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Relevant bibliographies by topics / Pentothal sodium

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Academic literature on the topic 'Pentothal sodium'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Pentothal sodium"

1

Orkaby, Asher, and Sukumar P. Desai. "The Death of Sodium Pentothal: The Rise and Fall of an Anesthetic Turned Lethal." Journal of the History of Medicine and Allied Sciences 76, no. 3 (July 1, 2021): 294–318. http://dx.doi.org/10.1093/jhmas/jrab016.

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Abstract For nearly a century, sodium pentothal was the undisputed king of anesthetics. Anesthesiologists were not, however, the sole consumers of pentothal, as psychiatrists used it to treat acute anxiety during psychoanalysis. The associated drug-induced inhibitions were attractive not only to psychotherapists, but also to a new generation of policing and Cold War espionage searching for the elusive truth serum. Cameo appearances of pentothal in media, film, and popular culture propagated the anesthetic’s negative public image. While legal challenges to the admissibility of pentothal-induced confessions and congressional investigations of clandestine truth serum programs may have tainted the popular anesthetic, it was pentothal’s widespread adaptation as part of the lethal injection cocktail that finally killed the king of anesthetics as pharmaceutical companies around the world refused to manufacture what had been transformed into a largely unprofitable drug, associated with capital punishment.

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2

Pernak, J., and W. Erdmann. "Thiopentone (pentothal-sodium) in the treatment of chronic pain." Pain 41 (January 1990): S289. http://dx.doi.org/10.1016/0304-3959(90)92693-k.

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3

Dabholkar, P. "Use of ECT in Hysterical Catatonia." British Journal of Psychiatry 153, no. 2 (August 1988): 246–47. http://dx.doi.org/10.1192/bjp.153.2.246.

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Catatonia is now accepted as a non-specific syndrome. Hysteria can very rarely be a cause. A case of hysterical catatonia developing twice in a year, and on both occasions responding to ECT, is presented. Initial diagnostic difficulties, and use of the sodium pentothal interview as a diagnostic test, are also described.

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4

Popovic, Robert, Richard Liniger, and Philip E. Bickler. "Anesthetics and Mild Hypothermia Similarly Prevent Hippocampal Neuron Death in an In Vitro Model of Cerebral Ischemia." Anesthesiology 92, no. 5 (May 1, 2000): 1343–49. http://dx.doi.org/10.1097/00000542-200005000-00024.

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Background General anesthetics reduce neuron loss following focal cerebral ischemia in rodents. The relative efficacy of this action among different anesthetics clinically used for neuroprotection is uncertain. In addition, it remains unclear how anesthetics compare to neuroprotection afforded by mild hypothermia. This study was performed to evaluate the comparative effects of isoflurane, sodium pentothal, and mild hypothermia in a hippocampal slice model of cerebral ischemia and to determine if the mechanism of neuroprotection of isoflurane involves inhibition of glutamate excitotoxicity. Methods Survival and morphology of CA1, CA3, and dentate gyrus neurons in rat hippocampal slices were examined after 10 or 20 min of combined oxygen-glucose deprivation (in vitro ischemia) followed by a 5-h recovery period. Results 10 or 20 min in vitro ischemia at 37 degrees C killed 35-40% of neurons in CA1 (P < 0.001), 6% in CA3 (not significant) and 18% in dentate (P < 0.05). Isoflurane (0.7 and 2.0%, approximately 0.45 and 1.5 minimum alveolar concentration), pentothal (50 microm, approximately 1 minimum alveolar concentration equivalent) and mild hypothermia (34 degrees C) all reduced CA1 cell loss and morphologic damage to similar degrees in 10- and 20-min periods of ischemia (P < 0.001). The noncompetitive N-methyl-D-aspartate antagonist MK-801 prevented cell damage, showing that N-methyl-D-aspartate receptor activation is an important mechanism of injury in this model. Glutamate (1 mm) produced cell loss similar to in vitro ischemia. Isoflurane (2%) prevented cell damage from glutamate exposure. Conclusions In hippocampal slices, neuron death from simulated ischemia was predominately due to activation of glutamate receptors. Isoflurane, sodium pentothal, an N-methyl-D-aspartate receptor antagonist, and mild hypothermia prevented cell death to similar degrees. For isoflurane, the mechanism appears to involve attenuation of glutamate excitotoxicity.

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Simon, Eric P., and Lynn F. Dahl. "The Sodium Pentothal Hypnosis Interview with Follow-up Treatment for Complex Regional Pain Syndrome." Journal of Pain and Symptom Management 18, no. 2 (August 1999): 132–36. http://dx.doi.org/10.1016/s0885-3924(99)00047-0.

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Russo, Michael B., Franklin R. Brooks, Jason P. Fontenot, Bruce M. Dopier, Edward T. Neely, and Alan W. Halliday. "Sodium Pentothal Hypnosis: A Procedure for Evaluating Medical Patients with Suspected Psychiatric Co-Morbidity." Military Medicine 162, no. 3 (March 1, 1997): 215–18. http://dx.doi.org/10.1093/milmed/162.3.215.

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7

Thomas, Dale, and Sydney Aidinis. "Objective Documentation of Musculoskeletal Pain Syndrome by Pressure Algometry during Thiopentone Sodium (Pentothal) Anesthesia." Clinical Journal of Pain 5, no. 4 (December 1989): 343–50. http://dx.doi.org/10.1097/00002508-198912000-00012.

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8

Aggarwal, Naresh. "Pro: Propofol Is a Better Induction Agent than Etomidate." Journal of Cardiac Critical Care TSS 05, no. 01 (January 2021): 070–71. http://dx.doi.org/10.1055/s-0041-1726173.

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AbstractInduction refers to the start of anesthesia when the patient is rendered unconscious. The intravenous induction agents allow the patient to experience a pleasant loss of consciousness while also rapidly achieving surgical levels of anesthesia. An ideal induction agent must have a rapid onset and offset of action, and must be easy to administer and without significant side effects. Currently, the commonest used agents include sodium pentothal, propofol, ketamine, and etomidate. Unfortunately, none of these agents possess the characteristics of an ideal induction agent. In this article, we will discuss the merits of propofol as an ideal induction agent for cardiac surgery and how it scores over etomidate for the same purpose.

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9

INTRONA, R. P. S., J. K. PRUETT, D. C. MARTIN, D. JOSEPHSON, and M. MANABE. "Effects of Sodium Pentothal and Sufentanil on Serotonin Induced Constriction of Canine Coronary Artery Rings Without Endothelium." Survey of Anesthesiology 36, no. 4 (June 1992): 134. http://dx.doi.org/10.1097/00132586-199206000-00009.

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Introna, R. P. S., J. K. Pruett, D. C. Martin, D. Josephson, and M. Manabe. "Effects of Sodium Pentothal and Sufentanil on Serotonin Induced Constriction of Canine Coronary Artery Rings Without Endothelium." Survey of Anesthesiology 36, no. 3 (June 1992): 134–35. http://dx.doi.org/10.1097/00132586-199236030-00009.

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Book chapters on the topic "Pentothal sodium"

1

Gilsanz, F. J., R. Garcia de Sola, J. I. Lora-Tamayo, P. Mateos, and C. Hernandez. "Effects of Etomidate, Sodium Pentothal and Lidocaine on Cerebral Elastance." In Intracranial Pressure VI, 736–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70971-5_140.

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