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H2 receptor antagonists are often used to reduce gastric acidity prior to general or regional anaesthesias. However cimetidine and ranitidine have been found to increase plasma levels of local anaesthetics such as lidocaine. This study aimed to compare famotidine--another H2 receptor antagonist--with cimetidine in this respect. 33 male patients 70 years old or more, scheduled for surgery under spinal anaesthesia and randomized into 3 groups, received either diazepam 0.15 mg.kg-1 and famotidine 20 mg (group A) or diazepam and cimetidine 200 mg (group B) or diazepam only (group C) on the previous night and 90 minutes before spinal anaesthesia by hyperbaric lidocaine 5%, 3 ml. Arterial blood samples were taken 3 minutes after spinal injection then every 15 minutes unto 90 minutes after the first sampling. Lidocaine plasma levels were measured by fluorescence polarization immunoassay and the results were statistically analyzed. In famotidine group lidocaine levels were intermediate between B and C groups levels, and the increase was of lesser duration than in B group. Elimination mechanism of lidocaine with and without H2 inhibitor is briefly discussed. Therefore famotidine would appear to be more convenient than other H2 receptor inhibitors whenever antacid protective effects are sought after prior to regional anaesthesia.

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As fast-acting, water-soluble compounds, like midazolam (MID) are increasingly used in anesthetic practice, the need for quick and effective reversal of benzodiazepine actions in accidental overdoses is obvious. Quite a few drugs have been used in both animal models and clinically towards this aim, including: physostigmine (PHYS), naloxone (NAL), aminophylline, doxapram, in the past and, more recently, flumazenil (FLU) or Ro-15-1788. In the present study we assessed the relative potency, safety and efficacy of the antagonistic actions of PHYS (0.06 and 0.6 mg/kg), NAL (2 mg/kg) and FLU (2.5 mg/kg) on the state of sleep induced by MID (2.5 mg/kg) in 50 male, drug-naive rats. Time of induction of anesthesia and duration of sleep were measured with digital chronometer. Level of consciousness was determined by pain reactivity, spontaneous motor activity and computer-aided analysis of cumulative EEG patterns. Times obtained were integrated as mean values and statistical analysis was made using the t-test (Student's criterion). Rats were given MID followed 30 min later by an i.p. injection of either vehicle (VEH = water for injection = control group) or low-dose PHYS or high-dose PHYS or NAL or FLU (n = 10 in each group). We measured the duration of anesthesia following the injection of each antagonist. The following results were obtained: [table: see text] Thus, the relative potency scale of MID antagonism in this series of experiments is: FLU = High-dose PHYS greater than low-dose PHYS much greater than NAL VEH. Although FLU has a strong duration and rapid awakening action, this action is of short duration and the animals are resedated after 33.3 +/- 7.14 min. PHYS does not appear to show this resedation effect, while in high doses is equipotent to FLU. Nevertheless, in these excessive doses, the animals become restless and excited, showing phenomena of an acute, severe nicotinic crisis. In conclusion, FLU appears to have much more specific and reliable effects upon reversing MID-induced anesthesia in comparison to either PHYS or NAL. In fact, PHYS must reach toxic levels to counteract MID effects, while FLU is very safe. The existence of the resedation effect is due to the short t1/2 of FLU and can be overcome by continuous i.v. infusions or repeated bolus injections.

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Various agents used in the practice of anesthesia were applied in fifty five healthy postmenopausal female volunteers in order to investigate their hypothalamo hypophyseal response to these drugs, by measuring PRL and TSH levels in peripheral blood. Selection of volunteers, separation of blood specimens and RIA techniques were performed according to international standards. Our results show that thiopental, ketamine and dehydrobenzperidine increase PRL levels significantly (p less than 0.05-0.0025) while fentanyl and diazepam do not alter basal PRL values (p greater than 0.10). It is assumed that thiopental and ketamine may affect the hypothalamo hypophyseal axis through a cholinergic mechanism, whereas dehydrobenzperidine through a dopaminergic one. Atropine reduces the increase in PRL levels caused by thiopental and ketamine, while it does not affect PRL high levels induced by dehydrobenzperidine. TSH levels remain unaffected by all drugs, though ketamine shows a statistically indicative mild tendency to increase PRL levels (p less than 0.10). The fact that TSH values remain the same may be due either to the slower release of TSH stores, or to the involvement of a somatostatin-related mechanism in addition to the one described herein.

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The surface potential changes produced by three alcohols on the phosphatidylcholine (PC) monolayer, either alone or in combination with piracetam were studied. The PC monolayer was formedon 145 mM KCL in a teflon trough and the surface change was measured by means of a Kiethley electrometer, with the high impedence output connected to an Americium 241 air electrode and the low impedence output to a calomel reference electrode. The alcohols produced a negative going change in the surface charge of the monolayer, proportional to the chain length of carbon atoms and amount of alcohol added. 10 microliter (2 mg) of piracetam applied to the PC monolayer before adding the alcohols partially inhibited the changes produced by them. It seems that in vitro piracetam opposes the action of alcohols on this membrane model.

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The effect of enflurane and methoxyflurane on the permeability of liposomes to H+ was rested. Liposomes were prepared with phospholipids alone or as mixtures of cholesterol and phospholipids having the ratios of 1:2 or 1:1. Both anaesthetic drugs facilitated the release of H+ from pure phospholipid liposomes and from those with a 1:2 ratio. The facilitated release of H+ was prevented by the presence of high concentrations of cholesterol. As the cholesterol:phospholipid ratio in synaptic vesicles is of the order 1:2, it is expected that their permeability might be affected by volatile anaesthetics, leading to a modification of synaptic transmission.

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The effect of SNP on arterial blood gases was studied in a series of 25 patients undergoing neurosurgical operations. The PaO2 was slightly decreased after SNP infusion. The PaCO2 and the pH remained unchanged. Though this decrease in PaCO2 was not statistically significant the possible mechanisms and the clinical importance of this effect are discussed.

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The intranasal administration of nitroglycerine (NTG) was undertaken in 35 adult female patients 1 min before the induction of anaesthesia. A control group consisting of 32 patients did not receive NTG. Systolic arterial pressure (SAP) and heart rate (HR) were recorded before the induction of anaesthesia and at 0, 3, and 5 min after tracheal intubation. SAP did not increase significantly in the NTG group immediately after intubation, while significant decreases in SAP were observed at 3 and 5 min (P less than 0.005 and P less than 0.001 respectively). SAP did increase significantly in the control group. HR was increased in both groups immediately after intubation (P less than 0.001 and P less than 0.001 respectively). NTG administered intranasally is a safe, simple and effective method to attenuate the hypertensive response to laryngoscopy and tracheal intubation.

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Ten postmenopausal women were divided into two groups. In five patients (group 1) four venous blood samples were collected at 5-minute intervals before and after thiopental sodium, 6 mg/kg IV, for determination of serum levels of prolactin and thyroid-stimulating hormone. In the other five patients (group 2) the procedure followed was as in group 1, but thiopental administration was preceded by atropine, 0.1 mg/10 kg. Prolactin levels increased significantly after thiopental injection in group 1, but not in group 2. Thyroid-stimulating hormone levels in both groups remained virtually unaltered. The fact that atropine prevented the increase of prolactin due to thiopental suggests that thiopental may have an indirect effect on the hypothalamohypophyseal axis through a cholinergic mechanism.

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Enflurane dissolved in oil was injected subcutaneously in 20 Wistar rats under various conditions of environmental and body temperature. Five Wistar rats (control group) received only the solvent. Liver damage and decrease of glycogen storage was observed in the group of animals where endogenous temperature was increased deliberately, while in livers of animals where environmental temperature was increased, only slight changes were observed.

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Fifty one patients undergoing fiberoptic bronchoscopy were premedicated with atropine and anesthetised with thiopental, nitrous oxide and succinylcholine as a muscle relaxant. Twenty-six patients consisted the control group while twenty-five were given alcohol orally for three consecutive days before the procedure. The treatment group had no cardiac arrhythmias during bronchoscopy while six of the control subjects developed arrhythmias. Heart rate and mean arterial pressure were maintained significantly lower in the treatment group, thus the hypertensive response to tracheal intubation and bronchoscopy was significantly attenuated by atenolol.

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Serum cortisol levels were determined in 44 patients who underwent hysterectomy under enflurane or under halothane anesthesia by means of a radioimmunoassay technique. Of the 44 patients, in 21 anesthesia was maintained by enflurane and d-tubocurarine and 23 patients maintenance of anesthesia was carried out by halothane and d-tubocurarine. Blood samples for serum cortisol estimations were obtained from each patient before induction of anesthesia, 10 min. after induction, 10 min. after skin incision, at the end of the operation and in the ward on the fourth postoperative day. Cortisol levels increased in both groups at the end of the operation with a significantly higher mean value in the enflurane group (p less than 0.05) compared to that of the halothane group.

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Serum cholinesterase levels were determined in 180 patients with carcinoma and in 146 normal subjects. Serum cholinesterase activity was significantly lower in patients suffering from cancer than in normal controls, though still within the normal range. The degree of depression of serum cholinesterase activity was influenced by the extent to which the malignancy had spread and by the site of the primary lesion.

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Asymptomatic myasthenia gravis firstly manifested as total paralysis in patients submitted to a surgical procedure should be considered extremely rare. Two cases of latent myasthenia gravis manifested after thoracotomy for removal of mediastinal tumor are reported. Prolonged apnoea and need for postoperative mechanical support of respiration was most likely due to non-depolarizing relaxants administration. In both cases edrophonium test was positive and the histology of the tumor showed thymoma. The further recovery after pyridostigmine treatment was uneventful for both patients.

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Serum cholinesterase activity was determined in 30 female patients anaesthetized with enflurane for excision of lump in the breast. In all 30 patients biopsy of the tumor was negative for carcinoma. Blood samples were taken before induction of anaesthesia, at the end of the operation and 24 hours after the operation. Enzymatic determinations were performed by the Boerhinger cholinesterase kit. Enzyme levels were found sufficiently high at the end of the operation and returned to the preoperative levels 24 hours post-operatively.

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