Disease relevance of amobarbital

• Brain injury, handedness, and speech lateralization in a series of amobarbital studies [1].
• At the end of the experiment, recovery of left ventricular end-diastolic and of developed pressure was significantly greater in those hearts that had been treated with Amytal during ischemia and early reflow, as compared to untreated hearts.(ABSTRACT TRUNCATED AT 400 WORDS)[2]
• Respiratory failure after clonazepam and amobarbital [3].
• In 1 baby whose mother had membranous glomerulonephritis, plasma amobarbital concentration did not significantly change over the period of the study [4].
• Plasma half-lives of amobarbital were determined in newborn children of 10 mothers who had been treated with barbiturates for hypertension in pregnancy for 6 to 42 days prior to delivery [4].

Psychiatry related information on amobarbital

• Controlled investigation of the amobarbital interview for catatonic mutism [5].
• Amytal interviews have a valid role in the assessment and initial management of catatonia, hysterical stupor, and unexplained muteness as well as in distinguishing between depressive, schizophrenic, and organic stuporous states [6].
• Use of the amobarbital interview to determine appropriate behavior therapy [7].
• After the conversion symptom was removed with amobarbital, his depressive symptoms became more obvious and subsequently improved with imipramine treatment [8].
• Right hemisphere speech perception revealed by amobarbital injection and electrical interference [9].

High impact information on amobarbital

• Inhibition of mitochondrial respiration by cyanide, azide, or Amytal abolished acid secretion; the subsequent addition of ATP to shocked glands increased the aminopyrine accumulation ratio to 47 and resulted in an acridine orange fluorescence indistinguishable from that of histamine-stimulated, unshocked glands [10].
• Amytal, a blocker of site I of the mitochondrial respiratory chain, abolished the K+ effect, indicating a mitochondrial origin for the recorded changes [11].
• We compared (15)O water positron emission tomography (PET) auditory and visual confrontational naming activation with an intracarotid amobarbital (Amytal) injection procedure (IAP) for language lateralization in 12 patients with intractable epilepsy [12].
• Brain single photon emission computed tomographic (SPECT) images acquired after injecting Tc-99m-HMPAO into the internal carotid artery (ICA) during an intracarotid amobarbital procedure (IAP SPECT) provide anatomical information on the blood flow distribution from the ICA [13].
• Three patients undergoing selective amobarbital test of the posterior cerebral artery were included [14].

Chemical compound and disease context of amobarbital

• Six patients suffering from status epilepticus were refractory to parenteral treatment with either diazepam, amobarbital or both, and were given sodium valproate 200 to 800 mg every 6 hours [15].
• The relationship between myocardial cell contracture and injury during total metabolic inhibition (amylobarbital and iodoacetic acid) and ischemia was examined, using 5-50 mM butanedione monoxime (BDM) as an inhibitor of contracture [16].
• Indeed, whereas 27% of control cells became necrotic after 1 h of chemical hypoxia with 10 mM deoxyglucose and 5 mM amobarbital (Amytal), only 11% of the glucose-treated cells became necrotic [17].
• Methylphenidate in amytal-resistant mutism [18].
• In all four patients, the use of lidocaine detected clinically significant neurologic deficits that amobarbital alone did not, likely because of the pharmacodynamic differences of the two agents [19].

Biological context of amobarbital

• When these uncoupled cells were inhibited with Amytal to lower the rate of oxygen consumption to that of resting cells, the P50 fell to 1.25 +/- 0.14 microM [20].
• Membrane lipid peroxidation of reperfused hearts was also reduced by treatment with Amytal, but not with KCN [2].
• Heart rate does not decrease after right hemispheric amobarbital injection [21].
• Genetic study of amobarbital elimination based on its kinetics in twins [22].
• An Oriental male with only trace capacity for amobarbital hydroxylation was found in the second part [23].

Anatomical context of amobarbital

• Isolated myocyte suspensions were incubated with 3 mmol/l (millimolar) iodoacetic acid and 6 mmol/l amytal (inhibited) or were pelleted into a slurry and layered with oil (ischemic) in the presence and absence of 10 or 50 mumol/l (micromolar) mepacrine [24].
• METHODS: Thirty male Wistar rats were anaesthetised with amobarbital, the femoral veins were cannulated and laparotomies were performed [25].
• These results indicate that relying solely on amobarbital memory testing to assess the functional ability of the contralateral temporal lobe to sustain global memory prior to temporal lobectomy may needlessly exclude patients from a viable therapeutic option [26].
• Ten patients for whom follow-up neuropsychological assessment was available failed either the early or late item recognition portions of their amobarbital evaluation ipsilateral to seizure onset, but had hippocampus included in the temporal lobectomy by virtue of satisfactory performance on other tests of hippocampal function [26].
• Carotid artery dissection after the intracarotid amobarbital test [27].

Associations of amobarbital with other chemical compounds

• SATSCOM (Selective amobarbital test intraarterial SPECT coregistered to MRI) was performed by skull extraction in SPECT and MRI followed by surface matching [14].
• The effects of pentobarbital, phenobarbital, amobarbital, and diphenylbarbituric acid were studied by examining the average lifetime and conductance of acetylcholine-activated sodium channels in Aplysia neurons [28].
• Mild inhibition of the respiratory chain with Amytal reversed the effects of hormone treatment on mitochondrial pyruvate metabolism and ATP concentrations, but not on citrulline synthesis [29].
• Moreover, the addition of adenosine, inosine, or guanosine immediately before the amobarbital retarded the decline in ATP and preserved cell viability [30].
• Anatomic correlates of memory from intracarotid amobarbital injections with technetium Tc 99m hexamethylpropyleneamine oxime SPECT [31].

Gene context of amobarbital

• Intracarotid amobarbital procedure memory results were related to CA3 neuronal loss only [32].
• In addition, the activity of AS-3201 N-glucosyltransferase significantly correlated with that of amobarbital N-glucosyltransferase in microsomes from sixteen human livers (r=0.964, P<0.01), indicating that UGT2B isoforms were also involved in the barbiturate N-glucosidation in humans [33].
• Results indicate that hGH slows the metabolism of amobarbital, probably through an effect on the hepatic microsomal drug-oxidizing system [34].
• In an effort to identify patients at risk for behavioral complications, we reviewed 92 patients undergoing ISA evaluation and found five with severe changes in affect and behavior following amobarbital injection, ranging from prolonged coma to an extended confusional state [35].
• Carbonic anhydrase inhibitors and amobarbital resistance [36].

Analytical, diagnostic and therapeutic context of amobarbital

• To visualize individual amobarbital perfusion patterns, simultaneous injection of (99m)Tc-HMPAO was performed previously [14].
• The present study describes for the first time a method of coregistration of intraarterial SPECT during selective amobarbital test to MRI [14].
• Results obtained by fMRI are closely correlated with invasive procedures such as electrical stimulation mapping or the intracarotid amobarbital test [37].
• Contraction bands occurred following oxygenated, but not anoxic, reperfusions and were inhibited by Amytal [38].
• False positives in the differential diagnosis of confusion with amytal [39].

References