Biomedical subjects

P Sribanditmongkol

Publications and source records attributed to P Sribanditmongkol.

7 recordsLinked to original sources

PubMed2001

Children's plasma cholinesterase activity and fatal methomyl poisoning.

There is a case of a couple who intentionally killed their children with methomyl insecticide. This was presented as our initial investigation of plasma cholinesterase (ChE) activity in Thai children. A hundred and five healthy Thai children 5-6 years of age, participated in the project. Their plasma was drawn to measure ChE activity. Mean +/- standard deviation of the children ChE was 7,417 +/- 1,620 U/L. The enzyme activity of the children was not significantly different between gender and parents' occupations. However, the mean of female ChE activity appeared to be lower than male ChE. Children whose parents were farmers appeared to have lower ChE activity than those whose parents were employees, merchants, government officers, unemployed parents, or private business owners. Two victims of child homicide were presented with ChE activity approximately 6 and 9 per cent of the average, considering healthy children. It was concluded that children's plasma ChE activity lower than 10 per cent of normal, could be a lethal indicator of anti-ChE insecticide poisoning.

Adult↗

PubMed2000

Methamphetamine overdose and fatality : 2 cases report.

Methamphetamine abuse is an important problem in Thailand. The number of addicts and abusers is increasing. Abusers usually use speed pills by oral ingestion or inhalation. The dose used is about 5-60 mg of methamphetamine while the lethal dose reported is 200 mg. Death due to methamphetamine toxicity is uncommon. In this paper, we report two cases of methamphetamine fatalities. Both cases were drug dealers. They swallowed a handful of methamphetamine tablets while being arrested. The autopsy revealed nonspecific findings. Using thin layer chromatography technique, methamphetamine was detected in the urine, blood, stomach and liver of the corpses. This circumstance has been reported elsewhere and might be increased in Thailand as more speed pills are circulated in illegal markets.

Adult↗

PubMed1998

Inhibition of morphine tolerance and dependence by diazepam and its relation to mu-opioid receptors in the rat brain and spinal cord.

We have recently observed that concomitant administration of diazepam to morphine pellet implanted rats results in the inhibition of the development of morphine tolerance and dependence. We have now analyzed mu-opioid receptors in rats treated with morphine and diazepam for 5 days by using [3H]-DAMGO for binding studies. Male Sprague-Dawley rats were made tolerant and dependent by subcutaneous (s.c.) implantation of six morphine pellets (two pellets on the first day, and four on the second day). Diazepam (0.25 mg/kg b.wt) was injected once daily intraperitoneally (i.p.) for 5 days. Control rats were implanted with placebo pellets and injected once daily with saline or diazepam (i.p.). Animals were administered s.c. naloxone (10 mg/kg) to induce naloxone-precipitated withdrawal syndrome on the final day of the experiment (day 5). There was an up-regulation of mu-receptor (Bmax increased) in the spinal cord of morphine tolerant (+139%) and dependent (+155%) rats compared to saline treated animals. Diazepam treatment abolished the up-regulation of mu-receptors in spinal cord of morphine treated rats. In the cortex, Bmax was not affected in morphine tolerant or dependent rats but it decreased by 38% in morphine tolerant and 65% in morphine dependent rats treated with diazepam. The Kd of mu-receptors increased in the cortex, striatum and hypothalamus of morphine dependent rats. Diazepam treatment decreased the Kd of mu-receptors in the cortex of morphine tolerant and hypothalamus of morphine-dependent rats. These results suggest that diazepam treatment antagonizes the up-regulation of CNS mu-receptors observed in morphine tolerant rats. In addition, morphine tolerance and dependence may be associated with conversion of mu-opioid receptors to mu-constitutive opioid receptors that are less active, and this conversion is prevented in the brain of animals treated with diazepam.

Analgesics, Opioid↗

PubMed1995

Inhibition of morphine tolerance and dependence by diazepam and its relation to cyclic AMP levels in discrete rat brain regions and spinal cord.

Diazepam inhibits morphine tolerance and dependence and reverses a decrease in the met-enkephalin level in brain induced by morphine. In this study, we investigated whether inhibition of morphine-induced tolerance and dependence by diazepam involved a change in cyclic AMP levels in discrete rat brain regions and spinal cord. Male Sprague-Dawley rats were made tolerant and dependent by subcutaneous (s.c.) implantation of six morphine pellets (two pellets on the first day, and four on the second day). Diazepam (0.25 mg/kg b. wt) was injected once daily intraperitoneally (i.p.) for 5 days. Control rats were implanted with placebo pellets and injected once daily with saline or diazepam (i.p.). Tail-flick antinociception was measured 1 h after injections everyday. Animals were administered s.c. naloxone (10 mg/kg) to induce naloxone-precipitated withdrawal syndrome on the final day of the experiment (day 5), and the jumping behavior was observed for 30 min. Concomitant treatment with diazepam (0.25 mg/kg) significantly decreased the development of morphine tolerance and dependence. Diazepam (0.25 mg/kg) treated rats also showed a significant decrease in the jumping behavior compared to animals treated with morphine alone. Rats were sacrificed 2 h after the injection of saline or diazepam (0.25 mg/kg) on the fifth day. Cyclic AMP was estimated by RIA. In the control rats, the concentration of cyclic AMP in cortex was > hippocampus > cerebellum > hypothalamus > striatum > midbrain > pituitary > pons/medulla > spinal cord. There was no change in the concentration of cyclic AMP in any of the brain regions examined from morphine tolerant animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Inhibition of morphine tolerance and dependence by diazepam and its relation to the CNS Met-enkephalin levels.

The effect of diazepam on the development of morphine tolerance and dependence was investigated. Male Sprague-Dawley rats were rendered tolerant and dependent by subcutaneous implantation of six morphine pellets. Diazepam (0.025, 0.25 or 2.5 mg/kg body weight) was once daily injected intraperitoneally into rats starting on the first day of implantation. Antinociception was measured by tail-flick (TF) and hot plate (HP) tests, and the extent of sedation determined by a rotarod test before and one hour after diazepam injections everyday for 5 days. Physical dependence on morphine was assessed by an antagonist-precipitated abstinence syndrome on the fifth day of treatment by injecting naloxone 10 mg/kg subcutaneously. Diazepam (0.025-2.5 mg/kg body weight) did not produce significant antinociception or sedation (sensorimotor impairment) in rats implanted with placebo pellets. Diazepam (0.25 and 2.5 mg/kg) inhibited tolerance to TF antinociception in rats implanted with morphine pellets. Sedation as evidenced by sensorimotor impairment induced by morphine pellet implantation was not influenced by diazepam (0.025-2.5 mg/kg). Diazepam administration (0.25 mg/kg) also decreased the degree of jumping behavior observed following naloxone injection in morphine pellet implanted rats. Serum morphine concentration in morphine-diazepam treated rats was not significantly different from that in morphine-saline treated rats. Finally, a decrease in the Met-enkephalin levels observed in the hypothalamus, hippocampus, cortex and spinal cord of morphine dependent rats was reversed by injecting diazepam along with morphine pellet implantation. These results suggest that diazepam inhibits morphine tolerance and dependence, and also prevents morphine-induced decrease in the CNS Met-enkephalin levels in morphine dependent rats.

Animals↗

PubMed1994

Effect of morphine-induced catalepsy, lethality, and analgesia by a benzodiazepine receptor agonist midazolam in the rat.

Previously we have shown that intrathecal administration of midazolam can increase or decrease morphine-induced antinociception, depending upon relative concentration of these drugs by modulating spinal opioid receptors, and it also can inhibit morphine-induced tolerance and dependence in the rat. Now we report that midazolam also influences catalepsy, lethality, and analgesia induced by morphine in the rat. In the acute treatment, animals were first treated with saline or midazolam (0.03 to 30.0 mg/kg, b.wt., IP), and 30 min later with a second injection of saline or morphine (1.0 to 100.0 mg/kg, b.wt., SC). The catalepsy was measured 60 min after the second injection and lethality was checked after 24 h. Midazolam injection increased the morphine-induced catalepsy and lethality. In the chronic treatment, animals were injected with two injections daily for 11 days. The first injection consisted of saline or midazolam (0.03 to 3.0 mg/kg, b.wt., IP), and 30 min later with a second injection of saline or morphine (10.0 mg/kg, b.wt., IP) was given. Lethality, antinociception, and body weight were measured. Chronic morphine treatment also increased lethality in a dose-dependent manner. Chronic treatment with midazolam and morphine increased the antinociception on day 11, as measured in the tail-flick and hot-plate tests. Midazolam administration also prevented the morphine-induced weight loss. These results suggest a strong interaction between midazolam and morphine in altering catalepsy, lethality, and analgesia in rat.

Analgesics↗

PubMed1993

Inhibition of morphine-induced tolerance and dependence by a benzodiazepine receptor agonist midazolam in the rat.

We investigated whether midazolam administration influenced morphine-induced antinociception and tolerance and dependence in the rat. Antinociception was assessed by the tail-flick (TF) and the hot-plate test (HP 52 degrees C). Morphine tolerance developed after daily single injections of morphine for 11 days. The effect of midazolam on morphine-induced antinociception and tolerance was assessed by giving daily injections of various doses of midazolam for 11 days. The first injection of saline or midazolam was given intraperitoneally and 30 min later morphine (10 mg/kg body weight) was administered subcutaneously. Antinociception was monitored by measuring TF and HP latencies 60 min after the second injection. Midazolam was injected at four different concentrations: 0.03, 0.1, 0.3, and 3 mg/kg body weight. Chronic administration of morphine resulted in the development of tolerance to antinociception in both TF and HP tests, with rats exhibiting baseline antinociception on Day 9. Animals treated with midazolam alone showed little antinociception on Days 3-9. However, midazolam administration in morphine-treated animals attenuated morphine-induced tolerance to antinociception on Days 1-11 as measured by the tail-flick test. Midazolam also decreased the jumping behavior following naloxone injections in morphine-dependent rats. These results suggest that midazolam may prolong the effects of morphine by delaying morphine-induced development of tolerance to antinociception. Midazolam also attenuated a decrease in weight gain induced by chronic injections of morphine.

Animals↗