ABSTRACT
Resumen: Durante la sedación en procedimientos endoscópicos del tubo digestivo alto y bajo, es frecuente que se susciten complicaciones ventilatorias y hemodinámicas. Se presenta una revisión de las estrategias para prevenir y tratar las complicaciones ventilatorias más frecuentes: espasmo laríngeo, apnea por fármacos anestésicos endovenosos y broncoespasmo. También se revisan las complicaciones hemodinámicas: reflejo vagal e hipotensión aguda. Se propone un algoritmo de manejo que sintetiza y esquematiza las medidas profilácticas y terapéuticas descritas en la literatura, ordenándolas de acuerdo a su prioridad y eficacia, permitiendo identificar con claridad el nivel de tratamiento necesario y la viabilidad del procedimiento endoscópico.
Abstract: During sedation in endoscopic procedures of the lower and upper digestive tract, it is common for ventilatory and hemodynamic complications to arise. This article presents a review of the strategies to treat and prevent the most common ventilatory complications: laryngeal spasm, apnea due to intravenous anesthetic drugs and bronchospasm. Hemodynamic complications are also reviewed: vagal reflex and acute hypotension. A management algorithm is proposed which synthesizes and schematizes the prophylactic and therapeutic measures described in the bibliography, ordering them by their priority and effectiveness, allowing to clearly identify the degree of treatment necessary and the viability of the endoscopic procedure.
ABSTRACT
BACKGROUND AND OBJECTIVES: Acute hypotension induces expression of c-Fos protein and phosphorylated extracellular signal-regulated kinase (pERK), and glutamate release in the vestibular nuclei. Expression of c-Fos protein and pERK is mediated by the excitatory neurotransmitter, glutamate. In this study, the signaling pathway of glutamate in the vestibular nuclei following acute hypotension was investigated. MATERIALS AND METHODS: Expression of metabotropic glutamate receptors (mGluRs) was measured by Western blotting in the medial vestibular nucleus following acute hypotension in rats. RESULTS: Expression of pGluR1 Ser831, a subtype of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, peaked at 30 minutes after acute hypotension insult, and expression of pNR2B, a subtype of N-methyl-D-aspartate (NMDA) receptors, peaked at 2 hours after acute hypotension insult. Acute hypotension induced expression of Homer1a and group I mGluR in the medial vestibular nucleus. Expression of mGluR1 and mGluR5 peaked at 6 hours following acute hypotension insults. CONCLUSION: These results suggest that afferent signals from the peripheral vestibular receptors, resulting from acute hypotension insult, are transmitted through group I mGluRs as well as AMPA and NMDA receptors in the vestibular system.
Subject(s)
Animals , Rats , alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid , Blotting, Western , Glutamic Acid , Hypotension , N-Methylaspartate , Neurotransmitter Agents , Phosphotransferases , Receptors, Metabotropic Glutamate , Receptors, N-Methyl-D-Aspartate , Vestibular NucleiABSTRACT
Acute hypotension induced excitation of electrical activities and expression of c-Fos protein and pERK in the vestibular nuclei. In this study, to investigate the excitatory signaling pathway in the vestibular nuclei following acute hypotension, expression of NR2A and NR2B subunits of glutamate NMDA receptor and GluR1 subunit of glutamate AMPA receptor was determined by RT-PCR and Western blotting in the medial vestibular nucleus 30 min after acute hypotension in rats. Acute hypotension increased expression of NR2A, NR2B, and pGluR1 in the medial vestibular nuclei. These results suggest that both of NMDA and AMPA glutamate receptors take part in transmission of excitatory afferent signals following acute hypotension.
Subject(s)
Animals , Rats , alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid , Blotting, Western , Glutamic Acid , Hypotension , N-Methylaspartate , Receptors, AMPA , Receptors, Glutamate , Vestibular NucleiABSTRACT
The role of peripheral vestibular receptors in acute hypotension was investigated in anesthetized rats. Acute hypotension was induced by either intravenous infusion of sodium nitroprusside (SNP) or by experimental hemorrhage, and electrical activity and expression of cFos-like immunoreactive (cFL) protein were measured in the medial vestibular nuclei (MVN). Blood pressure decreased proportionately to the does of intravenous SNP and to the volume of the hemorrhage. Blood pressure decreased 10, 30, 50% for the 5, 10, 15ng/kg SNP injection, respectively, and also decreased 30 and 50% after 1- and 2-ml blood loss, respectively, due to hemorrhage. In animals with intact labyrinths, acute hypotension induced by either intravenous infusion of SNP or hemorrhage produced different electrical activities with three different patterns in type I and II neurons of MVN. The responses of type I neurons showed excitatory in 2/3 of recorded neurons and inhibitory or no change in 1/3 of neurons, while the responses of type II neurons showed inhibitory in 2/3 of recorded neurons and excitatory or no change in 1/3 of neurons. In unilateral labyrinthectomized animals, 2/3 of type I neurons ipsilateral to the lesion showed an inhibitory response, and 2/3 of contralateral type I neurons showed an excitatory response after the induction of acute hypotension. The response patterns of type II neurons were opposite from those of the type I neurons. After 30% decrease in blood pressure, cFL protein expressed in the bilateral vestibular nuclei of control animals with intact labyrinths. Expression of cFL protein increased significantly proportionately to the reduction of blood pressure. The unilateral labyrinthectomized animals with acute hypotension produced expression of cFL neurons in contralateral vestibular nuclei to the lesion side, but not in ipsilateral vestibular nuclei. However, cFL protein was not expressed in bilateral vestibular nuclei after acute hypotension in bilateral labyrinthectomized animals. These results suggest that the peripheral vestibular receptors might play a significant role in controlling blood pressure following acute hypotension via activation of type I neurons and inhibition of type II neurons in the vestibular nuclei.