[Propofol-induced myocardial depression: possible role of atrial muscarinic cholinergic receptors]. / Depresión de la función mioc irdica inducida por propofol: posible participación del receptor colinérgico muscarínico auricular.

OBJECTIVE: To investigate the possible role of muscarinic cholinergic receptors (MCRs) in the depression of myocardial function induced by propofol, an intravenous anesthetic chemically unrelated to other drugs. Although adverse effects are rare, bradycardia has been reported and this can lead to cardiac arrest in some patients. The mechanism behind this effect is still unknown but a possible role for MCRs has been suggested. MATERIAL AND METHODS: The interaction of propofol with human atrial MCRs was determined by means of inhibition tests using [3H] quinuclidinyl benzilate ([3H] QNB). RESULTS: The displacement of [3H] QNB binding to human atrial MCRs by propofol was concentration dependent but the observed effect was not consistent with a model of simple competition between propofol and [3H] QNB. CONCLUSION: Propofol appears to have the ability to modify the activity of human atrial MCRs and this effect may be related to its ability to induce bradycardia.

Depresión de la función miocárdica inducida por propofol: posible participación del receptor colinérgico muscarínico auricular / Propofol-induced myocardial depression: possible role of atrial muscarinic cholinergic receptors

OBJETIVO: Investigar la posible participación de la transmisión muscarínica en la depresión miocárdicainducida por propofol, anestésico intravenoso no relacionadoquímicamente con otras drogas. A pesar de que los efectos adversos son raros, se ha reportado la aparición de bradicardia, que puede llevar incluso a paro cardíaco en algunos pacientes. En la actualidad se desconoce elmecanismo de este efecto, pero se ha sugerido la posible participación de los receptores colinérgicos muscarínicos(RCMs).MATERIAL Y MÉTODOS: La interacción del propofol con RCMs de aurícula humana se determinó por ensayos deinhibición usando benzilato de [3H]-quinuclidinilo ([3H]- QNB).RESULTADOS: El propofol desplazó la unión de [3H]- QNB de los RCMs de aurícula humana, de maneradependiente de la concentración; no obstante, el efecto observado no fue consistente con un modelo de simplecompetición entre propofol y [3H]-QNB.CONCLUSIÓN: El propofol parece tener la capacidad de modificar la actividad de los RCMs de aurícula humana,siendo éste un efecto que podría estar relacionado con su capacidad de inducir bradicardia (AU)

OBJECTIVE: To investigate the possible role of muscarinic cholinergic receptors (MCRs) in the depression ofmyocardial function induced by propofol, an intravenous anesthetic chemically unrelated to other drugs. Althoughadverse effects are rare, bradycardia has been reported and this can lead to cardiac arrest in some patients. Themechanism behind this effect is still unknown but a possible role for MCRs has been suggested.MATERIAL AND METHODS: The interaction of propofol with human atrial MCRs was determined by means ofinhibition tests using [3H] quinuclidinyl benzilate ([3H] QNB).RESULTS: The displacement of [3H] QNB binding to human atrial MCRs by propofol was concentrationdependent but the observed effect was not consistent with a model of simple competition between propofol and [3H]QNB.CONCLUSION: Propofol appears to have the ability to modify the activity of human atrial MCRs and this effectmay be related to its ability to induce bradycardia (AU)

An unusual presentation of opioid-like syndrome in pediatric valproic acid poisoning.

We report a 3-y-o boy who accidentally poisoned himself with valproic acid (VPA). Clinical features included profound coma, depressed respiration and miosis. Treatment included naloxone, gastric lavage, and activated charcoal and a saline cathartic. The patient fully recovered and was discharged 24 h after the admission. Prompt use of naloxone is advised whenever the triad of coma, pinpoint pupils and depressed respiration concur with the clinical possibility of VPA intoxication.

Partial characterization of endogenous modulators of muscarinic acetylcholine receptors in human frontal cortex.

A soluble fraction from human frontal cortex with molecular weight less than 10 kD was tested for the presence of endogenous substances capable of modulating the [3H]-QNB binding to crude P1 + P2 fractions from the same region. The soluble fraction was able to decrease [3H]-QNB binding in a dose-response manner with an IC50 of about 30 micrograms/ml. The effect appeared to be noncompetitive in nature, since Bmax but not Kd was significantly affected; however, in some specimens a biphasic profile, with an initial inhibition of 88-90% of [3H]-QNB binding and 50-60% ulterior binding recuperation was also found. The modulator appeared to have a molecular weight less than 10,000 Daltons and was heat and trypsin resistant. These results point out the existence of an endogenous factor, which could be heterogeneous in regard to its molecular nature or to its action sites.