The Psychopharmacological Revolution
Petteri Pietikainen in Madness, 2015
Opium-based drugs were welcomed as painkillers in general medicine, and henbane extracts were useful in dampening manic and nervous excitation. Asylums were also in need of drugs that would put the patients to sleep. One of the first sleeping aids was chloral hydrate, synthesized in 1832 and used as a sedative and hypnotic from 1869 onwards. Chloral hydrate is soluble in both water and alcohol, and it became known as ‘knockout drops’ when it was mixed with alcohol – it was put into a drink surreptitiously to render the drinker temporarily unconscious so that the victim could then be robbed. As a drug, chloral hydrate was anything but safe, because it could cause rashes, gastric discomfort and severe renal, cardiac and hepatic failure. Overdosage could be fatal. Another widely used sleeping aid or ‘hypnotic’ was paraldehyde, a bitter-tasting liquid of penetrating odour (Jones 1983, 42–3). Memories of the unpleasant odour of paraldehyde haunted many patients and nurses until the mid-twentieth century, and these olfactory memories were certainly very unlike the French novelist Marcel Proust’s evocative memory of a lovely madeleine biscuit that he had tasted as a child.
Barbiturates, Alcohol, And Tranquilizers
S.J. Mulé, Henry Brill in Chemical and Biological Aspects of Drug Dependence, 2019
Abrupt withdrawal from chloral hydrate results, within a few hours, in agitation, restlessness, and disorientation. After 48 to 72 hours the symptoms of acute chloral delirium appear. Auditory and visual hallucinations occur, as well as delusions and illusions. Fear and acute paranoid reactions appear to be common. In addition, feelings of unreality, impaired insight, euphoria, agitation, impaired memory, and dream states may be seen. Suicide may be attempted because of depression, paranoia, or confusion. The symptoms of chloral withdrawal are largely mental (although any of the physical manifestations may occur during acute abstinence) and the state is often referred to as “chloral delirium”. The duration of the withdrawal syndrome varies from one to three weeks. No cases of death attributable to chloral hydrate withdrawal appear to have been reported.
Procedural and Perioperative Pain Management for Children
Mark V. Boswell, B. Eliot Cole in Weiner's Pain Management, 2005
Chloral hydrate’s hepatotoxic metabolites and structural similarity to several known carcinogens have prompted considerable concern. Toxicologic studies suggest increased incidence of malignancy, particularly hepatocellular carcinoma, in rodents following chronic chloral hydrate administration (Salmon, Kizer, Zeise, Jackson, & Smith, 1995; U.S. Department of Health and Human Services National Toxicology Program, 2002), but such an association has never been observed in humans despite many decades of widespread use. Disadvantages of chloral hydrate include pungent preparations, slow onset of action, prolonged recovery, lack of reversal agent, and significant rates of agitation and inadequate sedation. Risk of respiratory and hemodynamic depression with higher doses warrants continuous cardiorespiratory monitoring. Nevertheless, due to relative ease of administration and overall safety, chloral hydrate remains a popular sedative for nonpainful procedures in children such as CT scanning and magnetic resonance imaging (MRI) (Keeter, Benator, Weinberg, & Hartenberg, 1990). Because chloral hydrate lacks analgesic properties, appropriate analgesia should be provided for painful procedures.
Control strategy for intraspinal microstimulation based on central pattern generator
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Xiongjie Lou, Yan Wu, Song Lu, Xiaoyan Shen
The purpose of this experiment was to obtain the angle sequence of the right hindlimb knee joint of SCI rats under the stimulation of positive and negative PA sequences. Five Sprague Dawley rats of both sexes, weighing approximately 250 g, were used as experimental subjects and numbered 1–5. Chloral hydrate (10%) was intraperitoneally injected into the rats. After anaesthesia administration and preoperative skin preparation, the skin surface of the rats was disinfected with 75% alcohol, and the epidermis was cut off. The segment lamina of the T12 − T13 vertebrae was removed to expose the spinal cord, and the T9 segment of the spinal cord was hammered at a height of 6.25 mm using a 10 g hammer with a diameter of 2.5 mm. The ankle, knee, and hip joints of the rats' right hindlimbs were marked.
Open hepatic artery flow with portal vein clamping protects against bile duct injury compared to pringles maneuver
Published in Scandinavian Journal of Gastroenterology, 2023
Siliang Zhang, Pingli Cao, Pinduan Bi, Fu Yang, Ming Wu, Ding Luo, Bin Yang
Rats were fasted overnight before operation and had free access to water. Anesthesia was carried out the intraperitoneal injection of 10% chloral hydrate at a dose of 3 mL/kg. All operational steps were taken with microsurgery instruments (Shanghai Medical Instruments, Shanghai, China). In all groups, after a midline laparotomy, the ligaments around the liver were divided, the hepatic portal triad was removed, and collateral vessels to the hepatic hilum were disconnected. The HA and PV were meticulously freed individually. In the sham group, no further steps were performed except for the closing abdomen. In the CPM group, the hepatic portal triad was occluded for 45 min with two microvascular clamps. In the IPM group, the hepatic portal triad was clamped for 15 min and then reperfused for 5 min, for a total of 3 cycles. In the CHAFO group, after being meticulously with microsurgical instruments, the PV was clamped with a microvascular clamp and the HA were kept open for 45 min. In the IHAFO group, the portal vein were clamped for 45 min, while the hepatic artery was clamped for 5 min and re-open for 15 min, and these steps were alternate for 45 min. After completing the steps relevant to at the HA and PV in CPM, IPM, CHAFO and IHAFO groups, the liver perfusion was restored and the abdomen was closed.
Activation of the Nrf2-ARE signal pathway after blast induced traumatic brain injury in mice
Published in International Journal of Neuroscience, 2019
Yuan Zhou, Mi Tian, Han-Dong Wang, Chao-Chao Gao, Lin Zhu, Yi-Xing Lin, Jiang Fang, Ke Ding
The bTBI model referred to a modified blast shock tube model that has been described in our previous article [15]. First, 1% chloral hydrate was given by intraperitoneal (i.p.) injection into mice at a dose of 5 ml/kg for anesthesia. Then, the mice were moved to an animal holder with shielding of the head, neck and torso. Next, the holder was placed into the driven tube of the blast model. The driver chamber pressure was increased with compressed air, eventually leading to rupture of the polytetrafluoroethylene (JVS; Shenzhen, China) film, and a shock wave that rushed the mice. Atmospheric temperature, pressure and humidity were consistent during each test. Pressures and durations of all procedures were recorded by the software.
Related Knowledge Centers
- Chloral
- Clinical Trial
- Insomnia
- Reagent
- Hypnotic
- Geminal Diol
- Chemical Formula
- Sedative
- Medication
- Indication