Disease relevance of Surital

• This study investigated the effects of thiamylal on the activities of KATP channels in isolated rat ventricular myocytes during simulated ischemia [1].
• The tonic movements were associated with respiratory alkalosis and were not abolished by an i.v. injection of thiamylal 75 mg [2].
• A barbiturate (thiamylal) was administered at a rate of 3 mg . kg-1 . hr-1 for 2-5 days to four patients who had suffered cardiac arrest, four with acute focal ischemia, two with postoperative brain edema after neurosurgery, and one with brain damage due to asphyxia [3].
• Using a replicated Latin square design, all dogs were given placebo (saline solution) and 0.025, 0.05, 0.1, and 0.2 mg of midazolam/kg of body weight prior to IV administration of thiamylal sodium [4].
• Increases in arterial blood pressure may predispose to arrhythmia formation during thiamylal anesthesia [5].

Psychiatry related information on Surital

• The "second" component of the P2 wave appeared during excitement or following strong stimulation and disappeared after thiamylal administration and during natural slow-wave sleep [6].
• Electroconvulsive therapy with thiamylal or propofol during pregnancy [7].

High impact information on Surital

• For high-performance liquid chromatography (HPLC) of thiamylal, one of the barbiturates, the drug in serum samples was extracted by two alternative liquid-liquid extraction techniques using hydrophilic acetonitrile as a solvent and subzero-temperature and salting-out methods [8].
• A comparison of the long-term follow-up results of chronic motor cortex stimulation therapy revealed that thiamylal and ketamine-sensitive and morphine-resistant cases displayed long-lasting pain reduction with chronic motor cortex stimulation therapy, whereas the remaining cases did not show good results [9].
• During 105 min of anesthesia (induced by thiamylal sodium and maintained by halothane and oxygen), PRL increased (8.2 +/- 1.9 ng/ml) in all gilts [10].
• The plasma PRL and TSH responses to TRH injected iv at different stages of the estrous cycle in normal rats under Surital anesthesia were maximal during the afternoon of proestrus and morning of estrus and lowest on diestrus I [11].
• Measurement of thiamylal and thiopental in plasma by electron capture and flame photometric gas-liquid chromatography [12].

Chemical compound and disease context of Surital

• Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and halothane (1.25 minimal alveolar concentration) in 100% oxygen [13].
• The doses studied were 7.1, 10.0, 14.1, 20.0, and 28.3 mg of thiopental/kg of body weight; 5.7, 8.0, 11.3, 16.0, and 22.6 mg of thiamylal/kg; and 3.5, 5.0, 7.1, 10.0, and 14.1 mg of methohexital/kg [14].
• Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and isoflurane (1.25 minimal alveolar concentration) in 100% oxygen [15].
• A cumulative dose plus infusion technique and integrated EMG monitoring of the first dorsal interosseous muscle were used to determine the potency of vecuronium in 20 normal patients and in ten patients with myasthenia gravis under thiamylal, N2O, O2, fentanyl anaesthesia [16].
• Effect of hypercapnia on the arrhythmogenic dose of epinephrine in horses anesthetized with guaifenesin, thiamylal sodium, and halothane [17].

Biological context of Surital

• Blood pressure (BP), heart rate (HR), and arterial oxygen saturation were recorded every minute from the beginning of injection of thiamylal for 5 min [18].
• We found that the enantioselectivity of thiamylal existed in protein binding and metabolism [19].
• Both propofol and thiamylal depressed slow action potentials and contractile force in guinea pig papillary muscles depolarized by 25 mM K+ solution [20].
• Anesthesia was induced with thiamylal, followed by inhalation of 0.9 minimum alveolar anesthetic concentration (MAC) of the anesthetic in 100% oxygen via mask [21].
• IMPLICATIONS: Thiamylal enhances but pentobarbital suppresses human platelet aggregation in vitro [22].

Anatomical context of Surital

• In the mesenteric artery soaked in Ca++-free media, the addition of Ca++ produced only a slight contraction, which was potentiated by thiamylal (10(-4) and 10(-3) M) [23].
• Blockade of adenosine triphosphate-sensitive potassium channels by thiamylal in rat ventricular myocytes [1].
• METHODS: The authors used inside-out patch clamp configurations to investigate the effects of propofol and thiamylal on the activity of recombinant KATP channels using COS-7 cells transfected with various types of KATP channel subunits [24].
• The thiamylal-induced contraction appears to be associated mainly with influx of Ca++ from extracellular fluids [23].
• In helical strips of dog cerebral, coronary, mesenteric, renal, and femoral arteries, the addition of thiamylal and thiopental, 10(-5) to 10(-3) M, caused a dose-related contraction; the contraction was significantly more intense in cerebral than in extracerebral arteries [23].

Associations of Surital with other chemical compounds

• CONCLUSIONS: These results suggest that the major effects of both propofol and thiamylal on KATP channel activity are mediated via the Kir6.2 subunit [24].
• After obtaining informed consent, anesthesia was induced with sodium thiopental or thiamylal, fentanyl, and vecuronium in 61 ASA physical status II-IV patients [25].
• Circulatory responses after thiamylal (4 mg/kg) and succinylcholine (SCh) (2 mg/kg) administration followed by direct laryngoscopy and tracheal intubation were measured in 20 patients before elective aortocoronary vein bypass graft operations [26].
• Hepatic injury was measured in enzyme-induced rats following ligation of the hepatic artery performed under anesthesia with thiamylal, halothane, enflurane, or isoflurane [27].
• A randomized, double-blind controlled study was conducted to evaluate the effect of premedication with oral clonidine on thiamylal requirement for the induction of anesthesia and on associated hemodynamic changes in children [18].

Gene context of Surital

• CYP2C9 showed a significantly rapid metabolism of R(+)-enantiomer, suggesting that CYP2C9 is mainly involved in the enantioselective metabolism of thiamylal [19].
• Site-directed mutagenesis study suggests that propofol and thiamylal may influence Kir6.2 activity by different molecular mechanisms; in thiamylal, the SUR subunit seems to modulate anesthetic sensitivity [24].
• Thiamylal inhibited KATP channel activity without changing the single-channel conductance [1].
• Inhibition by six somatostatin analogs of plasma growth hormone levels stimulated by thiamylal and morphine in the rat [28].
• Although the increases in [Ca2+]i caused by membrane depolarization with high K+ were reduced equally with thiamylal and thiopental, thiamylal was more effective in attenuating the increase in [Ca2+]i produced by NMDA receptor activation than thiopental [29].

Analytical, diagnostic and therapeutic context of Surital

• Intraarterial injection of 2.5% thiamylal does cause gangrene [30].
• Motor unit spikes elicited during the TVR were recorded before and after an intravenous injection of thiamylal sodium [31].
• Thiopental and an internal standard (carbamazepine for HPCE and thiamylal for HPLC) were extracted from serum or plasma using pentane and a phosphate buffer (pH 6.4) [32].
• All patients received intramuscular morphine as preanesthetic medication 60 to 90 minutes before intravenous thiamylal anesthetic induction [33].
• Following immediate cardiopulmonary resuscitation, the patient was treated with an i.v. infusion of thiamylal sodium 2-4 mg kg-1 h-1 and his lungs were mechanically ventilated [34].

References