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PubMed1988

Combined atropine and 2-PAM Cl effects on tracking performance and visual, physiological, and psychological functions.

Combinations of atropine (up to 4 mg.70 kg-1) and 2-PAM Cl (up to 1200 mg.70 kg-1) were studied for their effects on a pursuit tracking task, six visual functions, heart rate and blood pressure, and cognitive functions as measured by six psychological tests. Tracking performance in both bright light and dim light was significantly degraded up to 3.5 h after injection. High- and low-contrast near acuity was significantly altered up to 6 h after injection, whereas accommodation and pupil size remained altered for 24 h. Elevated pulse rates were observed for 4 h. Elevated systolic blood pressures were observed for 2 h while diastolic pressures remained elevated for 6 h. No drug effects were found for the psychological tests. Overall, the observed effects of these two drugs in combination are qualitatively similar to those of atropine alone although they are of greater magnitude. On two measures (accommodation and diastolic blood pressure), 2-PAM Cl was found to significantly potentiate the atropine effect.

Accommodation, Ocular↗
PubMed1987

[Effect of cholinesterase (ChE) reactivators on hemodynamics in animals. II. Reactions of the circulatory and respiratory systems of dogs after administration of ChE reactivators].

Different actions of pralidoxim and obidoxim were shown in studies on the influence of ChE reactivators (administered in doses of 10, 20, 40 mg/kg) on the circulatory and respiratory system. Blood flow velocity, arterial blood pressure in the carotid artery, the frequency and amplitude of breathing were recorded continuosly 60 min before and after intravenous injection of the reactivator. From these data the pulse rate, blood flow rate and the coefficient of the peripheral vascular resistance were calculated. At the same time pulse pressure was determined. Pralidoxim (PAM) acts parasympathicolitically on the heart-vascular system. It causes blood vessel shrinkage and decreases blood flow which is accounted for by increased vascular resistance by 20-40%. Such reactions cause, particularly after lower doses, increased arterial pressure and pulse rate by 15%. A 10 mg/kg dose of obidoxim increased pulse rate and blood flow for 15 min after the injection after 15 min the blood flow gradually decreased with simultaneous increase of the vascular resistance by 30%, as compared with the initial values. At larger doses it evoked mainly vascular reactions characterized by a constant increase of blood flow with simultaneous decrease of the vascular area. The ChE reactivators used stimulated the function of the respiratory system, which becomes apparent by increasing frequency of breathing with simultaneous increase of its amplitude. In these studies no differences were found in the action of obidoxim: Toxogonin (E. Merck) and Toxobidin (Polfa).

Animals↗
PubMed1977

Human leukocyte migration inhibitory factor (LIF) III. Further investigations on the serine protease nature of this lymphokine and its preference for arginine amides.

Previous findings suggesting an esterase and protease nature of human leukocyte migration inhibitory factor (LIF) were extended by testing the ability of different protease and esterase inhibitors to reduce LIF activity. The serine-specific inhibitors phenylmethylsulfonyl fluoride (PMSF) and physostigmine (eserine) markedly reduced LIF activity, whereas the histidine-specific inhibitors N-tosyl-L-lysine chloromethyl ketone (TLCK) and L-tosylamide-2-phenylethyl chloromethyl ketone (TPCK) were inactive. That LIF might act as an esterase and a protease was further strengthened by the ability of pralidoxime methansulfonate (2-PAM) to reestablish LIF activity of supernatants previously inactivated by PMSF. Furthermore, the arginine amides N-benzoyl-L-arginine-p-nitroanilide (BApNA) and N-benzoyl-L-phenylalanyl-L-valyl-L-arginine-p-nitroanilide (BPVApNA) were shown to satisfy the substrate specificities of the putative LIF enzyme. Indeed, BPVApNA seemed to possess a particularly strong affinity for LIF, indicating its potential role in an enzymatic LIF assay.

Amides↗
PubMed1988

Pharmacokinetics of pralidoxime chloride and its correlation to therapeutic efficacy against diisopropyl fluorophosphate intoxication in rats.

A two compartment system is used to study the therapeutic efficacy of pralidoxime chloride (1) along with a suitable pretreatment against diisopropyl fluorophosphate (2) intoxication in rats. The data were analyzed by standard techniques. Though thiamine hydrochloride pretreatment prolonged the biological half-life of 1 but it failed to increase the protective efficacy of 1, on the other hand sodium hydrogen carbonate pretreatment augmented the protective action of 1 without altering its biological half-life appreciably, through increased distribution of 1 into tissue compartment.

Animals↗
PubMedDate not supplied

Effects of pralidoxime applied locally into the midbrain reticular formation on the hippocampal theta rhythm induced by acetylcholinesterase inhibition.

After local administration into the midbrain reticular formation of an acetylcholinesterase reactivator--Pralidoxime, a significant decrease of intensity of hippocampal theta rhythm induced by previous inhibition of acetylcholinesterase by DFP was observed already after 10 min. This result suggests that cholinergic structures are localized in midbrain reticular formation and that they play a role in the origin of hippocampal theta rhythm.

Animals↗
PubMed1988

In vitro and in vivo effects of dichlorvos on blood cholinesterase activities of cattle.

Studies were conducted to ascertain in vitro effects and effects of percutaneous application (in vivo) of dichlorvos (2,2-dichlorovinyl dimethyl phosphate; DDVP) on cholinesterase activities in bovine erythrocytes and plasma. Treatment in vitro of erythrocytes and plasma with DDVP resulted in concentration- and time-dependent inhibition of erythrocyte acetylcholinesterase (AChE) and plasma cholinesterase (ChE) activities. Mean (+/- SD) DDVP concentrations required to cause 50% enzyme inhibition were 15.7 +/- 3.3 microM and 43.1 +/- 5.7 microM for AChE and ChE, respectively; however, these values required to achieve this inhibition were markedly decreased with increasing incubation time. The inhibited AChE activity failed to be reactivated after incubation of erythrocytes with 2-pyridine aldoxime methiodide (2-PAM); however, limited reactivation of inhibited AChE and ChE activities was observed with excess concentration of 2-PAM. Percutaneous application of a DDVP-containing livestock spray on cattle also caused a marked decrease in the in vivo activities of AChE and ChE; however, the inhibited enzyme activities were reactivated rapidly after incubation with 2-PAM.

Acetylcholinesterase↗
PubMed1978

[Toxicity of oximes and their effect on acetylcholinesterase activity in the blood and myoneural synapses of animals].

The effect was followed up of 2-PAM and Toxogonin (T), reactivators of choline esterase, at a single muscular application on the activity of acetylcholine esterase (ES 3.1.1.7) (ACE) of whole blood (WB) and the myoneural synapses (MS) of an interrib muscle. It was found that a species-specific effect was produced by T and 2-PAM on ACE of WB and MS in lambs and sheep. Optimal doses of 50 and 80 mg/kg led to a slight drop in the activity of ACE at the 2nd hour following injection, after which it rose gradually up to values that were higher than the initial ones for more than ten days. 100 and 200 mg/kg led to a more sensitive and long-term drop in the activity of ACE (up to 48h--72nd hour), after which it likewise rose above the initial value, and came back to normal on the 13th day. With lambs the reaction was analogous, though weaker. In rats and rabbits there was no change in the activity of ACE of WB and MS following the use of oximes. The optimal nontoxic and inductoenzyme rates of the two oximes for lambs and sheep proved to be about 50 mg/kg. It was established that both for rats and for sheep and lambs T was almost twice as toxic as 2-PAM. Intoxication with T was characterized by severe hemorrhagic and necrotic nephroso-nephritis, acute toxic dystrophy of the liver, and ulcerous, necrotic enteritis. 2-PAM was found to potentiate the toxic effect of T.

Acetylcholinesterase↗
PubMed1987

Human thermoregulation after atropine and/or pralidoxime administration.

The effects of intramuscular saline (control), atropine (2 mg), and/or pralidoxime (600 mg) on heat exchange was evaluated in four healthy males during seated, cycle exercise (55% Vo2 peak) in a temperate environment (Ta = 30.3 degrees C, Pw = 1.0 kPa). Esophageal (Tes), rectal (Tre), and mean skin temperatures (Tsk), and chest and forearm sweating (ms) were continuously measured. Skin blood flow (FBF) from the forearm was measured twice each minute by venous occlusion plethysmography. Whole body sweating was calculated from weight changes. The expected result of atropine injection, decreased eccrine sweating (-60%, p less than 0.05) and elevated esophageal (+0.4 degree C, p less than 0.05) and skin temperatures (+2.1 degrees C, p less than 0.05) was observed relative to control. Heart rate (+28 b X min-1) and FBF (+9 ml X 100 ml-1 X min-1) were higher after atropine. Pralidoxime, in general, did not affect the core and skin temperature responses to the exercise differently from control; however, a slightly elevated FBF (+3 ml X 100 cc-1 X min-1, 33%) compensated for the reduction in whole body sweating (-45%, p less than 0.05] that we observed. The combination of the drugs resulted in significantly higher esophageal (0.4 degree C) and skin (0.9 degree C) temperatures than atropine alone, as has been previously shown. The thermoregulatory disadvantage of inhibited sweating by atropine was partially compensated for by enhanced skin blood flow in this environment where Ta less than Tsk. Pralidoxime was shown to decrease whole body sweating, by a mechanism as yet unexplained.

Adult↗
PubMed1987

Effects of atropine and 2-PAM chloride on vision and performance in humans.

These experiments assessed the time course and severity of effects of atropine and 2-PAM chloride on selected visual functions, physiological measures, and a tracking performance task. Atropine up to 4 mg X 70 kg-1 body weight and 2-PAM Cl in doses up to 1200 mg X 70 kg-1 body weight were administered intramuscularly in a double-blind Latin square design. A long lasting and dose-related increase in pupillary diameter and decrease in accommodative amplitude with accompanying loss of near visual acuity was found following atropine administration. These functions returned to baseline 2 d after injection. Distance acuity, contrast sensitivity, color vision, and intraocular pressure showed no changes after atropine. Tracking performance was significantly decreased by 4 mg of atropine. The changes in vision function cannot readily explain the tracking performance loss, since the tracking involved a distant visual target while the atropine produced degradation of near vision. Most of the physiological tests, tracking performance and all visual functions were unaffected by 2-PAM Cl.

Accommodation, Ocular↗
PubMed1986

Oxadiazolidinones: irreversible inhibition of cholinesterases and effects on acetylcholine receptors.

Inhibition of four acetylcholinesterases (AChE) and a butyrylcholinesterase (BuChE) by 3-(2,3-dihydro-2,2-dimethyl-benzofuran-'7-yl)-5-methoxy-1,3,4-oxadiaz ol-2(3H)-one (DBOX) and 3-(2-methoxyphenyl)-5-methoxy-1,3,4-oxadiazol-2(3H)-one (MPOX) was measured by the Ellman spectrophotometric method. Both oxadiazolidinones inhibited AChE and BuChE irreversibly and with quasi first order kinetics. DBOX was 2-3 orders of magnitude more potent than MPOX. Housefly brain AChE and horse serum BuChE were more sensitive than AChEs of red blood cells or eel and Torpedo electric organs. Aldicarb, a carbamate anticholinesterase, which protected Torpedo AChE against irreversible phosphorylation by DFP, also protected it against irreversible inhibition by DBOX and MPOX. It is suggested that the nonesteratic oxadiazolidinones are converted to carbanillates on the surface of the enzyme, then acylate the active site of ChEs, producing carbanillated enzymes. At higher concentrations, the two oxadiazolidinones also affected the specific binding of (125I) alpha-bungarotoxin (alpha-BGT) and [3H]perhydrohistrionicotoxin (H12-HTX) to Torpedo nicotinic ACh-receptors, but did not affect the specific binding of [3H]quinuclidinyl benzilate (QNB) to rat brain muscarinic ACh-receptors.

Acetylcholinesterase↗