Biomedical subjects

M Y Chan

Publications and source records attributed to M Y Chan.

At least 55 records · Page 3Linked to original sources

PubMed1990

Controlled ovarian hyperstimulation for in vitro fertilization using buserelin and gonadotropin in patients with previous failed cycles.

Fifteen patients who had had previous unsuccessful in vitro fertilization and embryo transfer (IVF) cycles were treated with intranasal buserelin, a gonadotropin releasing hormone agonist (GnRH-a), commencing in the mid-luteal phase prior to ovarian stimulation in the next cycle. The use of buserelin was associated with the suppression of spontaneous luteinizing hormone (LH) surges (nil versus 6), an increase in gonadotropin requirements (27.3 versus 13.7 ampoules), higher serum estradiol peak levels (8, 154 versus 4,446 pmol/l), more oocytes retrieved (87 versus 20) as well as more embryos being transferred (28 versus 7). In buserelin-treated cycles, 2 pregnancies resulted but no oocyte was recovered in 2 of the 3 poor responders.

Adult↗

PubMed1989

The identification of pyrrolizidine alkaloid-containing plants--a study on 20 herbs of the Compositae family.

Twenty Chinese medicinal herbs of the Compositae family were investigated for the presence of pyrrolizidine alkaloid. Of these, only the Eupatorium species were shown to contain pyrrolizidine alkaloid. The amount present was found to vary with species, parts of the plant used, purchase sources and extraction methods. Possible toxicity from the use of these herbs is discussed.

Drugs, Chinese Herbal↗

PubMed1989

A comparative study on the hepatic toxicity and metabolism of Crotalaria assamica and Eupatorium species.

The oral LD50 of Crotalaria assamica, which contains mainly monocrotaline, was found to be 154 mg/kg in mice. Neither liver necrosis nor morbidity was demonstrated with Eupatorium extract at a dose level of 144 mg/kg, which was equivalent to the LD20 of Crotalaria. Pretreatment with phenobarbitone enhanced the toxicity of both plant extracts in mice. In in vitro studies, "metabolic pyrrole" was formed by incubating Eupatorium japonicum extracts with liver microsomes. The rate of "pyrrole" formation was similar to that of Crotalaria extract and pure monocrotaline alkaloid, but was much slower than retrorsine. The rate of N-oxide formation was, in descending order, retrorsine, Eupatorium japonicum and Crotalaria/monocrotaline. It is concluded that the alkaloid in Eupatorium species is metabolized to "pyrrole" and an N-oxide metabolite in the liver, but hepatotoxicity is much lower when compared with that caused by Crotalaria.

Alkaloids↗

PubMed1989

Traumatic intracorneal cyst.

We describe clinical and pathologic characteristics of two cases of traumatic intracorneal cyst. Both patients were children, without a history of ocular surgery, but they had been injured by scissors many years before the corneal lesion was noted. The corneal lesion was characteristically circular, opalescent, quiet, and slowly progressive. Histopathologically it formed within the corneal lamellae and was lined by corneal epithelium. Some epithelial debris was noted in the cyst contents. The first case was treated with penetrating keratoplasty, and the graft remained clear after 11 months of follow-up. The second case received simple aspiration, and recurrence of the cyst was noted at a nine-month follow-up. Excision of the anterior cyst wall and chemical cauterization using aqueous iodine 1% was done subsequently.

Child↗

PubMed1988

Ventricular histamine concentrations in naive and morphine-treated rats during acute myocardial ischaemia.

The ventricular histamine concentrations of naive and morphine-treated rats subjected to acute left coronary artery ligation were examined. In naive animals, there was a significant increase in the right ventricular histamine level at 5 min following ligation, but not at 3 or 10 min. Left ventricular histamine concentrations tended to decrease, but the changes were not statistically significant. In shamoperated rats, neither acute nor chronic morphine treatment significantly altered either right or left ventricular histamine levels. Acute morphine treatment also did not significantly affect the ventricular histamine content at 5 min following coronary artery ligation. However, both right and left ventricular histamine concentrations were found to be significantly lower in chronic morphine-treated rats than in the naive animals when they were subjected to acute myocardial ischaemia. If the hypothesis that histamine release may contribute to the genesis of early ventricular arrhythmias resulting from acute myocardial ischaemia is accepted, the present findings suggest that the previously reported decreased incidence and delayed onset of early ventricular arrhythmias induced by acute left coronary artery ligation in chronic morphine-treated rats may be attributed to the reduced ventricular histamine concentrations.

Animals↗

PubMed1988

Cardiovascular responses to acute myocardial ischaemia in morphine-dependent rats.

1. The cardiovascular responses to acute myocardial ischaemia were studied in opiate-dependent animals before and after 2 weeks morphine withdrawal. 2. Rats were treated with morphine sulphate in drinking water for 2, 3 or 5 weeks. The development of morphine tolerance and dependence was verified by the tail-immersion test for analgesia and the naloxone-precipitated withdrawal syndrome, respectively. 3. Acute left coronary artery ligation induced a decrease in blood pressure, a slight increase in heart rate and ventricular tachycardia or fibrillation in anaesthetized naive rats. 4. Chronic morphine treatment did not alter the haemodynamic responses to coronary artery ligation. However, a significantly lowered incidence, and prolonged time of onset, of ventricular arrhythmias was found in 3 and 5 week morphine-treated rats. This phenomenon did not occur in animals receiving morphine for 2 weeks and in a 3 week morphine-treated group which was subsequently withdrawn for 2 weeks. 5. It is suggested that the decreased occurrence of early ventricular arrhythmias resulting from acute myocardial ischaemia in chronic morphine-treated rats may be related to the degree of opiate tolerance and dependence.

Animals↗

PubMed1988

Influence of acute myocardial ischaemia on ventricular cyclic AMP concentrations in naive and morphine-treated rats.

1. Ventricular cyclic AMP (cAMP) concentrations of naïve and morphine-treated rats subjected to acute myocardial ischaemia were examined. 2. In naïve rats, ventricular cAMP levels were increased at 3 min but decreased 5 and 10 min after left coronary artery ligation. Statistically significant changes were observed in the right ventricle after 3 min and in the left ventricle after 10 min. 3. Acute morphine treatment did not significantly alter ventricular cAMP content in rats subjected to either sham operation or acute left coronary artery ligation. 4. Ventricular cAMP concentrations were significantly lower in sham-operated rats after 5 weeks of chronic morphine treatment while after 3 weeks of chronic morphine treatment, this phenomenon was seen only after acute coronary ligation. The reductions were reversed by opiate withdrawal. 5. These observations support the theory that elevated cAMP levels may contribute to the production of early ventricular arrhythmias during acute myocardial ischaemia. It is suggested that the reduction in ventricular cAMP concentrations may partly account for the previously reported decreased occurrence of early ventricular arrhythmias in chronic morphine-treated rats subjected to acute left coronary artery ligation.

Animals↗

PubMed1988

Ventricular noradrenaline concentrations in naïve and morphine-treated rats subjected to acute myocardial ischaemia.

1 Ventricular noradrenaline concentrations in morphine-treated rats subjected to acute left coronary artery ligation were measured by high performance liquid chromatography with electrochemical detection. 2 In naïve rats, acute left coronary artery ligation induced a significant increase in right ventricular noradrenaline concentration at 5 min and significant decreases in left ventricular noradrenaline concentration at 3 and 10 min. 3 Acute morphine treatment did not significantly alter ventricular noradrenaline concentrations in rats subjected to acute coronary artery ligation. 4 Chronic morphine treatment caused significant declines in ventricular noradrenaline concentrations in rats subjected to acute coronary artery ligation. The reductions increased with duration of opiate treatment, and were reversed by opiate withdrawal. 5 These findings indicate that there is an increase in sympathetic activity during acute myocardial ischaemia. It is suggested that chronic morphine treatment may be able to retard this response, and consequently to lessen the occurrence of early ventricular arrhythmias resulting from acute myocardial ischaemia.

Animals↗

PubMed1987

Effects of morphine on cardiovascular responses to acute myocardial ischaemia in rats.

The effects of acute coronary artery ligation on cardiac rhythm and haemodynamics were studied in rats receiving either acute or chronic morphine-treatment. In chronic opiate-treated animals, increasing concentrations of morphine sulphate were administered in drinking water over a 3 week period, and the development of morphine tolerance and dependence was verified by decreased analgesic responses to morphine in the tail-immersion test and the occurrence of naloxone-precipitated withdrawal syndromes, respectively. Acute coronary artery ligation induced a decrease in blood pressure, a slight increase in heart rate, and ventricular tachycardia or fibrillation in anaesthetized rats. The changes in blood pressure and heart rate following acute coronary artery ligation were not significantly altered by acute or chronic morphine administration. The incidence and the time of onset of ventricular tachycardia or fibrillation were found to be significantly reduced and prolonged, respectively, in chronically morphine-treated rats, but were not significantly affected by acute morphine administration in naïve animals. These findings suggest that chronic morphine treatment lessens the occurrence of early ventricular arrhythmias caused by acute myocardial ischaemia in rats. The mechanism of this effect is unclear.

Animals↗

PubMed1987

Effects of Sophora flavescens Ait. on haemodynamics and ventricular fibrillation threshold in anaesthetized dogs.

The effects of an ethanol extract of the plant Sophora flavescens Ait. on haemodynamics and ventricular fibrillation threshold were studied in pentobarbitone-anaesthetized dogs. It was found that intravenous injection of the extract, 120 mg/kg, caused transient but significant depression in systolic and diastolic blood pressure, heart rate, left ventricular pressure and dLVP/dtmax, as well as elevation of ventricular fibrillation threshold. These preliminary findings suggest that the ethanol extract of Sophora flavescens Ait. possesses pharmacological activities resembling those of antiarrhythmic agents, but the mechanisms of action are unclear.

Anesthesia, Intravenous↗

PubMed1987

A comparative study on the pyrrolizidine alkaloid content and the pattern of hepatic pyrrolic metabolite accumulation in mice given extracts of Eupatorium plant species, Crotalaria assamica and an Indian herbal mixture.

Plants belonging to the Eupatorium species, E. japonicum Thunb, E. fortunei and E. chinense, were found to contain very low concentrations of pyrrolizidine alkaloid compared with a known hepatotoxic Indian herbal mixture and Crotalaria assamica. High concentrations of pyrrolic metabolite were detected in livers of mice given a single oral dose of extracts of Indian herbal mixture or C. assamica but not in the case of the Eupatorium species. Also, accumulation of pyrrole metabolites was not demonstrated with chronic administration of decoctions prepared from herbs of the Eupatorium species.

Animals↗

PubMed1987

Effects of acute and chronic morphine administration on glucose tolerance in mice.

The effects of acute and chronic morphine treatment on glucose tolerance were investigated in mice. In acute experiments, a single dose of morphine (20 mg/kg i.p.) increased the serum and muscle glucose level. After glucose loading (1.5 g/kg), the rate of increase and the peak of serum glucose concentration were significantly lowered in morphine-treated mice, while the availability and the half-life of glucose were similar to those of controls. In morphine-dependent mice, the fasting serum and muscle glucose levels were similar to those of control but the liver glucose was significantly greater. After glucose loading the rate of increase in serum glucose level was faster and the availability of glucose was 10% greater than that in naive mice. Again, there was no difference in the half-life of serum glucose between naive and morphine-dependent mice.

Animals↗

PubMed1986

Blood pressure homeostasis in the snake, Ptyas korros.

Three putative pressor systems, the alpha-adrenergic system (AS), the renin angiotensin system (RAS), and the arginine vasotocin system (AVT-S), were studied for their roles in blood pressure regulation and their possible interactions in the rat snake. Ptyas korros. Norepinephrine (NE), angiotensin I (ANG I), and arginine vasotocin (AVT) increased the mean arterial pressure (MAP) of the snake while administration of phentolamine, an alpha-adrenergic antagonist, and captopril, an ANG-converting enzyme inhibitor, but not KBIV24, an AVT antagonist, decreased the MAP. Treatment with any combination of two of these antagonists/inhibitor invariably decreased the MAP. Treatment with the agonist of the remaining third system invariably returned the MAP to normal or above. Phentolamine and KBIV24 attenuated the vasopressor effect of ANG I. Phentolamine and captopril enhanced the vasopressor effect of AVT. The pressor effect of NE was not altered by KBIV24 and captopril. It was concluded that there were at least two pressor systems (AS and RAS) regulating the basal MAP in the snake. There was also interaction among the three systems which could affect the MAP.

Angiotensin I↗

PubMed1986

The antiarrhythmic effects of Sophora flavescens Ait. in rats and mice.

The effects of an ethanol extract of the plant Sophora flavescens Ait. on cardiac arrhythmias induced by coronary artery ligation in rats, and by aconitine infusion in mice, were studied. Pretreatment with intravenous injection of the extract, 120 mg/kg, significantly reduced the incidence and delayed the onset of ventricular tachycardia in rats subjected to ligation of the left coronary artery. The time of onset of both initial cardiac arrhythmias and persistent ventricular tachycardia induced by aconitine infusion in mice was also significantly prolonged. These preliminary findings suggest that the ethanol extract of Sophora flavescens Ait. possesses antiarrhythmic activity.

Aconitine↗

PubMed1985

Changes induced by corticosterone and adrenalectomy in synaptosomal and platelet uptake and binding of 5-HT. The relationship to [3H]imipramine binding.

A comparative study of the effect of adrenalectomy, treatment with corticosterone, and imipramine on platelet an synaptosomal uptake was undertaken. One day after adrenalectomy, uptake of 5-hydroxytryptamine (5-HT) in the platelet and the hypothalamus was significantly decreased with an increase in the apparent Km, but the uptake of 5-HT of the cerebral synaptosomes was unchanged. In this group, the Kd of low affinity binding of 5-HT was also increased in the hypothalamic synaptosomes and in the platelet preparations. Treatment with corticosterone (5 mg/kg, i.m.) restored the decrease in the uptake of 5-HT induced by adrenalectomy in the hypothalamic synaptosomes and in the platelets, and significantly increased the uptake of 5-HT of these fractions in sham-operated rats. The binding of 5-HT was unchanged by acute treatment with corticosterone. The effectiveness of imipramine varied with the preparation and treatment group. The IC50 of the cerebral synaptosomal preparation was greater than that of the hypothalamic synaptosomal preparation. Using this latter preparation, the IC50 for imipramine in adrenalectomised, sham-operated and corticosterone-treated rats were found to be 0.04, 0.09 and 0.25 microM, respectively. These changes in sensitivity to imipramine were not reflected in the binding of [3H]imipramine which was unchanged.

Adrenalectomy↗

PubMed1985

Serotonin uptake and imipramine binding in rat platelets after chronic dexamethasone and amitriptyline treatment.

Chronic adrenocorticotrophin treatment was shown to decrease platelet 5HT uptake, increase Km and decrease Vmax. Similarly, chronic dexamethasone treatment decreased 5HT uptake, but had no effect on the Kd and Bmax of high affinity imipramine binding sites in the platelets. Chronic amitriptyline treatment induced similar changes, with the exception that the drug induced a decrease in the number of high affinity imipramine binding sites. Chronic dexamethasone treatment potentiated the effects of amitriptyline and decreased the IC50 of imipramine and desipramine as 5HT uptake inhibitors in vitro. The results suggest that whereas 5HT uptake is related to high affinity imipramine binding sites, it can be modified independently of the high affinity imipramine binding.

Adrenocorticotropic Hormone↗

PubMed1985

Naloxone interaction with some CNS depressants.

Mice were either pretreated with naloxone (10 mg/kg i.p.) and then injected with a hypnotic, or given a similar dose of naloxone simultaneously with a hypnotic (combination treatment). Neither the naloxone pretreatment nor the combination treatment changed the time of on-set or the sleeping duration of urethane, chloral hydrate or ketamine. However, the naloxone pretreatment markedly decreased the on-set time and prolonged the sleeping duration of phenobarbitone and barbitone; naloxone in combination prolonged the sleeping duration of pentobarbitone, phenobarbitone and barbitone.

Animals↗

PubMed1984

Effect of steroids on the inhibition of platelet 5HT uptake by desipramine and other antidepressants.

The inhibitory effect of desipramine on platelet 5HT uptake was tested ex vivo and in vitro in control, adrenalectomised and triamcinolone-treated rats. In both situations, the inhibitory effect of desipramine was augmented in adrenalectomised rats and decreased in triamcinolone-treated rats. These changes in desipramine sensitivity were accompanied by changes in the uptake kinetic components, Km and Vmax. In in vitro studies, the IC50 of clomipramine, fluvoxamine, zimelidine, imipramine and nomifensine was decreased in adrenalectomised rat platelets and increased in corticosterone-, dexamethasone- or triamcinolone-treated rat platelets. Deoxycorticosterone had no effect. Testosterone only affected the IC50 of desipramine and nomifensine.

Adrenalectomy↗