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PubMed2002

[Quantitative analysis of plasma concentration of barbiturate for diagnosis of brain death].

Organ transplantation from brain death patients started in Japan in 1997. However it is difficult to diagnose brain death in patients treated with barbiturate therapy. In this study, the influence of long continuous administration of barbiturate on diagnosis of brain death was investigated by measuring plasma concentration of barbiturate. In 15 patients treated with barbiturate therapy, plasma concentrations of thiamylal were measured by liquid chromatographic apparatus every day until it's level decreased below 0.1 microgram/ml after cessation of continuous administration. At the same time, plasma thiamylal levels were checked on the day when burst-suppression (b-s) pattern had disappeared in 9 cases, light reflex of pupil appeared in 7 cases and spontaneous respiration had been detected by trigger lamp in 11 cases. The plasma concentrations of thiamylal on the day when b-s pattern had disappeared differed clearly among the cases in the range of 8.8 to 37.9 micrograms/ml. Those cases in which light reflex of the pupil had been recognized were also different in the range of 17.8 to 57.8 micrograms/ml. The cases in which spontaneous respiration had been detected were in the range of 4.4 to 23.0 micrograms/ml. These concentrations varied about 4, 3 and 5 times among the cases examined. The intervals between cessation of continuous administration of thiamylal and the decrease of plasma concentration to below 0.1 microgram/ml also varied from 2 to 14 days from case to case. The minimum concentration of thiamylal on the day when b-s pattern had disappeared, light reflex of the pupil had been recognized and spontaneous respiration had been detected was 8.8, 17.8 and 4.4 micrograms/ml respectively. These results suggest that diagnosis of brain death in patients treated with barbiturate therapy is able to be made when the plasma thiamylal level is below 4.4 micrograms/ml.

Adolescent↗
PubMed1991

The relaxing effects of barbiturates in vascular smooth muscle of rat aorta.

The effects of thiamylal and pentobarbital on contractions mediated through the influx of extracellular Ca(++) and the release of intracellularly stored Ca(++) were compared in rat aortic strips. Thiamylal (3 x 10(-5) M to 10(-3) M) and pentobarbital (10(-4) to 10(-3) M) significantly attenuated the contraction induced by KCl (20 mM), and shifted the dose-response curve for Ca(++) of KCl (20 mM)-treated strips downwards and to the right. Caffeine (10(-2) M)-induced contraction was significantly attenuated by thiamylal at concentrations greater than 10(-4) M and by pentobarbital at 3 x 10(-4) M. Only a high concentration (10(-3) M) of these barbiturates significantly inhibited the contractions induced by norepinephrine (NE, 10(-6) M) in Ca(++)-free medium. Contraction of strips without endothelium by a Ca(++) ionophore, A23187 (5 x 10(-6) M), in the presence of a Ca channel blocker, was relaxed by high concentrations of thiamylal (3 x 10(-4) M to 10(-3) M) and pentobarbital (10(-3) M). It is concluded that thiamylal inhibits contraction through an intracellular action as well as a Ca channel-blocking action in vascular smooth muscle of rat aorta. However, the intracellular action of pentobarbital is less potent than that of thiamylal.

Journal Article↗
PubMed1997

Pharmacological classification of central post-stroke pain: comparison with the results of chronic motor cortex stimulation therapy.

In an attempt to clarify the neurochemical background of central post-stroke pain and to undertake a pharmacological analysis, the basic pharmacological characteristics of this intractable pain syndrome were investigated by the morphine, thiamylal and ketamine tests. In addition, the correlation between the pharmacological characteristics and the effects of chronic motor cortex stimulation therapy was examined. The study employed 39 central post-stroke pain patients who had intractable hemibody pain associated with dysesthesias, and radiologically demonstrated lesions in the thalamic area (thalamic pain, n = 25) or suprathalamic area (suprathalamic pain, n = 14). The pharmacological evaluations showed that definite pain reduction occurred in eight of the 39 cases (20.5%) by the morphine test, in 22 of the 39 cases (56.4%) by the thiamylal test, and in 11 of 23 cases (47.8%) by the ketamine test. Based on these pharmacological assessments, there was no obvious difference between thalamic and suprathalamic pain. 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. We conclude that pharmacological classification of central post-stroke pain by the morphine, thiamylal and ketamine tests could be useful for predicting the effects of chronic motor cortex stimulation therapy. It has recently been suggested that excitatory amino acids may be involved in the development of central post-stroke pain. However, the fact that only 23 of the present 39 cases (59.0%) of thalamic and suprathalamic pain were sensitive to the thiamylal or ketamine test reflects the complex pharmacological background and the difficulties associated with treating central post-stroke pain.

Adult↗
PubMed1990

Responses to barbiturates of isolated dog cerebral and mesenteric arteries contracted with KCl and prostaglandin F2 alpha.

In helical strips of dog cerebral and mesenteric arteries previously contracted with KCl or prostaglandin F2 alpha (PGF2 alpha), the addition of pentobarbital (10(-5) to 10(-3) mol.l-1) caused dose-related relaxation, whereas thiamylal and thiopental in a low concentration (10(-5) to 10(-4) mol.l-1) caused further contraction and in a high concentration (10(-3) mol.l-1) profound relaxation. Thiobarbiturate-induced contractions were greater in mesenteric than in cerebral arteries previously contracted with PGF2 alpha. In cerebral and mesenteric arteries exposed to Ca(++)-free media for 60 min and treated with KCl or PGF2 alpha, reintroduction of Ca++ produced a transient contraction, a transient relaxation and a persistent contraction. The Ca(++)-induced persistent contraction was attenuated by pretreatment with pentobarbital (10(-4) to 10(-3) mol.l-1) and thiamylal (10(-3) mol.l-1); the attenuation was greater in arteries treated with KCl than with PGF2 alpha. The Ca(++)-induced contractions of mesenteric artery treated with PGF2 alpha were potentiated by 10(-4) mol.l-1 thiamylal. It is concluded that pentobarbital possesses only a vasodilator effect, whereas thiamylal and thiopental have both constrictor and dilator effects on vascular smooth muscle. The vasodilator effect of barbiturates is associated in part with inhibition of transmembrane influx of Ca++; the inhibition is more predominant on the influx evoked by KCl-induced depolarization than by a stimulation of PGF2 alpha receptors. Thiamylal in low concentrations appears to enhance Ca++ influx through a receptor-operated Ca++ channel for PGF2 alpha.

Animals↗
PubMed1991

[Effects of halothane and barbiturate on hepatic circulation and hepatic oxygen metabolism during hypoxia in dogs].

Hepatic oxygen metabolism and the hepatic energy charge were assessed in 21 mongrel dogs receiving 1 to 1.5 MAC of halothane or thiamylal (20-30 mg.kg-1.hr-1) intravenously while inhaling graded hypoxic mixtures (FIO2 0.21-0.08). Hepatic blood flow was measured using electromagnetic flowmetry: hepatic oxygen delivery and consumption were calculated from measured hepatic blood flow and oxygen content in hepatic arterial, portal venous blood and hepatic venous blood. In the hypoxia-halothane group, portal venous blood flow (FIO2 0.15-0.10), portal venous oxygen content (FIO2 0.10-0.08) and hepatic oxygen consumption (FIO2 0.08) significantly decreased compared with the hypoxia-thiamylal group. Arterial ketone body ratio (AKBR), which indicates the mitochondrial energy charge level, decreased with the development of hypoxia, and in the hypoxia-halothane group, the decrease of AKBR was significantly greater than in the hypoxia-thiamylal group at FIO2 0.08. The serum catecholamine levels, epinephrine and norepinephrine, increased in both groups at FIO2 0.08. In the hypoxia-halothane group, however, the increase of norepinephrine was significantly higher than in the hypoxia-thiamylal group at FIO2 0.08. These results suggest that, compared with halothane, thiamylal could suppress the exaggerated reaction to hypoxic hypoxemia, maintain hepatic circulation and hepatic oxygen metabolism and therefore maintain the hepatic mitochondrial redox state in better condition.

Animals↗
PubMed1990

[Does induction with midazolam decrease stress response during anesthesia?].

The effects of midazolam on stress response during surgery compared with thiamylal were studied. Twelve patients were divided into 2 groups at random; midazolam group and thiamylal group. Anesthesia was induced with midazolam 0.2 mg.kg-1 or thiamylal 4 mg.kg-1 in each group, and maintained with O2 2 l.min-1, N2O 4 l.min-1 and enflurane. The plasma concentration of catecholamine was measured at preinduction, 10, 30, 60, 120 and 180 minutes after intubation. No significant differences were seen between 2 groups in plasma concentration of catecholamine. In midazolam group, plasma concentration of epinephrine decreased significantly 10 minutes after intubation as compared with preinduction level. The plasma concentration of norepinephrine in midazolam group tended to decrease. In thiamylal group, plasma concentration of norepinephrine tended to increase and increased significantly at 120 and 180 minutes after intubation as compared with preinduction level. These results suggest that induction with midazolam suppresses stress response during anesthetic induction and surgery more intensely than induction with thiamylal.

Adult↗
PubMed1989

The contractile responses of isolated dog cerebral and extracerebral arteries to oxybarbiturates and thiobarbiturates.

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. Secobarbital caused a slight contraction only in the cerebral artery. In contrast, pentobarbital did not produce a contraction in any artery studied. The thiamylal-induced contraction was not affected by treatment with phentolamine, diphenhydramine, or cinanserin but was attenuated by treatment with Ca entry blockers, such as nifedipine or diltiazem. In the cerebral artery soaked in Ca++-free media for 60 min, the addition of Ca++ produced triphasic responses; a transient contraction followed by a relaxation and a slowly developing, persistent contraction. The persistent contraction was potentiated by 10(-4) M thiamylal but abolished at 10(-3) M. 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). It is concluded that thiobarbiturates are more potent vasoconstrictors than oxybarbiturates and that the barbiturates produce greater contraction in cerebral arteries than in extracerebral arteries. The thiamylal-induced contraction appears to be associated mainly with influx of Ca++ from extracellular fluids.

Animals↗
PubMed1993

Acute, chronic and differential effects of several anesthetic barbiturates on glutamate receptor activation in neuronal culture.

The acute and chronic effects of several anesthetic barbiturates, in therapeutic concentrations, on the excitatory amino acid (EAA)-induced elevation of intracellular calcium levels ([Ca2+]i) were examined in neuronal tissue culture. The ultrashort-acting barbiturate, thiamylal, was effective in blocking elevations of [Ca2+]i induced by kainate, N-methyl-D-aspartate (NMDA), and quisqualate or by membrane depolarization with 40 mM KCl. The structurally similar barbiturate, secobarbital which differs from thiamylal only by having an oxygen in place of a sulfur, was able to block elevations induced by the above EAAs but was less effective than thiamylal and did not significantly reduce [Ca2+]i that resulted from membrane depolarization with KCl. Pentobarbital, while differing from secobarbital by only a methyl group, was without effect on either the NMDA- or 40 mM KCl-induced elevations of [Ca2+]i. By contrast, cyproheptadine, a compound that has been shown to block Ca2+ channels, has a different profile from the above barbiturates in that cyproheptadine is more effective in blocking elevation of [Ca2+]i induced by membrane depolarization with KCl while the barbiturates are more effective in reducing [Ca2+]i induced by EAAs. An anticonvulsant barbiturate, phenobarbital, did not reduced elevations of [Ca2+]i induced by any EAA tested or by membrane depolarization with KCl. When cells were treated chronically with thiamylal for 4 days, 2-6 h after the abrupt drug withdrawal there was a hyperresponsiveness to the elevations of [Ca2+]i induced by both kainate and NMDA but not by quisqualate. A similar hyperresponsiveness was not seen after the chronic treatment with phenobarbital.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗