Sedative/Hypnotics
Frank A. Barile in Barile’s Clinical Toxicology, 2019
Although it has no analgesic effect, and more effective and less toxic S/H drugs are available, chloral hydrate is still used therapeutically, primarily as a hypnotic.† Currently available in oral liquid dosage forms only, the compound is lipid soluble and is a metabolite of chloral betaine and triclofos (see structure in Figure 13.3). The long-acting metabolite of chloral hydrate, trichloroethanol, is responsible for most of its toxicity, low therapeutic index, and undetectable presence in plasma. Signs and symptoms of toxicity include CNS depression, ataxia, gastrointestinal irritation, cardiovascular instability, and proteinuria. In addition, chloral hydrate significantly impairs myocardial contractility by sensitizing the myocardium to catecholamines. An increased risk of sudden death with chloral hydrate intoxication is a result of the development of arrhythmias. Emergency guidelines and assessment of vital signs include pear-like breath odor, hypotension, and dysrhythmias. Gastrointestinal irritation and bleeding are also a common occurrence. Structure of chloral hydrate.
The Treatment of the Special Forms of Mental Disease
Francis X. Dercum in Rest, Suggestion, 2019
Chloral is a poison depressant to the heart and vasomotor apparatus. Dyspnea, vertigo, and general sense of weakness are among the symptoms likely to be present. In well-established cases there are marked nervousness, marked insomnia, and a certain degree of mental weakness, as manifested by loss of will-power and failure of memory. In some cases an emotional depression is present which may simulate melancholia. The patient is weak, his movements are tremulous, and he frequently complains of palpitation of the heart. These symptoms must be combated by food, by rest and by other physiologic measures, and by tonics, such as digitalis, strophanthus, and strychnin. When the habit has been long continued and the doses large, the patient occasionally suffers from attacks of delirium closely resembling delirium tremens. Chloral, it should be added, has been so largely displaced by other hypnotics that chloralism is at present a very infrequent condition.
Barbiturates, Alcohol, And Tranquilizers
S.J. Mulé, Henry Brill in Chemical and Biological Aspects of Drug Dependence, 2019
Mental manifestations of chronic chloral intoxication may include apathy, depression, drowsiness, impaired memory and judgment, apprehension, restlessness, euphoria, hallucinations, impaired libido, and, commonly, paranoia. Physical symptoms of chronic chloralism include some which appear to be characteristic of the drug, such as suffusion of the conjunctivae, lacrimation, scaling of the eyelids and scalp, cutaneous vasodilatation, the tell-tale odor of the drug on the breath, and arthralgia and myalgia which may mimic arthritis. Other somatic symptoms are similar to those observed in chronic alcoholism. Loss of weight, hypovitaminosis, ataxia, incoordination, slurred speech, gastric irritation, skin eruptions, and grand mal seizures occur. A number of parenchymatous pathologies have been attributed to chloral hydrate including fatty degeneration of the heart, congestion of lungs and liver, and renal damage.
Ethanol extract of Schisandrae chinensis fructus ameliorates the extent of experimentally induced atherosclerosis in rats by increasing antioxidant capacity and improving endothelial dysfunction
Published in Pharmaceutical Biology, 2018
Xiu Chen, Jiahong Cao, Yong Sun, Yaolan Dai, Jiali Zhu, Xuemei Zhang, Xiaoqin Zhao, Liwen Wang, Tingting Zhao, Yongbiao Li, Youping Liu, Guihua Wei, Tiane Zhang, Zhiyong Yan
Schisandrin (HPLC >98%), schisandrin A (HPLC >98%), schisandrin B (HPLC >98%) were purchased from Chengdu Pusi Biotechnology Company (Chengdu, China). Chloral hydrate was obtained from Chengdu Kelong Chemical Reagent Factory (Chengdu, China). Triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), glutathione peroxidase (GSH-PX), catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), oxidized low-density lipoprotein (ox-LDL), endothelin-1 (ET-1), thromboxane B2 (TXB2) and 6-keto prostaglandin F1α (6-keto-PGF1α) assay reagent kits were purchased from Nanjing Jiancheng Biological Engineering Company (Nanjing, China). Primary antibody (anti-HO-1, No. ab85309, diluted 1:30) was obtained from Abcam trading company (Shanghai, China). Primary antibody (anti-Nrf-2, No. bs-1074, diluted 1:100) was obtained from Beijing Boaosen Biotechnology Company (Beijing, China). The secondary antibody (No. SP-9001), diaminobenzidine (DAB) reagent kits were purchased from Beijing Zhongshan Jinqiao Biological Company (Beijing, China).
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.
LIM kinase inhibitor T56-LIMKi protects mouse brain from photothrombotic stroke
Published in Brain Injury, 2021
Svetlana V. Demyanenko, Anatoly Uzdensky
After the longitudinal incision of the skull skin, the periostelium was removed. The Rose Bengal solution in PBS (15 mg/mL) was administrated intraperitoneally to a final level of 10 μg/g. Five minutes later, the sensorimotor cortex of the mice (2 mm lateral to the bregma) was irradiated by a diode laser (532 nm, 0.2 W/cm2, Ø 1 mm, 15 min) like in the previous work (31). Two mice groups, in which solvents PBS or carboxymethyl cellulose (CMC) were administrated without inhibitors, served as controls (Table 1). The animals were euthanized with a chloral hydrate overdose (600 mg/kg, i.p.) and decapitated 3, 7, or 14 days after PTS. These time intervals were of interest because brain reparation started to be visible at 72 h after PTS (32). Scar formation was observed on days 7 and 14 (33). The PTS-induced infarct volume significantly decreased (p < .05) within the recovery period, at 7–14 days after photothrombotic stroke in the mouse brain (33).
Related Knowledge Centers
- Acetaldehyde
- ADDuct
- Chloral Hydrate
- Ddt
- Organic Compound
- Sulfuric Acid
- Aldehyde
- Hypnotic
- Sedative
- Antimony Trichloride