Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glycolysis intensity in an intact and ischemized muscle of a limb was decreased by prozerin and carbacholine in experiments on 230 noninbred rats with 2 models of acute ischemia. A less pronounced decrease was caused by benzohexonium, cholinesterase and dipyroxim. Meanwhile atropine blocked the glycolysis.
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PMID:[Effect of agents that act in the area of cholinergic synapses on the glycolysis process in an ischemic extremity]. 48 16

Regional cerebral blood flow (CBF) and regional cerebral glucose utilization (CGU) were studied by quantitative autoradiographic techniques in rats. Animals were treated either with a toxic dose of soman, an irreversible organophosphorus cholinesterase inhibitor, that produced convulsions or with saline as controls. An increased arterial blood pressure (mean increase = 41% of control) always preceded onset of convulsions. Convulsive activity was associated with an increase of plasma glucose concentration and marked increases over controls of CGU [average of all regions: control = 75 +/- 5 mumol.100 g-1.min-1, n = regions/animals (304/8); seizures = 451 +/- 20 mumol.100 g-1.min-1, n = 190/5] and CBF [average of all regions: control = 135 +/- 6 ml.100 g-1.min-1, n = 190/5; seizures = 619 +/- 29 ml.100 g-1.min-1, n = 190/5). Regional distribution of these effects revealed a greater proportional increase of CBF over CGU in cingulate, motor, and occipital cortex and caudate-putamen. In contrast, a lower proportional increase of CBF over CGU in CA3 region of hippocampus, dentate gyrus, medial thalamus, and substantia nigra was observed, implying the existence of a relative ischemia in these brain areas. These findings may be relevant to the pathogenesis of brain lesions associated with soman-induced convulsions.
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PMID:Cerebral blood flow and metabolism in soman-induced convulsions. 161 57

The effects of pharmacologic modulation of vagal activity on ischemic ventricular tachycardia were evaluated in 21 conscious dogs after permanent left anterior descending coronary artery (LAD) occlusion. Studies were done on spontaneous ventricular tachycardia (cycle length 383 +/- 100 msec, n = 21), 24 to 72 hours after LAD occlusion, and on inducible sustained monomorphic ventricular tachycardia (cycle length 251 +/- 30 msec, n = 6), 4 to 7 days after LAD occlusion. Edrophonium (1 mg/kg intravenously), a cholinesterase inhibitor, and methacholine (0.1 to 1 mg intravenously), a muscarinic agonist, had no significant effect on the rate or QRS morphology of either type of tachycardia, despite severe slowing of the sinoatrial rate. Similarly, atropine (up to 60 micrograms/kg intravenously) had no effect on the rate and QRS morphology of either type of tachycardia. In an attempt to enhance myocardial drug delivery to the ischemic and infarcted left ventricle, edrophonium (1 mg/kg) and methacholine (0.1 to 0.2 mg) were injected retrogradely through the great cardiac vein. This did not impart any significant therapeutic advantage over the systemic intravenous route. Sympathetic beta blockade did not affect the therapeutic outcome (n = 5) with either edrophonium or methacholine. It is concluded that direct or indirect enhancement of cardiac vagal activity has no effect on ischemic ventricular tachycardia in this model of subacute myocardial infarction. The lack of efficacy appears to be independent of myocardial drug delivery to ischemic ventricular site(s) and background sympathetic activity. Such a lack of efficacy may be caused by ischemia-mediated degeneration of vagal nerve terminals, by altered responsiveness of muscarinic receptors at infarcted arrhythmogenic myocardial sites, or both.
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PMID:The role of enhanced vagal activity on ischemic ventricular tachycardia: pharmacologic basis of inefficiency. 167 35

The biochemical changes of the elements of cholinergic neurotransmission (choline acetyltransferase, ChAT; acetylcholinesterase, AChE; butyrylcholinesterase, BuChE; and muscarinic cholinergic receptors, mAChR) as well as the electrolyte content were studied in ischemic lumbar spinal cord segments of newborn pigs. Ischemia was elicited by ligating the aorta for 30 min. Although no significant changes were observed in the sodium, potassium and calcium content of ischemic spinal cords, the calcium content was slightly elevated, to 119.3% of the control value. Whereas significant depletions were observed in both AChE and ChAT activities (to 69.1 and 87.7% of the control value, respectively), there was no significant change in BuChE activity as compared to the control value. The mAChR were also decreased, from 33.25 +/- 2.2 to 27.18 +/- 1.9 fmol/mg protein, while the Kd value was not significantly altered. It is concluded that even a relatively brief interruption of the oxygen supply can cause severe damage in the lumbar spinal cord of the newborn pig, affecting the cholinergic neurotransmission elements. This animal model might be suitable for studying the effects of hypoxia in newborns and children during chest operations involving the descending aorta.
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PMID:Effects of ischemia on cholinergic neurotransmission and electrolyte content in newborn pig lumbar spinal cord. 215 20

The effect of ischemia on cholinergic presynaptic inhibition of exocytotic norepinephrine release was studied in the innervated perfused rat heart. In normoxic hearts, vagal nerve stimulation significantly reduced exocytotic norepinephrine overflow to 75% of control values. This inhibitory effect was not affected by 3 minutes of low-flow ischemia (67% of control overflow values), but was attenuated or abolished by 10-minute low-flow ischemia or by 1-, 3-, and 5-minute stop-flow ischemia (107%, 85%, 101%, and 120% of control overflow values, respectively). The alpha-adrenergic antagonist phentolamine could completely or partly restore the failure of vagally induced inhibition of norepinephrine overflow in hearts with 1-, 3-, and 5-minute stop-flow ischemia (72%, 73%, and 85% of control overflow values, respectively). The muscarinic agonist methacholine substantially inhibited norepinephrine overflow to 18% of control overflow values in normoxic hearts. This effect was also significantly attenuated by 10-minute low-flow ischemia or by 1-, 3-, and 5-minute stop-flow ischemia (46%, 38%, 53%, and 55% of control overflow values, respectively). The cholinesterase inhibitor physostigmine did not restore the methacholine-induced inhibition of norepinephrine overflow after 3-minute stop-flow ischemia to normoxic level (55% vs. 17%). These results indicate that myocardial ischemia interferes with endogenous and exogenous cholinergic presynaptic inhibition of norepinephrine overflow in the rat heart. The extent of this attenuation depends on the severity and duration of ischemia. Reduced exocytotic acetylcholine release, which is at least in part due to an enhanced adrenergic presynaptic modulation, and dysfunction of presynaptic muscarinic receptors are suggested as two possible mechanisms.
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PMID:Failure of the cholinergic modulation of norepinephrine release during acute myocardial ischemia in the rat. 218 May 89

The effects of Y-8894 on experimental amnesia in rats induced by transient cerebral ischemia (600 sec) according to the method of Pulsinelli and Brierley were studied using the one trial passive avoidance response and the pole climbing discrete avoidance response. All drugs were administered to the rats immediately after recirculation. The following results were obtained: 1) In the one trial passive avoidance response test, Y-8894 (2.5, 5 and 10 mg/kg, i.p.) improved significantly the decreased latency induced by the ischemia, and it was most effective at 5 mg/kg. Calcium-hopantenate (100, 250 and 500 mg/kg, i.p.) and dihydroergotoxine (5 and 10 mg/kg, i.p.) tended to increase the latency. On the other hand, physostigmine (0.025, 0.05 and 0.1 mg/kg, i.p.), a cholinesterase inhibitor, increased the latency significantly, and it was most effective at 0.05 mg/kg. 2) The pole climbing discrete avoidance response was significantly decreased by the ischemia compared with the sham operated group, and Y-8894 (5 mg/kg, i.p.) tended to improve this decreased avoidance response. 3) Y-8894 (5 mg/kg, i.p.) facilitated recovery from the changes in glycolytic metabolism, and inhibited the accumulation of choline due to the dysfunction of the neuronal membranes induced by the ischemia. These results show that Y-8894 has beneficial effects on experimental amnesia induced by transient cerebral ischemia.
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PMID:[Pharmacological studies on Y-8894. (VII). Effects on transient cerebral ischemia-induced amnesia in rats]. 344 14

Cerebral cortical ischemia was induced in anesthetized rats by occlusion of the middle cerebral artery (MCA). Cerebral blood flow (CBF) was measured with the H2 clearance technique in the center and periphery of the ischemic territory. A decrease of CBF to about 50% of pre-occlusion values was observed in both areas. Administration of Physostigmine, a cholinesterase inhibitor, at a dose of 0.15 mg/Kg by intravenous route, induced an increase of CBF in the ischemic cortex. This change in CBF reached 120% of pre-occlusion level in the periphery and 80% of pre-occlusion value in the center of the area of distribution of the occluded artery. Although Physostigmine induced an increase in arterial blood pressure, the cerebral hyperemia observed both in normal and ischemic cortex could still be demonstrated after blockade of the pressor effect by bleeding or Phentolamine administration.
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PMID:Physostigmine induced reversal of ischemia following acute middle cerebral artery occlusion in the rat. 376 45

The main objective of this study was to determine whether the excitotoxic cholinesterase inhibitor soman increases the catabolism of phospholipids in rat brain. Injections of soman (70 micrograms/kg, s.c.), at a dose that produced toxic effects, increased the levels of both free fatty acids (175-250% of control) and free choline (250% of control) in rat cerebrum 1 h after administration. All fatty acids contained in brain phosphatidylcholine were elevated significantly including palmitic (16:0), stearic (18:0), oleic (18:1), arachidonic (20:4), and docosahexaenoic (22:6) acids. The changes observed were consistent with those reported to occur following ischemia and the administration of other convulsants. Pretreatment of rats with the anticonvulsant diazepam (4 mg/kg, i.p.) prevented both the signs of soman toxicity and the soman-induced increase of choline and free fatty acids. Diazepam alone did not affect the levels of choline or free fatty acids, cholinesterase activity, or soman-induced cholinesterase inhibition, suggesting that soman toxicity involves a convulsant-mediated increase in phosphatidylcholine catabolism. In addition, administration of the convulsant bicuculline, at a dose that produces seizures and increases the levels of free fatty acids in brain, significantly increased the levels of choline. Results suggest that excitotoxic events enhance the hydrolysis of phosphatidylcholine in brain as evidenced by a concomitant increase in the levels of choline and free fatty acids.
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PMID:Concomitant increases in the levels of choline and free fatty acids in rat brain: evidence supporting the seizure-induced hydrolysis of phosphatidylcholine. 381 25

The effects of pre-treatment with ENA-713, an acetylcholinesterase (AChE) inhibitor, on changes in pre- and postsynaptic cholinergic indices in gerbil brain following transient ischemia were studied at 4 and 14 days after recirculation. In the ischemic group, hippocampal acetylcholine (ACh) level was significantly reduced (to 23% of sham-operated controls) at 4 days post-ischemia, but this reduction was completely prevented by ENA-713 treatment. Choline acetyltransferase (ChAT) and cholinesterase (ChE) activities were not significantly changed at 4 and 14 days post-ischemia. Although the maximum number (Bmax) of muscarinic ACh receptor (mACh-R) binding in the hippocampus was decreased (to 44%) without any change in affinity at 14 days post-ischemia, this decrease was also inhibited by ENA-713 treatment. In addition, histological experiment indicated that ENA-713 inhibited ischemia-induced pyramidal cell loss in the hippocampal CA1 regions. Thus, these findings suggest that ENA-713 has protective, neurotrophic and therapeutic effects on cerebrovascular type dementia due to cerebral ischemia.
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PMID:Acetylcholinesterase inhibitor ENA-713 protects against ischemia-induced decrease in pre- and postsynaptic cholinergic indices in the gerbil brain following transient ischemia. 818 20

Activities of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) were studied in the ventral and dorsal horns and the intermediate zone of the rabbit lumbar spinal cord (L4-7) 24 and 96 h after ischemia caused by 20 or 40 min occlusion of the abdominal aorta. Changes of AChE and butyrylcholinesterase (BChE) activities were also detected histochemically by the direct thiocholine method. No significant changes were found immediately after ischemia. The most remarkable change after 20 min ischemia and 1 or 4 d of reperfusion was heterogeneous decrease in ChAT and AChE activities in the examined parts of gray matter. The highest loss of enzyme activities was found in the ventral horns and the lowest in dorsal horns. Following 40 min ischemia and reperfusion the significant depletion in enzyme activities in all investigated zones of the gray matter was accompanied with necrotic degenerative changes. There was a relatively greater decrease in ChAT and AChE activities in the ventral horns that corresponded with a more prominent morphological damage of the cholinergic neurons in this zone of the spinal cord.
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PMID:Cholinergic enzymes in spinal cord infarction. Biochemical and histochemical changes. 839 88


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