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Biomedical subjects

C L Wong

Publications and source records attributed to C L Wong.

At least 55 records · Page 3Linked to original sources
PubMed1985

Effects of adrenalectomy and gonadectomy on the antinociceptive effect of morphine and naloxone antagonism in mice.

In the present study the effects of adrenalectomy and gonadectomy on the antinociceptive activity of morphine and its antagonism by naloxone were studied in male and female mice. In the female mice, it was found that adrenalectomy enhanced the antinociceptive activity of morphine by two-fold, while the antinociceptive effects of morphine measured in the presence of naloxone were similar to those of the sham-operated controls. The naloxone potency ratios, expressed as the ratios of morphine ED50s with naloxone to that without naloxone, were increased in adrenalectomised animals. Similar effects were observed in oophorectomised female mice though the influence of oophorectomy on naloxone antagonism was not as effective as adrenalectomy. In animals that were both adrenalectomised and oophorectomised the antinociceptive effect of morphine measured was similar to those animals receiving either operative procedure. However, the naloxone potency ratios determined were between those determined in adrenalectomised mice and oophorectomised animals. In male mice, the effect of adrenalectomy was similar to that observed in the female animals, namely both the antinociceptive activity of morphine and naloxone antagonism were enhanced. Orchidectomy enhanced the antinociceptive effect of morphine but not to the same extent as adrenalectomy. Furthermore, the enhancement of naloxone antagonism was also less than that induced by adrenalectomy. The effects of adrenalectomy and orchidectomy in male mice were similar to those of adrenalectomy alone. These results suggest that steroid hormones are involved in the actions of both morphine and naloxone.

Adrenalectomy↗
PubMed1984

Neonatal cytomegalovirus infections: the relative role of neonatal blood transfusion and maternal exposure.

A prospective study of premature infants admitted to an intensive care neonatal unit was undertaken to evaluate the relative role of blood transfusions and maternal exposure in infections caused by cytomegalovirus (CMV), varicella zoster virus (VZV) and herpes simplex virus (HSV). During the first year of life, 13.7%, 4.8% and 4% of the infants became infected with CMV, VZV and HSV, respectively, as determined by virus isolation or seroconversion. Transfusion in the newborn period did not influence the rates of VZV or HSV infections. A higher rate of CMV infections occurred in transfused (18.8%) than in non-transfused (11%) infants but the difference was not statistically significant. A significant correlation was found between maternal antibody titers and the rate of CMV infection in infants whether or not transfusion occurred. An even stronger association was found between breast feeding and CMV infections. The risk of alloimmunization to erythrocyte and leucocyte antigens was also assessed; no evidence of increased alloimmunization to these antigens was associated with transfusion.

Antibodies, Viral↗
PubMed1984

The effects of morphine and nalbuphine on intestinal transit in mice.

In the present study, the effects of morphine, a predominant mu-receptor agonist, and nalbuphine, a partial agonist supposedly acting on x-receptors, on intestinal motility were studied. The intestinal motility was measured by the transit of charcoal meal through the small intestine in mice. Morphine caused a dose-dependent slowing of the rate of intestinal transit in mice. This inhibitory effect of morphine was antagonised by naloxone administration. Nalbuphine also caused a dose-dependent inhibition of intestinal motility; the inhibition was less and showed a low-level plateau response, with a maximum of 40% inhibition. The effect of nalbuphine was antagonised by naloxone, but the antagonism was far less than that against morphine. Pretreatment with a single dose of morphine did not induce any change in the inhibitory effect of a second dose of morphine given four hours later. However, naloxone was more effective in antagonising the inhibitory effect of morphine in morphine-pretreated mice than in saline-pretreated animals. Pretreatment with morphine did not affect the inhibitory effect of nalbuphine, and the antagonistic potency of naloxone against nalbuphine was only marginally enhanced. Pretreatment with nalbuphine failed to alter the inhibitory effect of morphine as well as that of nalbuphine. Furthermore, nalbuphine pretreatment also had no effect on the antagonistic potency of naloxone against the inhibitory effects of nalbuphine and morphine on intestinal transit. These findings suggest that x-receptors are not important in the inhibitory effects of narcotic analgesics on intestinal transit and that a mu-receptor agonist is more effective in inducing enhancement of the antagonistic effect of naloxone.

Animals↗
PubMed1983

Canalicular function during herpetic keratoconjunctivitis in rabbits.

Canalicular function during acute herpetic keratoconjunctivitis was investigated in rabbits. Evidence of partial obstruction of the duct was obtained in the infected as compared with the mock-infected eyes. Direct damage of the ductal epithelium by virus could not be demonstrated by histologic and immunofluorescent studies. Our findings suggest that canalicular dysfunction associated with viral infection may result from accompanying inflammatory changes.

Animals↗
PubMed1981

The effect of prostaglandin E2 on increased naloxone potency induced by morphine pretreatment.

Pretreatment with prostaglandin E2 caused an increase in naloxone potency while the antinociceptive effect of morphine remained unaffected. These effects of prostaglandin E2 were not blocked by concomitant administration of naloxone in the pretreatment. Furthermore, when prostaglandin E2 was given together with morphine as pretreatment, the resulting naloxone antagonism measured was higher than those induced by pretreatment with the individual drugs. It is suggested that the induction of increased naloxone potency is likely to be mediated through a prostaglandin-linked process.

Analgesics↗
PubMed1981

Effects of aspirin and paracetamol on naloxone reversal of morphine-induced inhibition of gastrointestinal propulsion in mice.

In mice, morphine caused a dose-dependent slowing of the rate of intestinal transit of a charcoal meal. This inhibitory effect of morphine was antagonised by naloxone. Pretreatment with a single dose of morphine did not induce any detectable tolerance to the inhibitory action of a second dose of morphine given 4 h later. However, naloxone was more effective in antagonising intestinal inhibition by morphine in morphine-pretreated mice than in saline-pretreated animals. Pretreatment with either aspirin or paracetamol did not alter the inhibitory action of morphine given 4.5 h later. However, the antagonistic effect of naloxone was significantly augmented, though not to the same extent as that caused by morphine pretreatment. When either aspirin or paracetamol was given together with morphine as pretreatment, the resulting naloxone antagonism measured 4 h later was significantly higher than that induced by pretreatment with the individual drugs. Furthermore, combined pretreatment with aspirin 20.0 mg/kg and morphine 40.0 mg/kg induced detectable tolerance to the inhibitory effect of a second dose of morphine given 4 h later. The present study indicates that prostaglandins reduce the naloxone antagonism of the inhibitory action of morphine on the rate of intestinal transit in mice and may interfere with the development of morphine tolerance.

Acetaminophen↗
PubMed1980

The effect of aspirin and paracetamol on the increased naloxone potency induced by morphine pretreatment.

Using the abdominal constriction test in mice, it was shown that pretreatment with a single dose of morphine given 3 h previously caused a marked increase in the antagonistic effect of naloxone without any change in the antinociceptive action of morphine itself. Pretreatment with either paracetamol (10.0-20.0 mg/kg, s.c.) or aspirin (5.0-10.0 mg/kg, s.c.) caused a small but significant antagonism of the antinociceptive effect of morphine, while the antagonistic action of naloxone remained unaffected. However, when aspirin or paracetamol was administered with morphine in the pretreatment regime, the ability of morphine to induce an increase in naloxone potency was much attenuated. This inhibitory effect was dependent on the dose of aspirin or paracetamol used in the pretreatment regime. The antinociceptive effect of aspirin and paracetamol was also studied. In the doses used, they did have a mild antinociceptive effect, but the analgesic effect of morphine was not affected by the administration of these drugs 30 min beforehand. It is suggested that the antinociceptive effect of morphine is probably not dependent on prostaglandin, but that the induction of increased naloxone potency is likely to be mediated through prostaglandin synthesis.

Acetaminophen↗
PubMed1980

Effect of morphine and naloxone on intestinal transit in mice.

Morphine caused a dose-dependent slowing of the rate of intestinal transit in mice. This inhibitory effect of morphine was antagonised by naloxone administration. Pretreatment with a single dose of morphine did not induce any detectable tolerance to the inhibitory effect of a second dose of morphine given 5 h later. However, naloxone was more effective in antagonising this inhibitory effect of morphine in morphine-pretreated mice than in saline-pretreated animals. Molecular sieve morphine pellet implantation for 24 h induced detectable tolerance to the inhibitory effect of morphine administered 3 h after removal of the pellet. In addition, the antagonistic effect of naloxone was also augmented when compared with blank pellet-implanted control animals. The present study has shown that the enhanced naloxone potency against the inhibitory effect of morphine was intestinal transit was observalbe before the development of overt tolerance, and that tolerance to the effect of morphine on the small intestine could be induced by implantation of a molecular sieve morphine pellet for 24 h.

Animals↗
PubMed1980

The effect of phenobarbitone pretreatment on the narcotic antagonistic potency of naloxone in mice.

Pretreatment with phenobarbitone (5.0-20.0 mg/kg, s.c.) did not alter the antinociceptive effect (tail-flick assay) of morphine measured 4.5 h later. However, naloxone was more potent in antagonising this antinociceptive effect in phenobarbitone-pretreated mice than in saline-retreated animals. Concomitant administration of naloxone in the pretreatment regime did not alter the effect of phenobarbitone. The enhanced naloxone potency was related to the amount of phenobarbitone given, and was observable at 3.0 and 4.5 h after pretreatment. It was no longer apparent at 6.0 h. Because of a difference in time course and in the ability of naloxone to block the phenomenon, it is suggested that the mechanisms underlying the increase in naloxone potency induced by phenobarbitone pretreatment and morphine pretreatment may not be the same.

Analgesics↗
PubMed1980

The effects of cholinergic compounds on the development of morphine tolerance, dependence and increased naloxone potency in mice.

The effects of chronic treatment with morphine and cholinergic compounds on the development of morphine tolerance, physical dependence and increased naloxone potency were studied. Using the abdominal constriction method, it was shown that morphine tolerance was apparent after s.c. administration of morphine 20.0 mg/kg three times a day for four days. It was found that, in animals which showed a low degree of morphine tolerance, the naloxone potency was similar to that determined in mice which had been pretreated with only a single dose of morphine which causes no measurable tolerance. Thus, the development of increased naloxone potency and tolerance to morphine do not parallel each other. In addition, while atropine inhibited, and anti-cholinesterase drugs enhanced, the development of increased naloxone potency caused by morphine treatment they had no or little effect on the development of morphine tolerance. Furthermore, chronic treatment with cholinergic agonists reduced, while muscarinic antagonist enhanced, the development of physical dependence on morphine as assessed by withdrawal jumping and body weight loss. It is concluded that the increased potency of naloxone in antagonising the antinociceptive effect of morphine can be dissociated from the development of tolerance to, and physical dependence on, morphine in mice.

Animals↗
PubMed1979

The effect of morphine pretreatment on hypothermia induced by morphine in mice.

Morphine caused an apparently dose-dependent hypothermia in mice. Co-administration of naloxone antagonised this effect. Pretreatment with a single dose of morphine induced detectable tolerance to the hypothermic effect of a second dose of morphine given 3 h later and naloxone was more effective in antagonising the hypothermic effect of morphine in morphine-pretreated mice than in saline-pretreated animals. The present study has shown that morphine pretreatment can augment the antagonistic effect of naloxone towards the hypothermic action of morphine.

Animals↗
PubMed1979

Further studies on the role of cholinergic mechanisms in the development of increased naloxone potency in mice.

Using the abdominal constriction response in mice, it was shown that pretreatment with either pilocarpine (5.0 mg/kg, s.c.) or oxotremorine (0.05--0.10 mg/kg s.c) caused a small but significant potentiation of the antinociceptive effect of morphine and the antagonistic action of naloxone. The potentiation of naloxone was considerably augmented following pretreatment with morphine plus either pilocarpine (2.5--5.0 mg/kg) or oxotremorine (0.05--0.10 mg/kg) as compared with any of these drugs given alone. Pretreatment with atropine sulphate (2.0 mg/kg, s.c.) had no effect on naloxone potency nor on the antinociceptive activity of morphine, but somewhat reduced that of pilocarpine and oxotremorine. Atropine abolished the ability of morphine pretreatment to enhance naloxone potency, and greatly reduced the augmenting effect of morphine plus the muscarinic receptor agonist drugs. It was also shown that oxotremorine reduced the development of dependence on morphine as tested by naloxone-precipitated jumping. These results agreed well with those reported using anticholinesterase drugs and add further evidence that the cholinergic system does play a role in the development of increased naloxone potency caused by morphine pretreatment. The increased naloxone potency does not seem to be related to the development of "acute dependence" on morphine.

Abdominal Muscles↗
PubMed1978

The role of the cholinergic system in the development of increased naloxone potency in mice.

Pretreatment of mice with the anticholinesterase (anti ChE) drugs tacrine or physostigmine augmented the antinociceptive potency of morphine given 3 h later, but had no effect on the antogonist potency of naloxone. Pretreatment with either of these anti ChE drugs together with morphine not only augmented the potency of a subsequent dose of morphine, but also enhanced the antagonist potency of naloxone to a greater extent than after pretreating with morphine only. Neostigmine did not affect the potency of either morphine or naloxone, suggesting that this phenomenon involved central cholinergic mechanisms. Atropine prevented the increase in naloxone potency caused by morphine pretreatment, and greatly reduced the effect of morphine plus the anti ChE drugs. The effects of these various pretreatments on the development of "acute dependence" to morphine was also studied. None of the three anti ChE drugs caused any change in this phenomenon, as tested by naloxone-precipitated jumping, although this was significantly increased by pretreatment with either atropine sulphate or atropine methyl nitrate. It is concluded that the increase in naloxone potency following morphine pretreatment involves both a cholinergic mechanism plus narcotic analgesic action. This phenomenon does not seem to be related to the development of either acute tolerance or acute dependence.

Analgesics↗
PubMed1978

Increased antagonist potency of naloxone caused by morphine pretreatment in mice.

Using the writhing test in mice, it was shown that pretreatment with a single dose of morphine hydrochloride given 3 h previously caused a marked increase in the antagonistic effect of naloxone without any change in the antinociceptive action of morphine itself. It was shown that when mice were pretreated with different doses of either morphine alone, or in combination with naloxone, so that each treatment produced the same antinociceptive effect, the increase in naloxone potency was proportional only to the antinociceptive effect of the pretreatment and not to the total dose of morphine present. It was also found that the concurrent administration of naloxone plus morphine prevented the development of "acute dependence" to morphine, as measured by the jumping reaction after challenge with naloxone.

Analgesics↗