Electroencephalographic study of naloxone effects in the recovery of an acute alcoholic intoxication

Experimental assays analysing EEG changes during the recovery of an acute alcoholic intoxication were carried out in three groups of cats: 1) Recovery of acute alcoholic intoxication produced by continuous intravenous perfusion of ethanol, 0.06 g/kg/min, during 20 minutes. 2) Recovery of acute alcoholic intoxication by injecting naloxone (400 micrograms/kg), just after finishing alcohol perfusion. 3) Recovery of acute alcoholic intoxication by injecting naloxone (400 micrograms/kg), 15 min after finishing perfusion. Naloxone administered after an acute alcoholic intoxication worsens the recovery of EEG parameters; 1-2 (p less than 0.05), 1-3 (p less than 0.05).     

Acute alcoholic intoxication and naloxone. Effects on visual evoked potential.

Experimental assays analyzing visual evoked potential (VEP) changes during an acute alcoholic intoxication were carried out in two groups of cats: One with continuous ethanol (0.06 g/kg.min) i.v. perfusion. Another one with a naloxone (400 micrograms/kg) i.v. injection 10 min before ethylic perfusion. Naloxone potentiates alcohol effects on VEP parameters, and on the appearance of isoelectric postpotential and flat VEP.     

Effect of chronic intoxication and naloxone on the ethanol-induced increase in plasma corticosterone

Ethanol (0.5–4.0 g/kg) induced an immediate, dose-dependent rise in plasma corticosterone in the conscious, undisturbed male rat. Chronic intoxication for at least two days resulted in tolerance to this effect. Chronic intoxication also significantly elevated the morning trough levels of this steroid. Co-administration of naloxone (1 mg/kg) prevented the development of tolerance to the immediate stimulatory effect of ethanol but did not alter the elevated trough levels of corticosterone. Naloxene (1 mg/kg) did not alter the stimulatory effect of ethanol on corticosterone in ethanol-naive animals. These data suggest that the process of tolerance development to the ethanol-induced rise in corticosterone is mediated by an opiate receptor. Alterations in the ability of ethanol to stimulate corticosterone secretion may be a useful endpoint for future studies of tolerance development to ethanol.     

Effect of acute postexercise ethanol intoxication on the neuroendocrine response to resistance exercise.

This investigation was conducted to determine the effect of postexercise ethanol intoxication (21.97 +/- 1.09 mmol/l blood) on the response of selected aspects of the neuroendocrine system to a resistance exercise (Ex) session. Nine resistance-trained men (25.0 +/- 1.4 yr, 179.4 +/- 3.4 cm, 79.7 +/- 3.3 kg) were used to compare three 3-day treatments: control, Ex, and ethanol after exercise (ExEt). Blood was collected serially from an antecubital vein before exercise, immediately after exercise, and for pooled analysis at 20-40 (2 samples), 60-120 (4 samples), and 140-300 (9 samples) min after exercise on day 1 and in the morning (2 samples each) on days 2 and 3. Ethanol did not increase circulating epinephrine, norepinephrine, or cortisol concentration (Cort) above Ex elevations. At 60-120 min, only ExEt Cort was greater than control Cort. Concentrations of testosterone, luteinizing hormone, and corticotropin were not affected by either treatment. It is concluded that, although this blood ethanol concentration is insufficient to acutely increase Cort above that caused by Ex alone, it appears that ethanol may have a prolonged effect beyond the Ex response. This blood ethanol concentration does not further stimulate the sympathoadrenal system during the postexercise response.     

Intravenous naloxone in acute respiratory failure.

A 58-year-old man presented with acute on chronic respiratory failure. In the acute stage of his illness an infusion of the opiate antagonist naloxone caused an improvement in oxygen saturation as measured by ear oximetry from 74% to 85%, while a saline infusion resulted in a return of oxygen saturation to the original value. When he had recovered from the acute episode the same dose of naloxone had no effect on oxygen saturation. These findings suggest that in acute respiratory failure there may be overproduction of, or increased sensitivity to, endorphins.     

Effect of naloxone on antinociceptive activity of phenoxybenzamine.

Phenoxybenzamine was found to have antinociceptive activity in the mouse writhing syndrome test. The percent protection against writhing was dose related from 2.0 to 164.6 μM/kg phenoxybenzamine (ED-50, 37.1 ± 2.0 μM/kg). The dose-response curve for phenoxybenzamine was shifted to the left when morphine was administered. Administration of morphine, 1.12 μM/kg, reduced the ED-50 for phenoxybenzamine to 4.5 ± 1.3 μM/kg. Administration of naloxone shifted the dose response curve for phenoxybenzamine to the right. Naloxone 0.03 μM/kg increased the ED-50 for phenoxybenzamine to 102.5 ± 22.7 μM/kg. Chronic treatment with phenoxybenzamine did not change the antinociceptive response to phenoxybenzamine. The α-adrenergic blockers, phenotolamine and tolazoline showed weak antinociceptive activity which was not blocked by naloxone.     

Effect of naloxone on coughing

Naloxone at doses of 200 micrograms X kg-1 increases cough, in experiments carried out on dogs. With stimuli of the same intensity, after naloxone, a significant increase in the number of coughs in each fit, is observed. Changes in the first cough burst, compared with spontaneous respiration at rest, are statistically significant and they contribute to define the characteristics of the cough burst. The increase of cough by naloxone blockade of endorphinic neurons of the respiratory center shows that usually the activity of these inhibitory neurons, tonically depresses the tussive response. The antitussive opiates would seem to operate by activating these inhibitory synapses.     

Lung function in acute paraquat intoxication.

Functional and morphological examination of the lungs was performed in rats 48 hours after intratracheal injection of 0.5 mg/kg of the herbicide paraquat. Pronounced tachypnoea was observed (235+/-20 c/min), which also persisted under urethane anaesthesia (210+/-18 c/min). In control rats the mean breathing rate was 115+/-11 and 90+/-9 c/min in wake and anaesthetized rats respectively. The rate of breathing decreased to comparable values in experimental and control rats after bilateral cervical vagotomy. The functional residual lung capacity was significantly increased in experimental rats. After vagotomy also this increase of functional residual capacity became normalized. Histologically the disease was characterized by focal formation of hyaline membranes and oedema with occasional haemorrhages and signs of inflammation. The significant role fo vagal function in lung pathology is demonstrated.     

Effect of acute sodium nitrite intoxication on some essential biometals in mouse spleen

Background and aimSodium nitrite (NaNO₂) is an inorganic salt with numerous applications in a variety of industries, as well as in medicine. Nevertheless, exposure to high levels of NaNO₂ is toxic for animals and humans. Sodium nitrite intoxication is shown to decrease the activity of major antioxidant defence enzymes which is dependent on the maintenance of specific ion equilibrium. The aim of the present study was to investigate the effect of acute NaNO₂ intoxication on the content of the essential metals iron (Fe), calcium (Ca) and zinc (Zn) in mouse spleen.MethodsMature male ICR mice were divided into four groups and subjected to acute NaNO₂ exposure by a single intraperitoneal injection of 120 mg/kg body weight. Animals in each group were sacrificed at certain time interval after treatment (1 h, 5 h, 1 day and 2 days). Spleens were excised and processed for atomic absorption spectrometry analysis of Fe, Ca and Zn content.ResultsAt the first hour after treatment, a decrease in Fe and Ca levels was observed. One day following NaNO₂ administration, Zn concentration reached its lowest value and Ca levels remained lower, compared to the untreated controls. In contrast, Fe concentration increased on the first and second day after treatment.ConclusionThe results of the present study demonstrate that acute NaNO₂ intoxication provokes changes in the endogenous levels of Fe, Ca and Zn in mouse spleen. These findings suggest disruption of the ionic balance and impact on the activity of antioxidant defence enzymes.     

Effect of acute ethanolic intoxication on the neuraminidase activity of rat liver golgi apparatus

Neuraminidase and galactosyltransferase were investigated in total Golgi apparatus and in the three fractions of increasing densities (GF₁, GF₂ and GF₂) isolated from the microsomal fraction of rat liver homogenates by flotation in a discontinuous sucrose density gradient (Ehrenreich, J.H., Bergeron, J.J.M., Siekevitz, P. and Palade, G.E. (1973) J. Cell Biol. 59, 45–72). About 50% decreases in neuraminidase content (units/g liver) and specifixc activity (units/ mg protein) were observed in total Golgi as well as in the three fractions isolated at 45 min, 90 min, 180 min and 16 h after administration of a single oral dose of 50% aqueous ethanol (0.6 g/100 g body weight). Colchicine administration (intraperitoneal injection, 0.5 mg/100 g body weight) caused a similar loss of neuraminidase activity; however, the effect of ethanol plus colchicine was not additive. Golgi galactosyltransferase, on the other hand, experienced marked increases of activity following ethanol administration but, unlike the results reported by others (Gang, H., Lieber, C.S. and Rubin, E. (1973) Nat. New Biol. 243, 123–125), significant increases in total activity and specific activity were already quite evident at 90 min after ethanol ingestion. In contrast with the decreased values observed in Golgi, the total particle-bound neuraminidase was significantly elevated following ethanol administration. Ultrastructural studies revealed increased lysosomal content and detachment of polysomes from the rough endoplasmic reticulum. A model, which takes into account these enzymological and ultrastructural findings and their biological significance, is proposed.