Placental Transmission of Nitrous Oxide
TL;DR: The data demonstrate rapid transmission of nitrous oxide across the human placenta as well as rapid uptake by the fetus.
Abstract: Placental transmission of nitrous oxide Was studied in 14 patients during elective cesarean section and in 26 patients during vaginal delivery. Duration of ancsthesia varied between 2, and 19 minutes. Randomly-selected patients were hyperor hyporcntilated. Umbilical vein nitrous oxide levels ranged
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TL;DR: BIS technology is moving out of the operating room and into diverse environments where conscious and deep sedation are provided, and anesthesiologists need to be actively involved in promoting patient safety and helping transition this technology into broader use.
283 citations
TL;DR: Nitrous oxide is not a potent labor analgesic, but it is safe for parturient women, their newborns, and health care workers in attendance during its administration and appears to provide adequately effective analgesia for many women.
246 citations
TL;DR: Although stress- induced glucose levels showed no circadiel rhythm, the stress-induced elevation of glucose above baseline showed a significant daily rhythm, indicating that stress elevated plasma glucose levels only during the scotophase in all three seasons.
245 citations
TL;DR: It is found that N2O inhibits both NMDA and non-NMDA receptor-mediated responses to exogenous agonist, and the effects of N2o on synaptic transmission are confined to postsynaptic targets.
Abstract: Nitrous oxide (N2O; laughing gas) has been a widely used anesthetic/analgesic since the 19th century, although its cellular mechanism of action is not understood. Here we characterize the effects of N2O on excitatory and inhibitory synaptic transmission in microcultures of rat hippocampal neurons, a preparation in which anesthetic effects on monosynaptic communication can be examined in a setting free of polysynaptic network variables. Eighty percent N2O occludes peak NMDA receptor-mediated (NMDAR) excitatory autaptic currents (EACs) with no effect on the NMDAR EAC decay time course. N2O also mildly depresses AMPA receptor-mediated (AMPAR) EACs. We find that N2O inhibits both NMDA and non-NMDA receptor-mediated responses to exogenous agonist. The postsynaptic blockade of NMDA receptors exhibits slight apparent voltage dependence, whereas the blockade of AMPA receptors is not voltage dependent. Although the degree of ketamine and Mg2+ blockade of NMDA-induced responses is dependent on permeant ion concentration, the degree of N2O blockade is not. We also observe a slight and variable prolongation of GABAA receptor-mediated (GABAR) postsynaptic currents likely caused by previously reported effects of N2O on GABAA receptors. Despite the effects of N2O on both NMDA and non-NMDA ionotropic receptors, glial glutamate transporter currents and metabotropic glutamate receptor-mediated synaptic depression are not affected. Paired-pulse depression, the frequency of spontaneous miniature excitatory synaptic currents, and high-voltage–activated calcium currents are not affected by N2O. Our results suggest that the effects of N2O on synaptic transmission are confined to postsynaptic targets.
213 citations