesterase-containing sympathetic nerves, some of the animals were treated with guanethidine for four weeks prior to being sacrificed. In cardiac muscle from the dog and the vervet monkey, cholinergic nerves were histochemically visualized in both small and large vessels. On the other hand, in cardiac muscle from baboons, cholinergic nerves were not seen in branches of the coronary artery with diameters between 0.6 mm to 1 mm and very few fibres were seen around smaller vessels of diameter less than 0.3 mm. The few fibres seen did not appear to penetrate the media of the vessels. These results support physiological findings that the baboon coronary vasculature is not innervated by parasympathetic cholinergic nerves.
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PMID:Histochemical localization of acetylcholinesterase in the wall of cardiac blood vessels in the baboon, dog and vervet monkey. 709 79

The influence of acetylcholine (ACh) on cardiac performance of larval (Taylor Kollros [TK] stages II-XVIII) and postmetamorphic (3-609 g) Rana catesbeiana was analyzed in situ (circulatory system intact) and in vitro (isolated heart or ventricular strip preparations). Topical application of ACh to the heart in situ resulted in a dose-dependent decrease in heart rate and in a slight decrease in systolic ventricular pressure in all developmental stages. Injection of acetylcholine into the ventricle lumen in situ caused a dose-dependent transient decrease in systolic ventricular pressure, with little heart rate effect. Intraventricular ACh injection also changed the hemodynamic coupling between ventricle and conus arteriosus, generating a biphasic pressure profile in the conus due to sequential contractions of the ventricle and of the conus. In situ the sensitivity of the ventricle to ACh decreased during larval development, with the lowest sensitivity in small postmetamorphic adults. ACh applied in vitro to cardiac muscle strips or small hearts produced a negative inotropic effect. The ACh dose necessary to induce a 50% reduction in muscle strip contraction force in vitro decreased substantially during larval development, indicating an increase in ACh sensitivity with development. The effects of ACh both in vitro and in situ were diminished or eliminated by topical application or injection of atropine, suggesting the presence of muscarinic cholinergic receptors. After preincubation with the acetylcholinesterase blocker eserine, injection of ACh into the conus arteriosus decreased systolic ventricular pressure with a delay of 4-10 seconds, probably representing the minimum blood circulation time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Developmental changes in the acetylcholine influence on heart muscle of Rana catesbeiana: in situ and in vitro effects. 837 48


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