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Biomedical subjects

S Dai

Publications and source records attributed to S Dai.

At least 127 records · Page 7Linked to original sources

Effects of blood gas/pH abnormalities on the cardiovascular actions of verapamil in rats.

1. The effects of hypoxaemia, hyperoxaemia, alkalosis, acidosis, hypocarbia with alkalosis or hypercarbia with acidosis on the blood pressure and pulse rate responses to verapamil were studied in chloralose-anaesthetized rats. 2. At a fixed stroke volume (10 mL/kg) and rate (80 strokes/min; except for the hypocarbic group at 160 strokes/min), hypoxaemia, hyperoxaemia, hypercarbia with acidosis, or hypocarbia with alkalosis was induced by artificial ventilation with gas mixtures containing 17% O2, 28% O2, 23% O2, with 5% CO2, or 17% O2, without CO2 respectively. Acidosis or alkalosis was produced by intravenous infusion of 1 mol/L HCl or 1 mol/L NaHCO3 respectively, in animals artificially ventilated with room air. 3. Changes in individual blood gas/pH parameters had no significant effect on blood pressure except for acidosis which caused a significant decrease. Effects on pulse rate were significant increases in the alkalosis and hypercarbia groups, decrease in the acidosis group, while in other conditions no significant changes were recorded. 4. In the controls, intravenous injections of verapamil 20-320 micrograms/kg caused dose-dependent increases in mean blood pressure, while effects on pulse rate were not marked. 5. The hypotensive responses to verapamil were significantly alleviated or enhanced in the presence of alkalosis or acidosis respectively. Verapamil also caused greater falls in pulse rate during acidosis. Effects of Po2 changes were not statistically significant. The influence of PCO2 changes remained unclear. 6. The present findings suggest that changes in blood pH may play a more important role than Po2 alterations in affecting the cardiovascular responses to verapamil in the presence of blood gas abnormalities.

Acid-Base Imbalance↗

Cardiovascular responses to verapamil and nifedipine in hypoventilated and hyperventilated rats.

1. The influence of hypoventilation or hyperventilation on blood pressure and pulse rate responses to verapamil and nifedipine was studied in chloralose-anaesthetized rats. 2. Artificial ventilation with room air at a fixed volume of 10 ml kg-1 successfully induced combinations of hypoxaemia, hypercarbia and acidosis at a ventilator rate of 37 strokes min-1 and of hyperoxaemia, hypocarbia and alkalosis at 160 strokes min-1. 3. Hypoventilation caused significant decreases in both the blood pressure and pulse rate, whereas hyperventilation produced significant increases in these parameters. 4. In the controls, intravenous injections of graded doses of either verapamil or nifedipine caused dose-dependent decreases in mean blood pressure. The effects on pulse rate were not marked. 5. The hypotensive effects of verapamil were significantly more intense in hyperventilated rats, whereas those of nifedipine were significantly less pronounced in hypoventilated animals. The hypoventilated rats exhibited a significant dose-dependent decrease in pulse rate in response to verapamil administration. 6. It is concluded that cardiovascular responses to verapamil, nifedipine and probably other calcium antagonists are altered in the presence of blood gas abnormalities.

Animals↗

Changes in preganglionic sympathetic nerve function following chronic morphine treatment in rats.

1. The effects of acute or chronic morphine treatment on the changes in blood pressure and pulse rate in response to ganglionic stimulation or blockade and to vagal stimulation, and of isolated atria to field stimulation or noradrenaline, were studied. 2. In pithed rats, intravenously injected hexamethonium significantly depressed the blood pressure responses to sympathetic nerve stimulation. The ganglionic blocking effects of hexamethonium were significantly greater in chronically morphine-treated rats, but were not significantly affected by acute morphine administration in naive animals. 3. Intravenous administration of nicotine dose-dependently increased blood pressure and pulse rate. The magnitudes of these changes were not significantly affected by acute or chronic morphine pretreatment. 4. Studies with rat isolated atrial preparations revealed that the changes in atrial contractile rate and force in response to noradrenaline or field stimulation were not influenced by either acute or chronic morphine treatment. 5. Cervical vagal stimulation produced voltage- or frequency-dependent decreases in pulse rate and blood pressure. The responses were not significantly affected by chronic morphine treatment. 6. These findings suggest that the site of the changes in sympathetic function following prolonged exposure to the opiate appears to be on the preganglionic nerve fibres.

Animals↗

Age-related differences in the cardiovascular responses to haemorrhagic shock in rats.

The cardiovascular responses to haemorrhagic shock were studied in male Sprague-Dawley rats of different age groups, ranging from 6-15 weeks (body weight 250-460 g). Haemorrhagic shock was induced by bleeding (2% body weight), under urethane anaesthesia, from the cannulated femoral artery at a rate of 1 ml/min. It was found that the younger rats had significantly smaller values of left ventricular pressure and dLVP/dtmax following haemorrhage and a greater mortality rate. Older animals exhibited significantly greater falls in blood pressure and pulse rate during the bleeding procedure, and slower recovery in these parameters after the bleeding was stopped. However, these rats had a significantly higher left ventricular pressure and dLVP/dtmax following haemorrhage, and a markedly lower mortality rate. The findings demonstrate the existence of age-related cardiovascular responses to haemorrhagic shock in rats.

Aging↗

[Survey of Bacillus thuringiensis and Bacillus sphaericus from soils of four provinces of China and their principal biological properties].

A number of isolates of Bacillus thuringiensis and Bacillus sphaericus were obtained from soils of Southwestern Area and Shaanxi Province of China. Among isolates of B. thuringiensis were under 13 sorts of serotype in total of 23 sorts of B. thuringiensis and about 20% of auto-agglutinate strains. Rules of ecologic distribution of two sorts of bacteria were analysed. Toxicities on six species of insects, morphology and crystal proteins of B. thuringiensis, as well as toxicities, morphology and crystal proteins of B. sphaericus, were investigated. 22 strains of more efficient of B. thuringiensis and 2 strains of more efficient of B. sphaericus were obtained. It was shown that B. thuringiensis is actually soil microorganism, and resource of B. thuringiensis is much fruitful in Southwestern Area of China.

Bacillus↗

Heroin self-administration by rats: influence of dose and physical dependence.

Lever-pressing behavior reinforced by intravenous infusion of various concentrations of heroin, and consequent development of physical dependence, were examined in rats. In addition, the influence of opiate dependence, and of its disappearance following withdrawal, on heroin self-administration were investigated. It was found that intravenous self-administration of heroin at 0.03 mg/kg/infusion maintained self-administration behavior without producing physical dependence. Total responses per session decreased with increasing unit dose of heroin, whereas the total amount of drug self-administered was directly related to unit dose. Significantly greater numbers of withdrawal signs and percentage body weight losses in response to naloxone injections were observed following self-administration of heroin at 0.1, 0.3 or 0.6 mg/kg/infusion. Intake of heroin at 0.03 mg/kg/infusion, but not at 0.1, 0.3 or 0.6 mg/kg/infusion, was found to increase significantly in opiate-dependent and postdependent animals. These findings support the previous use of 0.03 mg/kg/infusion as a suitable dose for illustrating the reinforcing effect of heroin without the influence of physical dependence.

Animals↗

Plasma, cardiac tissue and brain morphine concentrations in acute and chronic morphine-treated rats.

1. The plasma, cardiac tissues and brain morphine concentrations in rats after acute or chronic morphine treatment were measured by high-performance liquid chromatography. 2. Morphine concentrations in plasma and cardiac tissues were found to be significantly higher than those in brain after acute morphine injection. However, after chronic oral administration, morphine concentrations in plasma, cardiac tissues and brain were similar. 3. Brain concentrations of morphine following chronic administration were higher than those obtained after acute administration although concentrations in plasma and cardiac tissues were lower.

Animals↗

Histamine enhances hypoxia-induced ventricular arrhythmias in isolated rat hearts.

1. The effects of hypoxia, histamine-receptor agonist perfusion, and their combination on cardiac rhythm were studied in isolated rat hearts. 2. While hypoxia induced a high incidence of ventricular tachycardia or fibrillation, only a few preparations developed ventricular arrhythmias in response to perfusion with high concentration of histamine, 2-pyridylethylamine or impromidine. 3. The times of onset of hypoxia-induced ventricular arrhythmias were significantly shortened by perfusion with either histamine, 2-pyridylethylamine or impromidine. The accelerated occurrence of hypoxia-induced ventricular arrhythmias by histamine was significantly abolished by pretreatment with either diphenhydramine or cimetidine. 4. The results indicate that hypoxia and histamine can increase ventricular vulnerability of the rat heart to each other. It is also suggested that the arrhythmogenic actions of histamine in hypoxic rat hearts are mediated by both histamine H1-and H2-receptors.

Animals↗

Arterial catecholamine levels in morphine-treated rats subjected to sympathetic nerve stimulation.

1. The effect of acute or chronic morphine treatment on the changes in arterial noradrenaline and adrenaline levels in response to sympathetic nerve stimulation was studied in rats. 2. Rats which had been chronically treated with morphine in their drinking fluid for 21 days were shown to be morphine-tolerant, as revealed by the tail-immersion test for analgesia. 3. It was found that animals given either acute or chronic morphine treatment had similar basal concentrations of arterial catecholamines to their controls. 4. Sympathetic nerve stimulation produced significant increases in arterial noradrenaline and adrenaline levels in both the control and morphine-treated animals. However, the degree of arterial noradrenaline elevation was significantly less in morphine-tolerant animals. 5. This phenomenon was not observed in acutely morphine-treated rats or at 2 weeks following opiate withdrawal in animals which had been treated previously with morphine for 3 weeks. 6. The findings suggest that chronic morphine treatment in rats not only leads to opiate tolerance but also reduces catecholamine release in response to sympathetic nerve stimulation.

Animals↗

Anaesthetic-related occurrence of early ventricular arrhythmias during acute myocardial ischaemia in rats.

The cardiovascular responses of rats anaesthetised with different anaesthetic agents to acute coronary artery ligation were studied. Before thoracotomy, urethane-anaesthetised animals exhibited significantly lower blood pressures. Ligation of the left coronary artery induced a high incidence of ventricular tachycardia or fibrillation in rats anaesthetised with pentobarbitone, urethane, or ether inhalation followed by chloralose. Ketamine-anaesthetised animals had a significantly lower incidence of ventricular arrhythmias. The mortality rate was also lower, though not statistically significant. However, all groups of rats showed essentially similar blood pressure and heart rate changes following coronary artery ligation as well as the time of onset of ventricular tachycardia or fibrillation. The findings demonstrate the influence of anaesthetics on the occurrence of early ventricular arrhythmias following acute coronary artery ligation in rats.

Anesthesia↗

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↗

Antigen-antibody complex-induced immunosuppression. Effect of F(ab')2 antibodies and protein A.

The addition of immune complexes (anti-horse red blood cell (HRC) antibodies plus HRC) to spleen cell cultures activated by lipopolysaccharide (LPS) selectively suppressed the anti-HRC plaque-forming cell (PFC) response, but did not affect the PFC response to sheep red blood cells (SRC). The degree of suppression was directly related to the concentration of immune complexes. F(ab')2 preparations suppressed as efficiently as intact IgG, although the ability of the F(ab')2 preparation to lyse the red cells was abolished. The addition of protein A to the immune complexes (using intact antibodies) did not affect the degree of suppression. The findings suggest that immune complex-induced suppression of polyclonal B cell activation is caused by constant parts of the light or heavy chains of the antibodies other than the Fc part.

Animals↗

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↗

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↗

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↗

Morphine reduces vagal-stimulated gastric acid secretion through a central action.

The influence of morphine on gastric acid secretion stimulated by 2-deoxy-D-glucose or electrical vagal stimulation was studied in anaesthetised rats with perfused stomachs. It was found that changes in gastric acid output induced by electrical vagal stimulation were not noticeably affected, whereas those evoked by 2-deoxy-D-glucose were significantly suppressed by morphine pretreatment. The depressant effect of the opiate on the acid secretion stimulated by 2-deoxy-D-glucose was abolished by naloxone pretreatment. It is suggested that morphine inhibits vagal-stimulated gastric acid secretion in rats by acting predominantly on opioid receptors in the central nervous system.

Animals↗