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PubMed1995

Effect of neostigmine at different levels of mivacurium-induced neuromuscular blockade.

The effectiveness of neostigmine 40 micrograms/kg for antagonism of two different levels of neuromuscular blockade, induced by a bolus dose of mivacurium 0.15 mg/kg, was studied in 45 patients. The patients were anaesthetized with thiopentone, fentanyl, nitrous oxide in oxygen, and enflurane. Neostigmine was administered at either 10% recovery of the twitch height (TH10) at the adductor pollicis muscle (n = 14) or upon reappearance of the first response at the orbicularis oculi muscle (OO1) after train-of-four (TOF) stimulation (n = 16), the latter representing a deeper degree of neuromuscular blockade. Fifteen of the 45 patients did not receive neostigmine (control group). Neostigmine administration at OO1 rather than at TH10 at the adductor pollicis muscle caused reversal of neuromuscular blockade to occur 8 min earlier and shortened the time to reach 25% recovery of the twitch height (TH25) at the adductor pollicis muscle by about 5 min, compared with the control group. However, the time needed to reach a T4/T1 ratio > or = 0.8 was similar in both the early and late neostigmine administration groups, being 9 min faster than in the control group. It can be concluded that there is no advantage in administering neostigmine at profound neuromuscular blockade to achieve clinically adequate recovery (T4/T1 ratio > or = 0.8). However, the time between injection of mivacurium and TH25 may be shortened by using neostigmine at profound neuromuscular blockade, a procedure which may be useful in case of unpredictably difficult intubation, since diaphragmatic movements usually reappear at TH25.

Adolescent↗
PubMed2006

Neostigmine-induced postprandial phasic contractility in the proximal stomach and dyspepsia-like symptoms in healthy volunteers.

BACKGROUND AND AIMS: In a subset of functional dyspepsia patients, we have recently described the association between unsuppressed postprandial phasic contractions of the proximal stomach and a specific symptom pattern. To better elucidate the role of phasic contractility of the proximal stomach in symptom generation, we aimed at inducing this motility pattern in healthy volunteers and we carefully monitored symptom onset. PATIENTS AND METHODS: Eleven healthy volunteers underwent gastric barostat on two separate days. Gastric tone and phasic contractility were evaluated for a 90-minute period. In particular, after 30 min of basal recording, a caloric liquid meal and neostigmine 0.5 mg IV or saline in a double-blind, randomized, crossover protocol were administered. During the measurement, severity of 9 dyspeptic symptoms was evaluated on a visual analog scale. Computer-aided baseline reconstruction allowed us to quantify phasic contractions as a motility index (MI), reflecting the area between signal and baseline normalized over time. Perception of contractions after placebo or neostigmine was evaluated. Moreover, we tested for influence of gastric tone and phasic contractility on symptoms. RESULTS: After neostigmine, gastric accommodation was not different than after placebo (225 +/- 36 vs 206 +/- 76 mL, P= NS). During the first 30-min postprandial period, the MI was significantly higher after neostigmine than after placebo (26.4 +/- 3 vs 21.4 +/- 3, P < 0.001), confirming the induction of unsuppressed postprandial phasic contractions. The postprandial total symptom score was significantly higher after neostigmine compared to saline; several individual postprandial symptom scores were also significantly higher after neostigmine-compared placebo. After neostigmine, a higher percentage of postprandial contractions was perceived compared to placebo. CONCLUSIONS: Unsuppressed postprandial phasic contractility of the proximal stomach is a mechanism potentially involved in the pathogenesis of dyspeptic symptoms.

Adult↗
PubMed1992

Mechanism of intrahippocampal neostigmine-induced hyperglycemia in fed rats.

We previously reported that the injection of neostigmine, an acetylcholine esterase inhibitor, into the dorsal hippocampus produced hepatic venous plasma hyperglycemia associated with an increase of epinephrine and glucagon in anesthetized fed rats. To evaluate the relative contribution of these glucoregulatory hormones and the nervous system to the net hyperglycemic response, we unilaterally injected neostigmine (5 x 10(-8) mol) into the dorsal hippocampus in the following groups of rats: intact rats with bilateral adrenalectomy to eliminate the action of epinephrine, and rats receiving a constant infusion of somatostatin and insulin to prevent the glucagon response and to maintain the basal insulin level. Hepatic venous plasma levels of glucose, immunoreactive glucagon, immunoreactive insulin, epinephrine, and norepinephrine were determined. The area under the glucose curve during the 120-min period following the injection of neostigmine was compared between groups. The areas under the glucose curve for rats receiving somatostatin and insulin, adrenalectomy rats, and adrenalectomy rats receiving somatostatin and insulin were, respectively, 82, 31, and 61% of that for intact rats. The fashion of hippocampal stimulated hyperglycemia with neostigmine was similar to that after injection of neostigmine into the third cerebral ventricle. Therefore, we investigated hyperglycemia in rats with lesions of ventromedial hypothalamus and found that the response to hippocampal neostigmine was significantly inhibited by the hypothalamic lesion. These findings suggest that the glucoregulatory hippocampal activity evoked by neostigmine may be transmitted to peripheral organs via the ventromedial hypothalamus.

Animals↗
PubMed2003

Interactions of edrophonium with neostigmine in the rat trachea.

UNLABELLED: The muscarinic M(3) receptor of airway smooth muscle has both an orthosteric binding site and an allosteric binding site. Edrophonium may bind to the allosteric site, resulting in the inhibition of the action of the orthosteric site. Therefore, we examined the effects of edrophonium on neostigmine-induced contractile and phosphatidylinositol responses of rat trachea. Neostigmine (100 micro M in final concentration) was added, and ring tension was examined by the addition of edrophonium. After the completion of the experiment, Krebs-Henseleit (K-H) solution containing both edrophonium and neostigmine was changed three times with fresh K-H solution, and the tension was recorded. Tracheal slices were incubated with [(3)H]myo-inositol and 100 micro M neostigmine in the presence or absence of edrophonium. The [(3)H]inositol monophosphate (IP(1)) was measured. Data were expressed as mean +/- SE. Statistical significance (P < 0.05) was determined with analysis of variance. Neostigmine-induced tension and IP(1) accumulation were attenuated by edrophonium at concentrations of 100 micro M or more. This attenuation was reversed to more than 80% of control levels by washing with fresh K-H solution. The results suggest that edrophonium would bind to the allosteric site, resulting in the inhibition of the action of the orthosteric site of muscarinic M(3) receptors of rat trachea. IMPLICATIONS: We examined the effects of edrophonium on neostigmine-induced contractile and phosphatidylinositol responses of rat trachea. Neostigmine-induced tension and inositol monophosphate accumulation were attenuated by edrophonium. This attenuation was reversed by washing. The results suggest that edrophonium would bind to the allosteric site.

Animals↗
PubMed2005

Does neostigmine administration produce a clinically important increase in postoperative nausea and vomiting?

Neostigmine is used to antagonize neuromuscular blocker-induced residual neuromuscular paralysis. Despite the findings of a previous meta-analysis, the effect of neostigmine on postoperative nausea and vomiting remains unresolved. We reevaluated the effect of neostigmine on postoperative nausea and vomiting while considering the different anticholinergics as potentially confounding factors. We performed a systematic literature search using MEDLINE, Embase, Cochrane library, reference listings, and hand searching with no language restriction through December 2004 and identified 10 clinical, randomized, controlled trials evaluating neostigmine's effect on postoperative nausea and vomiting. Data on nausea or vomiting from 933 patients were extracted for the early (0-6 h), delayed (6-24 h), and overall (0-24 h) postoperative periods and analyzed with RevMan 4.2 (Cochrane Collaboration, Oxford, UK) and multiple logistic regression analysis. The combination of neostigmine with either atropine or glycopyrrolate did not significantly increase the incidence of overall (0-24 h) vomiting (relative risk, 0.91; 95% confidence interval, 0.70-1.18; P = 0.48) or nausea (relative risk, 1.24; 95% confidence interval, 0.98-1.59; P = 0.08). Multiple logistic regression analysis indicated that there was not a significant increase in the risk of vomiting with large compared with small doses of neostigmine. Contrasting a previous analysis, we conclude that there is insufficient evidence to conclude that neostigmine increases the risk of postoperative nausea and vomiting.

Humans↗
PubMed2006

The efficacy of thoracic epidural neostigmine infusion after thoracotomy.

Few anesthesia studies have explored perioperative continuous epidural infusion of neostigmine. We examined such a regimen in thoracotomy patients. Ninety patients were randomized to one of three groups in this double-blind trial. Before anesthesia induction, an epidural catheter was inserted in all patients at T5-8 levels under local anesthesia. Pre-neo patients received bolus 500-microg epidural neostigmine before anesthesia induction followed by infusion of 125 microg/h until the end of surgery. Post-neo patients received epidural saline during the same time periods plus bolus 500-microg epidural neostigmine at end of surgery. Patients in the control group received saline placebo during all three periods. Patients in the neostigmine groups postoperatively received patient-controlled epidural analgesia with morphine 0.02 mg/mL, bupivacaine 0.08 mg/mL, and neostigmine 7 microg/mL. Control patient-controlled epidural analgesia excluded neostigmine. Data were recorded for 6 postoperative days. Daily patient-controlled epidural analgesia consumption (mL) for Pre-neo patients was significantly less than that of post-neo and control group patients for postoperative days 1-6 (at least 10% and 16% less, respectively; P < 0.05). There was a modest decrease in pain intensity on postoperative days 3-6 for pre-neo patients versus other groups (P < 0.05). These results suggest that continuous thoracic epidural neostigmine started before anesthesia provided preemptive, preventive analgesia and an analgesic-sparing effect that improved postoperative analgesia for these patients without increasing the incidence of adverse effects.

Adult↗
PubMed2001

Rise in plasma leptin levels after stimulation of hypothalamic cholinoceptive neurons by neostigmine in rats.

To investigate the role of hypothalamic cholinergic neurons in the regulation of plasma leptin levels, we injected neostigmine, a cholinesterase inhibitor, or vehicle alone into the third cerebral ventricle in free moving male Wistar rats and then measured plasma leptin levels. The administration of neostigmine (5 x 10(-9) or 5 x 10(-8) mol) increased plasma leptin levels 3-6 h after stimulation in a dose-dependent manner, while intravenous injection of neostigmine (5 x 10(-8) mol) had no effect. Atropine (5 x 10(-8) mol) concomitantly injected with neostigmine (5 x 10(-8) mol) prevented neostigmine-induced increase in plasma leptin. The expression of leptin messenger ribonucleic acid (mRNA) in epididymal white adipose tissue was significantly increased at 4 and 6 h after neostigmine injection compared with that before the injection. Plasma levels of corticosterone were significantly increased at 30 min after stimulation with neostigmine and this increase was sustained for 6 h after stimulation. Furthermore, bilateral adrenalectomized rats showed no increase in plasma leptin levels after stimulation. In conclusion, stimulation of hypothalamic cholinoceptive neurons increased plasma leptin levels in rats by increasing leptin production in adipocytes. This increase may be due to an increase in glucocorticoids from the adrenal glands. These results suggest that plasma leptin levels can be regulated by hypothalamic cholinoceptive neurons.

Adipocytes↗
PubMed1981

Reversal of neuromuscular blockade: dose determination studies with atropine and glycopyrrolate given before or in a mixture with neostigmine.

Glycopyrrolate and atropine were studied in doses of 5, 10, or 15 microgram/kg and 10, 20, or 30 microgram/kg, respectively, given intravenously either before or in a mixture with neostigmine, 50 microgram/kg, at the time of reversal of neuromuscular block. When given first, both anticholinergic drugs produced a dose-related increase in heart rate; following the administration of neostigmine the heart rates decreased. When administered in a mixture with neostigmine, the 20- and 30-microgram/kg doses, but not the 10-microgram/kg dose of atropine were associated with an initial increase in heart rate. This was, however, absent with all the doses of glycopyrrolate. The 5-microgram/kg dose of glycopyrrolate and 10-microgram/kg dose of atropine given either before or in a mixture with neostigmine were associated with unacceptable decreases in heart rate and needed further anticholinergic drug administration. The 10-microgram/kg dose of glycopyrrolate, when administered in a mixture with neostigmine, was associated with the most stable heart rates. Increasing the dose to 15 microgram/kg was not associated with undue tachycardia and is not hazardous. Atropine, 20 microgram/kg, necessitated a further administration of atropine in nearly a third of patients in this group due to bradycardia (heart rate of 50 beats/min or less) and would be considered inadequate. Increasing the dose to 30 microgram/kg prevented bradycardia but was accompanied by significant initial tachycardia and a higher incidence of dysrhythmias when administered before neostigmine. The frequency of dysrhythmias was otherwise similar. It is recommended that anticholinergic drugs be administered in a mixture with neostigmine. Glycopyrrolate, administered in this way in a dose of 10 microgram/kg, is associated with stable heart rates.

Atropine↗
PubMedDate not supplied

Subarachnoid neostigmine does not affect blood pressure or heart rate during bupivacaine spinal anesthesia.

BACKGROUND AND OBJECTIVES: Intraspinal administration of neostigmine has been shown to prevent induction of hypotension in rats by bupivacaine spinal block, and thus to provide greater hemodynamic stability. This study was undertaken to determine whether subarachnoid neostigmine would prevent bupivacaine spinal anesthesia from causing hypotension or bradycardia in patients undergoing abdominal hysterectomy. METHODS: Of 40 patients scheduled for abdominal hysterectomy under spinal anesthesia, 20 were randomly assigned to each of two groups. The control group (CG) received 1.5 mL subarachnoid saline followed by 15 mg (3 mL) of hyperbaric bupivacaine 0.5%. The neostigmine group (NG) received 75 micrograms (1.5 mL) of subarachnoid neostigmine followed by 15 mg (3 mL) of hyperbaric bupivacaine 0.5%. No preload was given. Hypotension was treated with 4-mg intravenous boluses of ephedrine to keep blood pressure above 75% of the baseline value. The skin body temperature was measured with probes at the suprascapular region and at the foot. RESULTS: Spinal neostigmine (75 micrograms) failed to prevent bupivacaine-induced hypotension. There was no statistical difference in the incidence of brady-cardia between the groups (NG, 2/20; CG 1/20), although the bradycardia appeared to be qualitatively different, being somewhat delayed in the NG. Spinal neostigmine did not alter the onset or duration of sensory block and did not affect skin body temperature in either anesthetized or unanesthetized sites. The incidence of intraoperative nausea was 20% in the NG and 5% in the CG. CONCLUSION: A 75-micrograms subarachnoid neostigmine dose does not affect blood pressure or heart rate during bupivacaine spinal anesthesia.

Adult↗
PubMed1997

Neostigmine requirements for reversal of neuromuscular blockade following an infusion of mivacurium.

PURPOSE: To study the efficacy of neostigmine compared with placebo for the antagonism of neuromuscular blockade at the end of a mivacurium infusion, and to determine its optimal dose. METHODS: One hundred adult patients undergoing an elective surgical procedure received a standardized anaesthetic with 20-30 micrograms.kg-1 alfentanil, a propofol infusion and nitrous oxide. Muscle relaxation was maintained at 90-95% T1 depression with 0.2 mg.kg-1 mivacurium followed by an infusion. Neuromuscular blockade was measured with an integrated evoked electromyogram in response to train-of-four (TOF) stimuli at the ulnar nerve every 20 sec. Patients were randomized into four groups. At the end of surgery, the mivacurium infusion was stopped and patients received, immediately, in a double-blind manner, neostigmine (10, 20, or 40 micrograms.kg-1) or placebo according to a random number table. The T1 and TOF ratio were recorded until adequate recovery of neuromuscular function (TOF ratio > 0.70). During the reversal period, non-invasive blood pressure and heart rate were recorded every minute. The incidence of postoperative nausea and vomiting (PONV) was recorded in the recovery room. RESULTS: Data from 94 patients who completed the protocol were analysed. Compared with placebo, neostigmine 10 micrograms.kg-1 did not reduce the time to TOF > 0.70 (17.0 +/- 5.1 vs 14.6 +/- 4.2 min respectively). However the time was decreased with neostigmine 20 micrograms.kg-1 and 40 micrograms.kg-1 (P < 0.001), but with no difference between these last two groups (11.4 +/- 3.0 and 11.4 +/- 3.5 min respectively). Changes in systolic blood pressure and heart rate were not different between the four groups. Very few PONV events were observed in all groups (global incidence 7.4%). CONCLUSION: Recovery of neuromuscular blockade following a mivacurium infusion is accelerated by neostigmine. A dose of neostigmine 20 micrograms.kg-1 appears optimal with no further reduction in recovery time obtained from a larger dose.

Adult↗
PubMed2004

Differential reversal of drug-induced small bowel paralysis by cerulein and neostigmine.

OBJECTIVE: Cerulein and neostigmine are prokinetic drugs whose potency and effective dose range are barely known. The aim of this study was to assess their benefit for normal and compromised peristalsis. DESIGN: In vitro, isolated segments of guinea pig small intestine. Setting : University laboratory. INTERVENTIONS: Small bowel segments were mounted in tissue baths and luminally perfused with Tyrode solution. Test drugs (prokinetic: cerulein, neostigmine; inhibitory: atropine, hexamethonium, epinephrine, sufentanil) were added to the tissue bath. MEASUREMENTS AND RESULTS: Peristalsis was quantified via changes in the peristaltic pressure threshold. One-way and two-way analysis of variance (ANOVA) were used for statistical analysis. Cerulein (0.03-100 nM) stimulated normal peristalsis in a concentration-dependent manner and reversed paralysis of peristalsis induced by all inhibitory test drugs to a similar extent. The properistaltic effect of neostigmine was limited to a narrow concentration range (0.03-0.1 micro M), whereas concentrations >0.3 micro M inhibited peristalsis. Neostigmine more effectively counteracted blockage of peristalsis caused by atropine than that caused by hexamethonium. The inhibitory effects of epinephrine and sufentanil on peristalsis were reversed only at the concentration range of 0.1-0.3 micro M neostigmine. CONCLUSIONS: Cerulein stimulates normal peristalsis in vitro at a wide concentration range and reverses blockage of peristalsis caused by drugs with a site of action either on the enteric nervous system or intestinal smooth muscle. Neostigmine's prokinetic effect, to the contrary, is limited to a small concentration range and best seen when peristalsis is depressed by blockage of cholinergic muscle activation.

Adjuvants, Anesthesia↗
PubMed1993

Effect of choline on basal and stimulated acetylcholine release: an in vivo microdialysis study using a low neostigmine concentration.

Using in vivo microdialysis, we examined the ability of choline (Ch) chloride (120 mg/kg i.p.) to amplify basal and stimulated acetylcholine (ACh) release from rat striatum in the presence of high (10(-5) M) and low (5 x 10(-8) M) neostigmine concentration. High concentrations might suppress ACh release, and thus Ch dependence, by excessively stimulating presynaptic cholinergic receptors; alternatively, they could enhance Ch dependence by depriving the cholinergic terminals of Ch that would otherwise be formed intrasynaptically from the hydrolysis of ACh. Both basal and stimulated ACh release were found to be tetrodotoxin (TTX) sensitive. The concentration of neostigmine in the microdialysis fluid positively affected basal ACh levels, but had no effect on Ch levels. Ch administration significantly increased ACh release (to 136% of basal values; P < 0.01) in the presence of the low neostigmine concentration, but failed to significantly increase ACh release following local electrical depolarization of striatal neurons. In contrast, Ch failed to affect basal ACh release in the presence of the high neostigmine concentration, but did increase electrically evoked release to 408% of basal values, as compared with 250% in rats receiving saline instead of the Ch (P < 0.05). Ch administration significantly increased microdialysate Ch levels in the presence of both of the neostigmine concentrations. Local administration of oxotremorine, a muscarinic agonist, to animals receiving the lower neostigmine concentration reduced basal ACh release and reduced the increase in basal release produced by Ch administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

Mechanisms of respiratory failure produced by neostigmine and diisopropyl fluorophosphate.

Acetylcholinesterase inhibitors produce diverse physiologic effects, but lethal exposure consistently produces respiratory failure due to neuromuscular paralysis or depression of respiratory control centers in the medulla. Simultaneous measurement of gastrocnemius muscle contraction and efferent phrenic nerve activity was used to determine the primary cause of respiratory failure produced by neostigmine and diisopropyl fluorophosphate (DFP) in anesthetized cats. Both neostigmine and DFP abolished phrenic nerve activity prior to producing neuromuscular blockade. Furthermore, neostigmine did not alter brain acetylcholinesterase activity and pretreatment with either atropine methylbromide or atropine increased the dose of neostigmine required to abolish phrenic nerve activity. In contrast, DFP abolished brain cholinesterase activity and only atropine inhibited its respiratory effects. Despite the loss of efferent phrenic nerve activity, there is no evidence of a direct effect of neostigmine on respiratory control centers. Neostigmine may instead alter afferent inputs which modulate respiration to produce a reflex respiratory failure.

Animals↗
PubMed1989

Use of low-dose neostigmine intravenously in the treatment of supraventricular tachycardia: an immediate bradycardic effect.

Neostigmine was first used 50 years ago to treat sinus tachycardia and paroxysmal auricular tachycardia. Then there were reports of successful treatment by neostigmine of other forms of supraventricular tachycardias. However, reports of sudden death using neostigmine for reversal of neuromuscular blockade at the end of an operation, which were not properly treated with atropine abandoned the use of neostigmine as an antiarrhythmic drug. Low-dose neostigmine intravenously was used in the treatment of supraventricular tachycardia in three patients described herein. It gave an immediate bradycardic effect in all three patients. The use of a low-dose neostigmine intravenously for an immediate treatment of supraventricular tachycardia is a novel suggestion. It has to be further evaluated and compared to the conventional drugs used like digoxin, verapamil, propranolol or esmolol.

Adolescent↗
PubMed2004

Postoperative analgesic effect of epidural neostigmine and plasma cortisol and IL-6 responses.

STUDY OBJECTIVES: To examine whether epidural administration of neostigmine reduces the stress and inflammatory responses thereby improving postoperative pain status. DESIGN: Randomized, double-blinded clinical study. SETTING: Operating rooms and wards of a university hospital. PATIENTS: 40 ASA physical status I patients undergoing lower open abdominal surgery for benign gynecological disease. INTERVENTIONS: Patients were randomly divided into four groups to receive different doses of epidural neostigmine (0, 0.05, 0.1, or 0.15 mg) with mepivacaine (100 mg) before general anesthesia induction. MEASUREMENTS: The plasma levels of cortisol and interleukin-6 (IL-6) were determined perioperatively. The patients' pain rating was assessed by visual analog scale (VAS) in the postoperative period. MAIN RESULTS: Epidural neostigmine at all doses significantly reduced the plasma levels of cortisol in the early surgical period; however, IL-6 levels were not affected by the neostigmine. The VAS scores were significantly decreased at 2 hours after the end of surgery by all doses of epidural neostigmine used in this study. CONCLUSIONS: The preincisional epidural neostigmine transiently suppresses the stress responses during surgery and improves postoperative analgesia in patients undergoing lower open abdominal surgery.

Adult↗
PubMed2005

Intrathecal neostigmine reduces the zymosan-induced inflammatory response in a mouse air pouch model via adrenomedullary activity: involvement of spinal muscarinic type 2 receptors.

Intrathecal (IT) injection of neostigmine (a cholinesterase inhibitor) has been reported to produce a significant anti-nociceptive effect in a number of inflammatory pain models. However, a potential anti-inflammatory effect of IT neostigmine in these models has not been investigated. In the present study, we have examined the 'anti-inflammatory effect of IT injection of neostigmine' (AI-NEO) using a standard mouse air pouch model by evaluating the effect of AI-NEO on zymosan-induced leukocyte migration and myeloperoxidase (MPO) release. IT neostigmine was found to suppress both leukocyte migration and MPO degranulation in a dose dependent manner. We then established which subtypes of cholinergic receptors were involved in this AI-NEO. IT pretreatment with atropine (a muscarinic receptor antagonist) but not hexamethonium (a nicotinic receptor antagonist) completely blocked the IT neostigmine anti-inflammatory effect. Subsequent experiments showed that IT pretreatment with methoctramine (a muscarinic type 2 (M2) receptor antagonist), but not pirenzepine (M1 receptor antagonist) or 4-DAMP (M3 receptor antagonist), suppressed the AI-NEO. We then evaluated whether adrenal glandular activity was important in the AI-NEO. Adrenalectomy significantly blocked the AI-NEO, while intraperitoneal pretreatment with the beta-adrenoceptor antagonist (propranolol), but not the corticosteroid antagonist (RU486) reversed AI-NEO. In conclusion, these results indicate that IT neostigmine facilitates the activation of spinal M2 receptors and this activation ultimately leads to release of adrenal catecholamines which contribute to the anti-inflammatory effect observed at the site of tissue inflammation.

Adrenal Cortex Hormones↗
PubMed2001

The elevation of plasma adrenocorticotrophic hormone and expression of c-Fos in hypothalamic paraventricular nucleus by microinjection of neostigmine into the hippocampus in rats: comparison with acute stress responses.

We have reported that the microinjection of neostigmine into the hippocampus of rats induced responses similar to stress responses in terms of catecholamines and glucose in plasma. In order to test the hypothesis that hippocampal neostigmine injection is a possible animal model of acute stress responses, we investigated c-Fos expression in the hypothalamic paraventricular nucleus (PVN) and plasma levels of adrenocorticotrophic hormone (ACTH) after hippocampal neostigmine injection and compared these levels with those resulting from stressful conditions such as immobilization and insulin-induced hypoglycemia. The patterns of expression of Fos-ir in the PVN after microinjection of neostigmine into the hippocampus were not different from those seen in the two stressful situations. After microinjection of neostigmine, plasma ACTH levels significantly increased. Taken together, the results of this study indicate that microinjection of neostigmine into the hippocampus is a potential experimental model for acute stress responses.

Adrenocorticotropic Hormone↗
PubMed2000

Efficacy of intrathecal neostigmine for the relief of postinguinal hemiorrhaphy pain.

BACKGROUND: Intrathecal administration of various doses of neostigmine has been reported to produce analgesia without neurotoxicity in both animal and human studies. The present study was undertaken to evaluate the efficacy and safety of intrathecal neostigmine for the relief of pain for patients having undergone inguinal herniorrhaphy surgery. METHODS: Sixty men scheduled for elective inguinal herniorrhaphy with spinal anaesthesia were randomly allocated to three groups: group I (n=20) received intrathecal (IT) tetracaine 15 mg, group II (n=20) received IT tetracaine 15 mg+ neostigmine 50 microg, and group III (n=20) received IT tetracaine 15 mg+neostigmine 100 microg. The onset of anaesthesia, duration of analgesia, time to use of first rescue analgesics, the overall 24 h VAS pain scores and the incidence of adverse effects were recorded for 24 h postdrug administration. RESULTS: Onset of anaesthesia (time to T6 sensory block) was significantly faster for group II and III patients compared with group I patients. Motor block (time to lift leg) was greatly prolonged for group III patients, with an average of 6.4 h, compared with 4.1 h for group II patients. Group III patients also showed a later onset of postsurgical pain, lower overall 24-h VAS pain score and prolonged time to first rescue analgesics than did group II patients. There was a significantly greater incidence of adverse effects associated with IT neostigmine, especially nausea and vomiting. CONCLUSION: Our study showed that intrathecal neostigmine at 50 pg or 100 microg enhanced the onset of tetracaine anaesthesia and provided analgesia lasting for 6-9 h, although increased incidences of prolonged motor blockade and nausea or vomiting were noted.

Adult↗