Moumlssbauer studies of Ta1-xFexS3 (0.0012 <= x <= 0.5) and their charge-density waves.
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Journal Article↗
Biomedical subjects
S Dai
Publications and source records attributed to S Dai.
Ventricular histamine concentrations and arrhythmias during acute myocardial ischaemia in rats.
The relation between ventricular histamine concentrations and the occurrence of early ventricular arrhythmias during acute myocardial ischaemia was investigated in pentobarbitone-anaesthetized rats. There was significant decrease in the left, but not the right, ventricular histamine level at 5 min following acute left coronary artery ligation. Pretreatment with rhodanine caused remarkable reduction in ventricular histamine concentrations as well as significantly lower incidence and slower onset of ventricular tachycardia and fibrillation resulting from acute myocardial ischaemia. On the contrary, aminoguanidine pretreatment did not significantly alter ventricular histamine levels nor did it influence the occurrence of early ventricular arrhythmias induced by coronary artery ligation. The responses of blood pressure and heart rate to acute coronary artery ligation were not noticeably affected by rhodanine or aminoguanidine pretreatment. These findings support the hypothesis that histamine release from cardiac tissues may contribute to the genesis of early ventricular arrhythmias, but not to the changes in blood pressure and heart rate, during acute myocardial ischaemia.
Acute Disease↗
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↗
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↗
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↗
Age-related cardiovascular responses of rats to coronary artery ligation.
The cardiovascular responses of rats of different ages, ranging from 4-15 weeks (body weight 115-490 g), to acute left coronary artery ligation under pentobarbitone anaesthesia were studied. In older animals, the responses included the occurrence of ventricular tachycardia and/or fibrillation, decrease in blood pressure, and a slight increase in heart rate. On the contrary, younger rats exhibited atrioventricular block followed by ventricular arrest, and decreases in both blood pressure and heart rate. The findings demonstrate the existence of age-related cardiovascular responses to acute myocardial ischaemia in rats, and suggest that 10-15-week-old male Sprague-Dawley rats are suitable experimental animals for producing early ventricular arrhythmias by acute coronary artery ligation.
Aging↗
Treatment of acute lymphoblastic leukemia in children. A 12-year experience with an analysis of the role of cooperative group (CCLSG) participation.
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Adolescent↗
Effects of morphine, hypoxaemia and hypercapnia on the rat stomach.
The effects of morphine, hypoxaemia or hypercapnia on gastric acid secretion, gastric mucus synthesis and the gastric mucosa were studied in conscious rats with pyloric occlusion. Hypoxaemia and hypercapnia were induced by morphine 32 mg/kg given i.p., or each condition was produced separately by adjusting the composition of respired air in the chamber where the animals were kept during the experimental period. Hypoxia significantly enhanced gastric mucus synthesis whereas hypercapnia significantly reduced gastric acid secretion. These effects were significantly alleviated by atropine pretreatment. Morphine-treated rats exhibited decreased gastric acid secretion, increased gastric mucus synthesis and a higher mean ulcer index but only the reduced gastric acid output was significantly prevented by atropine. It is suggested that the effect of morphine on gastric acid secretion may result from its respiratory depressant action and consequent acute stress production. However, the mechanisms by which morphine can increase mucus synthesis and produce ulceration remain obscure.
Animals↗
Morphine enhances gastric mucus synthesis in rats.
The effect of morphine on gastric mucus synthesis was studied in conscious rats, using the method of staining mucus with alcian blue then destaining it with magnesium chloride. It was found that morphine significantly enhanced gastric mucus synthesis, as did fentanyl, a non-histamine-liberating opioid. The effects of the opioids on mucus synthesis were significantly attenuated by pretreatment with naloxone 8 mg/kg or cimetidine 100 mg/kg. Cimetidine itself significantly suppressed gastric mucus production in saline-treated rats. These findings suggest that the increased gastric mucus synthesis caused by morphine is due to activation of opiate receptors and not to histamine release. It appears that cimetidine may counteract rather than block the receptor effects of the opioids by a direct action on the mucus-secreting glands.
Animals↗
Effects of ranitidine and cimetidine on experimentally induced ventricular arrhythmias in anaesthetized rats.
The effects of two histamine H2-receptor antagonists, ranitidine and cimetidine, on ventricular arrhythmias induced by acute coronary artery ligation and by aconitine infusion were studied in pentobarbitone-anaesthetized rats. The changes in arterial blood pressure and heart rate were also observed. It was found that both drugs significantly reduced the incidence, and prolonged the time of onset, of ventricular tachycardia and ventricular fibrillation following acute coronary artery ligation; however, they did not significantly alter the incidence or time of onset of ventricular dysrhythmias caused by aconitine infusion. These findings further support the hypothesis that histamine release may contribute to the genesis of early ventricular arrhythmias resulting from acute myocardial ischaemia. Since the decreased blood pressure induced by coronary artery ligation was not significantly prevented by pretreatment with either histamine H2-receptor blocker, this suggests that histamine may not be responsible for the blood pressure changes during acute myocardial ischaemia.
Aconitine↗
Cardiovascular effects of ranitidine and cimetidine during acute myocardial ischaemia in anaesthetized dogs.
The effects of ranitidine and cimetidine on ventricular fibrillation threshold and haemodynamics were studied in pentobarbitone-anaesthetized dogs subjected to acute coronary artery ligation. These drugs did not significantly change the ventricular fibrillation threshold nor haemodynamics before coronary artery ligation, except for remarkable haemodynamic depression by ranitidine 1 mg/kg. Ligation of the left anterior descending coronary artery reduced the ventricular fibrillation threshold, decreased systemic and left ventricular pressures and myocardial contractility, and slightly increased heart rate. Pretreatment with ranitidine 0.25 or 1 mg/kg, or with cimetidine 2 mg/kg, significantly abolished the reductions in ventricular fibrillation threshold, but did not noticeably alter the haemodynamic changes. These findings further support the hypothesis that histamine release may contribute to the increased ventricular vulnerability resulting from acute myocardial ischaemia. However, the role of histamine in the haemodynamic responses to coronary artery ligation remains obscure.
Animals↗
Gastric acid secretory responses to cholinergic and histaminergic stimulation in chronic morphine-treated rats.
The effects of chronic morphine administration on cholinergic and histaminergic activities were evaluated in rats by observing their gastric acid secretory responses to secretagogues. The responses of in-vivo perfused stomachs to 2-deoxy-D-glucose or pentagastrin, and of the isolated gastric mucosa to histamine or bethanechol, were not significantly different between naive and chronic morphine-treated animals. It is suggested that the chronic morphine-treated rats exhibit normal cholinergic and histaminergic activities as well as receptor sensitivities to acetylcholine and histamine.
Animals↗
Cardiovascular responses to sympathetic nerve stimulation in morphine-treated rats.
The effects of morphine on the responses of blood pressure and pulse rate to stimulation of sympathetic nerves or to intravenous administration of noradrenaline were studied in female rats which had been treated with either an increasing concentration of morphine sulphate in their drinking fluid (5% sucrose solution), or an acute intraperitoneal injection of morphine. Sympathetic nerve excitation was effected by electrical stimulation of the thoracic segments of the spinal cord in pithed rats. Both sympathetic nerve stimulation and noradrenaline produced dose-dependent changes in blood pressure and pulse rate in naive rats and in the sucrose-drinking controls. Animals which had been chronically treated with morphine in their drinking fluid for 21 days showed significantly less intense responses to sympathetic nerve stimulation. However, these decreased responses were not observed in rats given acute treatment with morphine. Chronic treatment with morphine did not significantly influence the changes in blood pressure or pulse rate induced by noradrenaline. These findings suggest that chronic treatment with morphine lessens the cardiovascular responses to stimulation of peripheral sympathetic nerves in rats. The mechanism is not clear, but it seems unlikely to be due to changes in the sensitivity, or perhaps the number, of adrenoceptors.
Animals↗
Rapid induction of dependence to morphine in rats.
The rate of development of dependence to morphine was studied in female rats which were given increasing concentrations of morphine sulphate in their drinking fluid (5% sucrose solution). The occurrence of physical dependence was determined by the naloxone-precipitated withdrawal syndrome at various times during the 3-week experimental period. It was found that a significant degree of the withdrawal syndrome precipitated by naloxone was evident at 24 hr after starting administration of morphine; the syndrome reached its greatest intensity after the rats had received the opiate for 7 days. This study shows that dependence on morphine can be induced in rats by administration of the opiate in drinking fluid for a period shorter than 7 days.
Animals↗
Production of physical dependence in rats by drinking a morphine solution.
The plasma concentrations of morphine and glucose, the body weight, and the severity of the naloxone-precipitated withdrawal syndrome were studied in female rats in which morphine dependence was induced by administration of the opiate, with or without sucrose, in their drinking water. It was found that sucrose encouraged the animals to consume more morphine and that the initial plasma concentrations of the opiate, as well as the rate of development of physical dependence, were higher than the group not given sucrose. Plasma glucose concentrations, maximum plasma morphine levels and the maximum severity of the naloxone-precipitated withdrawal syndrome were, however, not significantly different between the two groups. The findings suggest that both regimens of administering the opiate in drinking fluid are effective in inducing morphine dependence in rats; the addition of sucrose tends to speed up the development of physical dependence, probably by increasing intake of the opiate through consuming more sucrose solution.
Administration, Oral↗
Mechanisms of captopril-induced potentiation of the depressor responses to arachidonic acid in rats.
The mechanisms underlying potentiation by captopril of the depressor responses to arachidonic acid were studied in chloralose-anaesthetized rats. Captopril, in a dose (0.5 mg/kg, i.v.) which inhibited the pressor responses to angiotensin I (0.03-1 microgram/kg, i.v.), enhanced the depressor responses to bradykinin (3-300 micrograms/kg, i.v.) and potentiated the hypotensive action of arachidonic acid (3 mg/kg, intravenously). This phenomenon was observed not only when captopril and arachidonic acid were administered intravenously, but also when these compounds were injected directly into the aortic arch. The enhancement of arachidonic acid-induced hypotension by captopril was not significantly affected by pretreatment with a low dose of aprotinin (3 mg/kg, i.v.), but was abolished by bilateral nephrectomy or by pretreatment with a higher dose of aprotinin (6 mg/kg, i.v.). It is suggested that captopril augments the depressor responses to arachidonic acid by inhibiting angiotensin converting enzyme. This results in accumulation of bradykinin which in turn increases release of vasodilator prostaglandins, originating most probably, from the kidneys. The possibility that blockade of angiotensin II formation by captopril may leave the vasodilator action of prostaglandin unopposed cannot be excluded.
Angiotensin I↗
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↗
Effects of carbenoxolone sodium on gastric and duodenal mucus synthesis in mice.
Using the method of staining mucus with Alcian blue and destaining it with magnesium chloride, it was found that intragastric administration of carbenoxolone in mice did not significantly affect duodenal mucus synthesis at doses which remarkably increased gastric mucus synthesis. However, in vitro study showed that carbenoxolone significantly stimulated both gastric and duodenal mucus synthesis. It is suggested that carbenoxolone may also effectively increase mucus synthesis and probably accelerate ulcer healing in the duodenum if sufficient amounts can escape gastric absorption and reach this region.
Alcian Blue↗