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At least 19 recordsLinked to original sources
PubMed1977

Glycopyrrolate-neostigmine mixture for antagonism of neuromuscular block: comparison with atropine-neostigmine mixture.

Glycopyrrolate, a new anticholinergic agent, was evaluated and compared with atropine. Glycopyrrolate 0.2 mg to neostigmine 1.0 mg was found to be safe and effective. The heart rates remained more stable with glycopyrrolate, and the frequency of arrhythmia, which was both transient and of no consequence, was similar in the two groups. The antisialogogue action of glycopyrrolate was superior to that of atropine.

Anesthesia, General↗
PubMed1979

4-Aminopyridine potentiates neostigmine and pyridostigmine in man.

To elucidate the interaction of 4-aminopyridine with neostigmine and pyridostigmine, the authors studied 57 anesthetized surgical patients using a technique of constant infusion of pancuronium to quantitate antagonist activity. 4-Aminopyridine, 0.15 or 0.35 mg/kg, produced no antagonism, while 0.5 mg/kg produced a mean 24 +/- 6 per cent (peak) antagonism. The dose that produced 50 per cent antagonism (ED50) of neostigmine alone was 22 micrograms/kg; with 0.35 mg/kg 4-aminopyridine, it was 7 micrograms/kg. The ED50 of pyridostigmine alone was 110 micrograms/kg; with 0.35 mg/kg 4-aminopyridine, it was 27 micrograms/kg. 4-Aminopyridine prolonged the onset times of both neostigmine and pyridostigmine, but prolonged the duration of action of neostigmine only. At a given level of antagonism of pancuronium, adding 4-aminopyridine 0.35 mg/kg, to neostigmine and to pyridostigmine decreased the amounts of atropine needed to prevent a change in heart rate by 68 and 70 per cent, respectively. The authors conclude that 4-aminopyridine potentiates antagonism of a pancuronium-induced neuromuscular blockade by neostigmine or pyridostigmine. Also, less atropine is needed to prevent cardiac muscarinic stimulation when 4-aminopyridine is used with either neostigmine or pyridostigmine.

Adult↗
PubMed1992

Effect of intraperitoneal neostigmine on peritoneal transport characteristics in CAPD.

Lymphatics have been suggested to play a major role in the absorption of dialysate, which consequently affects the adequacy of peritoneal dialysis. Neostigmine has been found to decrease lymphatic absorption in rats, presumably by causing constriction of the lymphatic stomata. We investigated the effect of neostigmine on seven continuous ambulatory peritoneal dialysis (CAPD) patients in a prospective study. We performed modified peritoneal equilibration tests both with and without intraperitoneal neostigmine in a random order. Radiolabeled albumin (0.8 mg) was added to 2 liters of dialysate +/- 2.0 mg neostigmine. We evaluated ultrafiltration and creatinine, phosphate, and urea clearances. The dialysate bag and the peritoneum were scanned at the initiation and conclusion of the four-hour dwell period. We found no change in ultrafiltration, residual volumes, creatinine, phosphate and urea clearances, or albumin recovered. Of the seven patients exposed to neostigmine, four had diarrhea, abdominal cramps, nausea, and vomiting. In conclusion, we found that 2 mg i.p. neostigmine did cause significant side-effects and did not alter transport characteristics in CAPD patients.

Adult↗
PubMedDate not supplied

Antagonism of pancuronium and its metabolites by neostigmine in cats.

Antagonism by neostigmine of neuromuscular blockade produced by pancuronium or its metabolites was studied in the cat anterior or tibialis muscle-peroneal nerve preparation using constant infusions of muscle relaxants. The ED50 of neostigmine (dose which caused a 50% antagonism) was 16, 11, 29, and 26 micrograms/kg for pancuronium, 3-hydroxypancuronium, 17-hydroxypancuronium, and 3, 17-hydroxypancuronium, respectively. Times of onset of neostigmine action were shorter when antagonizing 17-hydroxypancuronium neuromuscular blockade. Duration of neostigmine action when antagonizing 17- or 3, 17-hydroxypancuronium blockade was shorter than with pancuronium or 3-hydroxypancuronium. We conclude that more neostigmine is required to antagonize 17- or 3,17-hydroxypancuronium neuromuscular blockade than is required to antagonize pancuronium. Conversely, less neostigmine was required to antagonize 3-hydroxypancuronium blockade.

Animals↗
PubMed1975

Central cholinergic control of cerebral blood flow in the baboon. Effect of cholinesterase inhibition with neostigmine on autoregulation and CO2 responsiveness.

Cerebral autoregulation and vastomotor responsiveness to carbon dioxide (CO2) were measured quantitatively by the use of the autoregulation index and chemical index, respectively, in normal baboons before and after intravertebral and intracarotid infusion of the anticholinesterase agent, neostigmine methylsufate (Prostigmin). Continuous measurements were made of cerebral blood flow (measured as bilateral internal jugular venous outflow), arterial and cerebral venous pO2 and pCO2, cerebral arteriovenous oxygen differences, and endotracheal CO2. The effect of intravertebral infusion of neostigmine (12.5 mug/kg body weight) was compared to intravertebral infusion of neostigmine (25 mug/kg body weight) for assessment of any specific action of the drug on a hypothetical cholinergic vasomotor center, presumed to be located in the territory of the vertebrobasilar supply. No significant or persistent changes in cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) followed either intravertebral or intracarotid infusion of neostigmine. Cerebral vascular resistance (CVR) and cerebral perfusion pressure (CPP), however, decreased significantly after intravertebral infusion. Cerebral autoregulatory vasoconstriction during increases of CCP was significantly reduced following both intravertebral and intracarotid infusion. Cerebral autoregulatory vasodilatation was not altered as CPP was lowered. Cerebral vasodilatory reactivity to CO2 inhalation was significantly enhanced following intravertebral neostigime but not following intracarotid neostigmine. Cerebral vasoconstrictive response to hyperventilation was not influenced by neostigmine. These results support the view that central cholinergic cerebrovascular influences exist, and are vasodilatory in nature.

Acetylcholine↗
PubMed1975

The effect of temperature on a d-tubocurarine neuromuscular blockade and its antagonism by neostigmine.

In 19 cats anesthetized with chloralose and urethrane, d-tubocurarine (d-TC) was continuously infused to produce constant 90% depression of twitch tension prior to injection of 5, 10 or 20 mug/kg of neostigmine. The required mean infusion rates of d-TC were 3.6 +/- 0.6, 5.1 +/- 0.3, 8.5 +/- 0.3 and 8.9 +/- 0.5 mug/kg/min at body and muscle temperatures of 28, 31, 37 and 41 degrees C, respectively. The doses of neostigmine needed for 50% antagonism of the d-TC-induced depression of twitch height were 8.7, 9.2, 10.5 and 12.0 mug/kg at 28, 31, 37 and 41 degrees, respectively. The time to peak effect and duration of action of 5 and 10 mug/kg of neostigmine were longer at 28 and 31 degrees C than at 37 and 41 degrees C. Although these times also were longer at 27 and 31 degrees C with the 20 mug/kg dose of neostigmine, they were not statistically different. We conclude that hypothermia augments a d-TC neuromuscular blockade. Hypothermia prolongs time-to-peak effect and duration of neostigmine but does not affect peak magnitude of antagonism of d-TC by neostigmine.

Animals↗
PubMed1978

Neostigmine-induced alterations at the mammalian neuromuscular junction. II. Ultrastructure.

Brief and chronic exposure of rats to neostigmine methylsulfate produced marked morphological alterations of the fine structure at the end-plate region of the extensor digitorum longus muscles. These changes were dose and time dependent and were restricted primarily to the subjunctional myofibrillar apparatus and membrane-bound organelles. In addition, significant presynaptic alterations were observed including synaptic vesicle depletion and the appearance of numerous coated vesicles and membrane cisternae, which indicated continuing nerve terminal hyperactivity. With chronic treatment, degeneration and partial recovery of the nerve axon also were observed. The morphological changes of the end-plate region induced by neostigmine did not occur in most fibers after brief denervation and were eliminated entirely by chronic nerve section. Thus, the postsynaptic degenerative changes caused by neostigmine treatment observed in nondenervated animals appear to result primarily from greatly increased synaptic activity and not primarily from a direct neostigmine reaction with the pre- or postsynaptic membranes. Since the myopathic changes observed in this study were produced by neostigmine, a drug which is commonly employed in the routine treatment of human patients with myasthenia gravis, continued use of neostigmine for long-term therapy in noncrisis situations may not be accepted as being free from risk.

Animals↗
PubMed1975

Neostigmine methylsulfate. Does it have a chronic effect as well as a transient one?

Three groups of 200-gm rats were injected subcutaneously with neostigmine methylsulfate (1 mg/kg/day) for 7, 30, and 100 days. Electrophysiological changes were assessed in vitro, using microelectrode techniques to examine diaphragm muscles of treated and untreated animals. Miniature end-plate potential (MEPP) amplitude decreased in neostigmine-treated preparations. Guanidine hydrochloride enhances transmitter release and increases MEPP frequency in control preparations. Neostigmine-treated animals examined between 6 to 72 hours after discontinuation of neostigmine therapy showed impaired response to the facilitating influence of guanidine. Recovery of response to guanidine was inversely related to length of treatment with neostigmine. Results of electron-microscopic examination of motor end-plates in treated animals revealed ultrastructural changes, including simplified end-plates, and, occasionally, multiple, separate, junctional regions. Therefore, the chronic administration of cholinesterase inhibitors in man may have a deleterious effect, as well as a transient beneficial one.

Animals↗
PubMed1992

Role of brain histamine H1- and H2-receptors in neostigmine-induced hyperglycemia in rats.

We previously reported that when neostigmine, an inhibitor of acetylcholine esterase, was injected into the third cerebral ventricle, the concentration of hepatic venous plasma glucose was increased via central muscarinic receptors in anesthetized rats. To determine whether brain histamine receptors are involved in cholinergic system transmission with regard to central nervous system (CNS)-mediated glucoregulation, we examined the effects of the H1 receptor antagonist pyrilamine and the H2 receptor antagonist ranitidine on neostigmine-induced hyperglycemia in anesthetized rats. The injection of pyrilamine (5 x 10(-9)-5 x 10(-7) mol) into the third cerebral ventricle suppressed hyperglycemia induced by intraventricular injection of neostigmine (1 x 10(-9) mol) in a dose-dependent manner. Injection of ranitidine (5 x 10(-9)-5 x 10(-7) mol) into the third cerebral ventricle did not suppress the hyperglycemia induced by neostigmine, but enhanced it in a dose-dependent manner. These findings suggest that neostigmine-induced CNS-mediated hyperglycemia is transmitted by not only brain cholinergic muscarinic receptors but also in part by histamine H1 receptors.

Animals↗
PubMedDate not supplied

Effects of intranasal neostigmine on oesophageal motility in man.

The effects of intranasally administered neostigmine on oesophageal peristalsis and lower oesophageal sphincter tone were investigated in 21 healthy volunteers. After 30 min of basal recording of oesophageal tracings, neostigmine (3 or 5.4 mg) or the inert vehicle were given. The oesophageal recording was continued for 45-60 min after administration. Neostigmine increased the amplitude and duration of the peristaltic waves without significantly affecting conduction. Lower oesophageal sphincter tone was also increased but post-swallowing relaxation was normal. At the highest dose, the effects of neostigmine lasted 45 min or more. There were no side effects and the heart rate was only slightly slowed. The results suggest that intranasal administration of neostigmine might be clinically useful for stimulation of upper gastrointestinal tract peristalsis.

Administration, Intranasal↗
PubMed1975

The effect of acid-base balance on neostigmine antagonism of d-tubocurarine-induced neuromuscular blockade.

d-Tubocurarine (dTc) was infused intravenously into 35 cats anesthetized with chloralose and urethane at a constant continuous rate to produce and maintain 90 per cent depression of twitch height of the anterior tibial muscle following supramaximal stimulation of the peroneal nerve. The mean infusion rates that produced 90 per cent depression were not significantly altered by respiratory acid-base changes. Metabolic alkalosis decreased (32.5 per cent) and metabolic acidosis increased (27.7 per cent) the required infusion rate of dTc. When pH and Paco2 were maintained at 7.37 and 38 torr, respectively, the addition of a bolus of neostigmine, 10.5 mug/kg, intravenously, to the continuing infusion of dTc produced 50 per cent antagonism of the dTc-depressed twitch. Respiratory alkalosis and metabolic acidosis did not alter the dose of neostigmine needed to produce 50 per cent antagonism. However, during respiratory acidosis (pH 7.13, Paco2 66 torr) and metabolic alkalosis (pH 7.59, Paco2 36 torr) 20.0 and 18.0 mug/kg neostigmine, respectively, were needed to produce 50 per cent antagonism. Still larger doses of neostigmine (75 mug/kg) could not completely antagonize the block unless pH and Paco2 were returned to 7.30-7.50 and 35-45 torr, respectively. It is concluded that respiratory acidosis and metabolic alkalosis limit and oppose antagonism of dTc by neostigmine.

Acid-Base Equilibrium↗
PubMed1979

Pharmacokinetics and pharmacological effects of neostigmine in man.

1 The pharmacokinetics of neostigmine was studied in six patients during the reversal of neuromuscular block induced by tubocurarine chloride. The effect of the drug on neuromuscular function was simultaneously assessed by electromyography. 2 Neostigmine was rapidly eliminated from plasma after intravenous administration. The decline in the plasma concentration of the drug was invariably resolved into two exponential components. The fast disposition (distribution) half-life of the drug was invariably less than 1 min; the slow disposition (elimination) half-life ranged from 15.4--31.7 min. 3 Neostigmine usually increased the amplitude of the compound muscle action potential and diminished electromyographic decrement within 2 min of intravenous injection. The pharmacological effect of neostigmine was usually maximal between 7 and 15 min. There was an inverse relationship between the plasma concentration of the drug and the facilitation of neuromuscular transmission. 4 Red cell acetylcholinesterase activity was almost completely inhibited within 2--3 min of intravenous injection of neostigmine. Enzyme activity recovered to approximately 28% of control values by 30 min and to 55% by 60 min.

Acetylcholinesterase↗
PubMed1978

Plasma clearance of neostigmine and pyridostigmine in the dog.

1 The pharmacokinetics of neostigmine and pyridostigmine was studied in conscious dogs by the use of a cross-over design. 2 Both neostigmine and pyridostigmine were cleared from plasma in a biexponential manner. 3 The apparent volume of distribution of pyridostigmine was invariably greater than that of neostigmine, and its fast disposition half-life was approximately three times longer. 4 The whole body clearance and the urinary elimination of pyridostigmine was approximately twice that of neostigmine. 5 The slow disposition half-life of pyridostigmine was approximately three times longer than that of neostigmine, suggesting that the longer duration of action of pyridostigmine is related to the differential clearance of the two quarternary amines from plasma.

Animals↗
PubMedDate not supplied

The interaction between d-tubocurarine, pancuronium, polymyxin B, and neostigmine on neuromuscular function.

The interaction between pancuronium, d-tubocurarine, polymyxin B, and neostigmine was studied in the rat diaphragm-phrenic nerve preparation. Polymyxin B (5 mug/ml) did not affect twitch tension alone but decreased the pancuronium ED50 from 0.8 mug/ml to 0.32 mug/ml and the d-tubocurarine ED50 from 0.25 mug/ml to 0.15 mug/ml. Neostigmine (0.2 to 10 mug/ml) antagonized pancuronium or d-tubocurarine-induced depression of twitch tension. In contrast, neostigmine (0.001 to 0.2 mug/ml) augmented polymyxin B depression. Similarly, neostigmine (0.1 mug/ml) augmented combined polymyxin B-pancuronium or polymyxin B-d-tubocurarine depression of twitch tension. The authors conclude that polymyxin B potentiates the neuromuscular blockade from pancuronium or d-tubocurarine and that neostigmine further augments this block.

Animals↗
PubMedDate not supplied

[Effect of x-irradiation, nicotinic acid and neostigmine methylsulfate on the interrelation between methylation and biosynthesis of tRNA].

Experiments on rats established that tRNA of the liver under the effect of total X-irradiation (800 R), nicotinic acid and neostigmine methylsulphate proves to be hypermethylated. In this case tRNA molecules undergo conformation changes. Nicotinic acid and neostigmine methylsulphate administered to the animals under experiment an hour before irradiation favour the normalization of these indexes. As a rule, a correlation is observed between changes in methylation of tRNA and activity of their methylases. Irradiation inhibits the processes of tRNA synthesis which are normalized under the effect of nicotinic acid administered before the irradiation. Nicotinic acid and neostigmine methylsulphate produce no effect on synthesis of tRNA in the liver of normal animals. The activity of acid tRNase under the effect of nicotinic acid is not changed, under other conditions of the experiment it decreases. Irradiation against a background of nicotinic acid and neostigmine methylsulphate administered to animals and neostigmine methylsulphate administration to the intact animals inhibit the activity of alkaline tRNase.

Animals↗
PubMed1975

[Effects of postoperative decurarization with neostigmine on digestive anastomoses].

A prospective study was undertaken to assess the influence of neostigmine, a reversal agent for curarimimetic myorelaxants, on the incidence of postoperative disruption of anastomotic sites. Over a period of one year, 400 patients had surgery, including anastomosis, on the digestive tract for a variety of surgical conditions (Table II). At the end of anaesthesia, 200 patients received doses of atropine and neostigmine, usually 1 mg and 2.5 mg of each, as indicated on clinical basis and neuromuscular stimulation. The other patients did not recieve these drugs and were ventilated till the myorelaxation vanished spontaneously. During the postoperative period of incidence of anastomotic breakdown was assessed by the surgeon, unaware of the use or the omission of neostigmine in his patients. Anastomotic leakage was classified in four groups, namely: proved, absent, likely and unlikely. In this series and according to these clinical criteria, both groups had an incidence of anastomotic breakdown which was not significantly different (Table III). Neostigmine as used in this work does not seem to compromise the normal healing of anastomotic sites on the digestive tract.

Adolescent↗
PubMed1992

Antagonism by beta-eudesmol of neostigmine-induced neuromuscular failure in mouse diaphragms.

beta-Eudesmol, a sesquiterpenol extracted from a Chinese herb, Atractylodes lancea, at 10-80 microM, did not affect muscle action potentials, miniature and evoked endplate potentials and acetylcholine-induced depolarization in the presence or absence of neostigmine in mouse phrenic nerve-diaphragms. However, the tetanic fade, muscle fasciculation and twitch potentiation induced by neostigmine were effectively antagonized by 20 microM beta-eudesmol. When trains of pulses were applied to the nerve in the presence of neostigmine, beta-eudesmol reduced the incidence of explosive depolarization of the endplate from 95% to 35-67% of junctions, and shortened the duration when it occurred. Moreover, both the maximal and steady-state depolarizations during repetitive stimulation were reduced while the amplitudes of steady-state endplate potentials were increased. The results suggest that beta-eudesmol antagonized neostigmine-induced neuromuscular failure mainly by a presynaptic action to depress the regenerative release of acetylcholine during repetitive stimulation. The mechanism of antagonism is obviously not tubocurarine-like and it is unrelated to desensitization of acetylcholine channels.

Acetylcholine↗