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Biomedical subjects

S Dai

Publications and source records attributed to S Dai.

At least 109 records · Page 6Linked to original sources

Hemodynamic and nonhemodynamic mechanisms of experimental pulmonary edema in rats and the effects of anisodamine and tetramethylpyrazine--estimation of blood gas analysis, RBC superoxide dismutase and prostaglandin E2 in plasma and bronchoalveolar lavage (Part 3).

Anisodamine (ADM, 654-2, 30 mg/kg) and tetramethylpyrazine (TMP, 120 mg/kg) have shown an apparent preventive effect on pulmonary edema (PE). In this study, the nonhemodynamic mechanism was studied: The dynamic changes of PaO2, O2Sat, PaCO2, and blood pH were measured, and RBC superoxide dismutase (SOD) and plasma and bronchoalveolar lavage (BAL) PGE2 levels were estimated. It was concluded that ADM and TMP exerted inhibitory effects on the hypoxic state. The ability of ADM and TMP to adjust RBC SOD and PGE2 levels may be one of the preventive mechanisms of the drugs.

Animals↗

[Histochemical studies on the glycoconjugates of experimental alkali burned cornea in rabbit].

The model of experimental alkali burn of cornea in rabbit was obtained using 1 mol/L NaOH solution. After being burned for 1, 3, 7 and 14 days, the histochemical changes of these models were studied by using labelled concanavalin A (ConA-FITC) and wheat germ agglutinin (WGA-FITC). The results showed that after being burned, the amount of glycoconjugates interacted with these lectins decreased, and increased gradually after 7 days, then reached the level higher than that in the normal cornea. These changes were related to the recovery of alkali burned cornea.

Animals↗

Hemodynamic and nonhemodynamic mechanisms of experimental pulmonary edema in rats and the effect of anisodamine and tetramethylpyrazine. Part 1: Survival rate, pulmonary index, pathological change and pulmonary vascular permeability.

Pulmonary edema (PE) which is similar to the neurogenic type was induced by adrenaline (AD) administration (0.1 mg/kg) in rats. Acute progressive respiratory distress, cyanosis and dyspnea occurred. All the experimental animals in the PE group died within 20 min after AD injection, with a pulmonary index (PI) of 1.70 +/- 0.47 (mean +/- S) which was much higher than that in the normal group. The mortality rate was 100%. It was found that in rats with PE, a protein-rich fluid filled the alveolar and interstitial spaces, and ecchymosis occurred. The capillary permeability as estimated by Evans blue injection showed that Evans blue from extraction fluid and bronchoalveolar lavage (BAL) in the PE rats was at a much higher level than that in the normal control (NC) rats. In anisodamine (ADM, 654-2) and tetramethylpyrazine (TMP) treated rats, almost all the damage was diminished or absent, and the mortality rates were decreased from 100% to 4.4% and 20%, respectively. 654-2 and TMP could significantly inhibit the increase of pulmonary permeability.

Animals↗

Blood pH and the actions of nifedipine on cardiac excitation-contraction coupling.

Hearts from male Sprague-Dawley rats were perfused, by the Lagendorff method, with calcium-free Krebs solution (containing either adrenaline or a high level of potassium) at pH 7.48 (control), 7.26 (acidosis) or 7.69 (alkalosis). When the hearts stopped contracting, a dose of nifedipine or its vehicle was given before measuring the force of contraction, coronary perfusion pressure and heart rate in response to graded doses of calcium. The calcium-antagonising efficacy of nifedipine was reduced during acidosis in both adrenaline- and potassium-stimulated hearts, but the reduction was greater in the adrenaline-stimulated hearts. Alkalosis led to a small increase in the efficacy of nifedipine on adrenaline- and potassium-stimulated contractions.

Animals↗

Role of peptido-leukotrienes in the genesis of early ventricular arrhythmias during acute myocardial ischaemia in rats.

Changes in cardiac ventricular concentrations of peptidoleukotrienes (peptido-LTs) following coronary artery ligation and the effects of lipoxygenase inhibition and leukotriene antagonism on the cardiovascular responses to acute myocardial ischaemia were studied in pentobarbitone-anaesthetised rats. It was found that the left ventricular peptido-LT levels significantly increased at 2.5 and 5 min after left coronary artery ligation while the changes in right ventricle were not statistically significant. Pretreatment with nordihydroguaiaretic acid 25, 50 or 100 mg/kg caused marked depletion of ventricular peptido-LT content, but did not significantly prevent the blood pressure or heart rate changes, the occurrence of ventricular tachycardia or fibrillation, or the mortality of the animals following coronary artery ligation. Administration of SK&F 102922, even at doses which caused marked decreases in blood pressure and heart rate, also did not significantly alter the cardiovascular changes and the mortality rate induced by left coronary artery ligation. It is, therefore, suggested that the occurrence of ventricular arrhythmias and haemodynamic changes during the early phase of acute myocardial ischaemia may not be due to the augmented synthesis of peptido-LTs in cardiac tissue.

Acute Disease↗

Effects of deoxycorticosterone acetate on glucose metabolism in nondiabetic and streptozotocin-diabetic rats.

A previous study in our laboratory showed that streptozotocin (STZ) induced diabetic, deoxycorticosterone acetate (DOCA) induced hypertensive rats exhibited significantly lower levels of plasma glucose than did normotensive diabetic animals. The present experiments further investigate the effects of DOCA treatment on fasting levels of plasma glucose and insulin and on their changes after oral glucose challenge in nondiabetic and STZ-diabetic rats. It was found that, in nondiabetic rats, DOCA-induced hypertension was associated with normal glucose levels and glucose tolerance but with significantly lower levels of plasma insulin. DOCA-treated diabetic animals showed significantly lower levels of plasma glucose, but their plasma insulin concentrations were not significantly different from those of the DOCA vehicle treated diabetic rats. DOCA-treated diabetic rats also had significantly higher plasma levels of cholesterol and triglycerides. It is suggested that DOCA may have a direct or indirect action on the assimilation, production, or utilization of glucose, perhaps leading to an improvement in insulin sensitivity and subsequently a decrease in insulin secretion.

Analysis of Variance↗

Effects of fructose loading in streptozotocin-diabetic and nondiabetic rats.

The present study compares the cardiovascular consequences of a 6-week fructose feeding in nondiabetic and streptozotocin-diabetic rats. Myocardial performance of these animals was determined using the isolated perfused working heart preparation. Systolic blood pressure, pulse rate, ventricular weight/body weight ratio, and plasma levels of glucose, insulin, triglycerides, and cholesterol were measured. In nondiabetic rats, fructose drinking caused significant increases in blood pressure, pulse rate, and plasma concentrations of insulin and triglycerides. Streptozotocin-diabetic animals exhibited significantly less body weight growth, slower pulse rate, higher plasma levels of cholesterol and triglycerides, ventricular enlargement, and functional impairment of the myocardium. The fructose-loaded diabetic rats had larger increases in plasma cholesterol and triglycerides than did control fructose-fed rats, but the fructose-induced increases in blood pressure and pulse rate were attenuated significantly. However, plasma levels of glucose and insulin and the degree of ventricular enlargement and myocardial dysfunction were not significantly different from those of control diabetic rats. These results show that fructose loading for 6 weeks can cause increases in blood pressure, pulse rate, and plasma lipids in both nondiabetic and diabetic rats. However, fructose ingestion does not significantly alter glycemic control or affect the development of myocardial dysfunction in streptozotocin-diabetic rats.

Animals↗

Myocardial performance of STZ-diabetic DOCA-hypertensive rats.

Myocardial performance of streptozotocin (STZ)-diabetic deoxycorticosterone acetate (DOCA)-hypertensive rats was examined using the isolated working heart apparatus at various time periods after induction of the experimental diseases. Blood pressure, pulse rate, and plasma levels of glucose, insulin, cholesterol, and triglycerides, as well as ventricular weight-to-body weight ratio, were also determined. In nondiabetic rats it was found that DOCA hypertension was associated with an increase in plasma cholesterol, a decrease in circulating insulin level, lower weight gain, and ventricular enlargement compared with control rats. Diabetic rats developed myocardial dysfunction in a time-dependent manner and exhibited hyperglycemia, hypoinsulinemia, bradycardia, and ventricular enlargement. Compared with the normotensive diabetic animals, STZ-diabetic DOCA-hypertensive rats showed a similar magnitude of myocardial dysfunction and a greater degree of ventricular enlargement, but significantly less severe hyperglycemia. It is concluded that DOCA-induced hypertension does not aggravate the severity of myocardial dysfunction developed in STZ-diabetic rats. It is also suggested that DOCA may have an action on glucose metabolism either directly or via an effect on insulin secretion.

Animals↗

[Morphology and delta-endotoxin proteins of Bacillus thuringiensis from soils and their toxicities to insects].

94 strains of Bacillus thuringiensis were isolated from soils in southwest and northwest of China. The morphology of cells, spores and parasporal crystals of these strains was investigated under transmission and scanning electro-microscope. Proteins of delta-endotoxins from all strains were analysed by rapid SDS-PAGE. 9 species of insects in Lepidoptera, Coleoptera and Diptera were tested for assay of delta-endotoxins. Some kinds of parasporal crystals were quite different in form and in composition of protein from those reported before. Most of strains were nontoxic to all of 9 species used in bio-assay. Some strains were very effective in species of Coleoptera or Noctuidae.

Animals↗

[Doppler and echocardiographic study of normal systolic murmurs].

To elucidate the genesis of normal ejection systolic murmurs, we performed phono and Doppler echocardiography in 42 normal subjects. Individuals with hypertension, ST.T changes on ECG, anemia or other cases with definite cardiovascular findings were excluded from the study. Their ages ranged from 22 to 61 years with an average of 48.1 years. They were classified in 2 groups; 9 with Levine 2/6 systolic murmur and 33 without murmur or with 1/6 murmur. Fifteen patients with pure aortic regurgitation or with aortic prosthesis but without significant stenosis, and 7 patients with pulmonic valvular stenosis were served as control. We correlated the intensity and timing of murmur with maximal flow velocity, acceleration time and other parameters. All systolic murmurs were early systolic. Mid-systolic murmur was not noted. Peak of flow velocity increased at the aortic orifice than at the left ventricular outflow tract or pulmonary orifice. Left-sided peak flow velocity occurred earlier than the right-sided peak flow velocity. Early systolic maximal flow velocity of the aorta significantly increased in 9 subjects with murmur than in the remaining 33 without significant murmur. Ejection fraction, hematocrit and body surface area did not differ between the groups with and without significant murmur. Systolic blood pressure and age, however, were higher in subjects with murmur. In aortic valvular disease, systolic murmurs and peak flow signals were early systolic, but in pulmonary stenosis these were mid-systolic in timing. In conclusion, normal ejection systolic murmurs were early systolic and originated at the aortic orifice. Mid-systolic murmurs were unlikely as left-sided murmur in origin. Flow velocity was the most important determinant of the intensity of ejection murmur.

Adult↗

[Cardiovascular risk factors of visitors to a mass-screening booth].

The attitude towards mass screening of serum cholesterol is controversial. In order to characterize the volunteers of such screenings and to test the representativity of its findings, we compared the data of 1686 adult health-screening participants collected during a trade fair in the city of Basel, Switzerland, with the results of two population-based studies, the Basel City Risk Factor Survey and the MONICA Project in Western Switzerland. Among those screened, there was an over-representation of women and older persons. The age-specific medians of blood cholesterol and proportions of hypercholesterolemic persons were consistently higher in female screenees--and marginally so in males--than in the reference populations, whereas higher proportions of persons with ideal cholesterol level in those screened were also observed, especially in younger males. Higher systolic blood pressure, lower relative body weight and less regular smoking were found consistently among the screenees. This cross-sectional study shows that the participants of such mass screening actions are a selective group of older, more frequently female health-conscious persons with a specific risk-factor pattern. Mass screenings of self-selected volunteers can, therefore, not be used for a reliable prediction of risk-factor distributions in the general population. Moreover, suggested further steps for those screenees with both health-conscious behavior and elevated biological risk-factor levels, such as second measurement, medical consultation and counselling, cannot be assured in the setting of a trade fair. The objectives and intentions of such mass screening activities should be reconsidered and discussed.

Adult↗

Influence of pH changes on the actions of verapamil on cardiac excitation-contraction coupling.

Langendorff preparations of Sprague-Dawley rat hearts were perfused with calcium-free Krebs solution of pH 7.48 (control), 7.26 (acidosis) or 7.69 (alkalosis) containing either adrenaline or potassium. The responses of the force of contraction, coronary perfusion pressure and heart rate to graded doses of calcium preceded by a single dose of verapamil were measured. Contractile responsiveness to calcium was reduced during acidosis in both adrenaline- and potassium-stimulated hearts but was increased or reduced during alkalosis with adrenaline- or potassium stimulation, respectively. The efficacy of verapamil as a calcium antagonist increased during acidosis or alkalosis in both adrenaline- and potassium-stimulated hearts. In conclusion, acidosis or alkalosis inhibits potassium-stimulated contractions of the heart and enhances the effects of verapamil on potassium- and adrenaline-mediated contractions. Acidosis inhibits and alkalosis enhances adrenaline-stimulated contractions.

Acidosis↗

Circulatory depression and ventricular arrhythmias induced by compound 48/80 in anaesthetized rats.

The effects of graded doses of compound 48/80 on various cardiovascular and respiratory parameters were studied in pentobarbitone-anaesthetized rats. Following intravenous injections, this compound significantly depressed the mean blood pressure (MBP), left ventricular pressure (LVP) and dLVP/dtmax, and caused ventricular tachycardia (VT) or fibrillation (VF) and death. Heart rate (HR) response were variable, and there were no marked changes in airway resistance or blood gases. Pretreatment of the animals with either cimetidine or diphenhydramine significantly prolonged the time of onset of VT/VF but failed to alter the changes in other circulatory variables. A combination of cimetidine and diphenhydramine significantly alleviated the decreases in MBP and LVP and prevented the occurrence of VT/VF. It is suggested that the circulatory depression and the occurrence of ventricular arrhythmias following the administration of compound 48/80 result from activation of H1- and H2-receptors by elevated blood histamine levels due to release of the amine from tissues.

Animals↗

Cardiovascular responses to nifedipine in anaesthetized rats with abnormal blood gas/pH levels.

1. Blood pressure and pulse rate responses to intravenously (i.v.) administered nifedipine were studied in chloralose-anaesthetized rats subjected to hypoxaemia, hyperoxaemia, alkalosis, acidosis, hypocarbia with alkalosis, or hypercarbia with acidosis. 2. Ventilation with a gas mixture of 17% O2, 28% O2, or 23% O2 with 5% CO2 at a fixed stroke volume (10 mL/kg) and rate (80 strokes/min) induced hypoxaemia, hyperoxaemia or hypercarbia, respectively. Hypocarbia was induced by ventilation with 17% O2 at 160 strokes/min. Acidosis or alkalosis was produced by intravenous infusion of 1 mol/L HCl or 1 mol/L NaHCO3, respectively, in animals ventilated with room air. 3. There were significant decreases in blood pressure and pulse rate during acidosis, and increases in pulse rate during alkalosis and hypercarbia. No marked changes in these parameters were observed under the other experimental conditions. 4. The control animals showed a dose-dependent decrease in blood pressure without marked changes in pulse rate in response to nifedipine injection. 5. Significant reductions in the hypotensive effect of nifedipine were observed in rats subjected to alkalosis, acidosis, or hypercarbia. A similar tendency was also found during hypocarbia while the responses to nifedipine during hypoxaemia and hyperoxaemia were statistically the same as those in the controls. 6. It is concluded that alterations of blood pH reduce the hypotensive effect of nifedipine, and we suggest that blood pH changes probably play a more important role than PO2 or PCO2 abnormalities in altering the cardiovascular responses to nifedipine in hypoventilated or hyperventilated rats.

Acidosis↗

Naloxone-induced cardiovascular depression in rats that had received chronic morphine-treatment.

1. Cardiovascular changes in response to intravenous injection of naloxone were studied in pentobarbitone-anaesthetized rats which had been given morphine in their drinking water for 1-21 days. The mechanisms of the observed changes were investigated in intact animals and in isolated hearts and tail arteries. 2. In rats that had received chronic morphine-treatment, intravenous administration of naloxone caused immediate decreases in blood pressure, heart rate, left ventricular pressure and dLVP/dtmax which were followed by the occurrence of atrial or ventricular extrasystoles and other signs of opiate withdrawal such as faecal passage and muscle twitching. 3. The intensities of the naloxone-precipitated cardiovascular changes were directly related to the duration of chronic morphine pretreatment, reaching statistically significant levels on day 2 or 3 and maximal levels on day 7 or 14. This phenomenon disappeared on days 3 to 14 following opiate withdrawal in animals which had been treated previously with morphine for 21 days. 4. Either atropine or clonidine pretreatment significantly prevented the occurrence of faecal passage or muscle twitching during naloxone-precipitated opiate withdrawal. However, clonidine, but not atropine or yohimbine, abolished the decreases in various haemodynamic parameters. The occurrence of cardiac extrasystoles was not affected. 5. In isolated heart or tail artery preparations from chronically morphine-treated rats, naloxone administration did not elicit reactions which differed from those of the preparations from naive animals. These findings suggest that under pentobarbitone anaesthesia, the cardiovascular systems of rats that had received chronic morphine treatment exhibit inhibitory, instead of excitatory, reactions to naloxone-precipitated opiate withdrawal.

Anesthesia↗

In-vivo and in-vitro studies on the effects of chronic dexamethasone treatment on cardiovascular responses to sympathetic stimulation.

Rats treated with dexamethasone, 1.5 mg/kg s.c. weekly for 3 weeks exhibited significantly greater increases in mean arterial pressure than their controls, following either sympathetic nerve stimulation or noradrenaline administration. The atria from dexamethasone-treated rats showed greater chronotropic activity in response to noradrenaline but not to field stimulation, whereas the force of contraction was significantly less than that of the controls after either field or noradrenaline stimulation. Isolated rat tail artery preparations from dexamethasone-treated rats were found to be twice more sensitive to noradrenaline than the controls. Prazosin antagonised the noradrenaline-induced pressor response to the same extent in control and dexamethasone-treated rats. Dexamethasone treatment did not significantly increase the sensitivity to KCl or the angiotensin-potentiated pressor response to noradrenaline. This study shows that dexamethasone treatment increases postsynaptic sensitivity of the cardiovascular system to noradrenaline in rats.

Animals↗

[Total cholesterol, HDL-cholesterol and blood pressure in relation to life style: results of the first population screening of the Swiss MONIKA Project].

To evaluate the association of individual health habits with levels of cardiovascular risk factors such as serum cholesterol and blood pressure, data from a representative population sample of 860 men and 788 women, aged 25 to 64 years and residing in Western Switzerland, were analyzed cross-sectionally. The data had been collected during 1984/85 as a part of the WHO MONICA project, an international research project on the epidemiology of cardiovascular diseases. In age-adjusted analysis, a score of prudent diet was a reasonably strong inverse correlate of total cholesterol in men (p less than 0.001) but less so in women (p = 0.11); the diet score was unrelated to HDL cholesterol. In both genders, alcohol consumption was associated with elevated levels of systolic and diastolic blood pressure (men: both p less than 0.001; women: p = 0.05 and 0.01 respectively) and of HDL cholesterol (men and women: p less than 0.001). Coffee consumption was unrelated to either blood lipids or blood pressure. In both men and women, leisure-time exercise was a predictor of a low-risk lipid profile, i.e. a low total cholesterol/HDL ratio (both p less than 0.001). Better educated persons, especially women, revealed consistently lower levels of cardiovascular risk factors. The independent character of these lifestyle-risk factor-associations was largely confirmed in a multivariate analysis, with cigarette smoking emerging as another significant predictor of a deteriorated lipid profile, while education was not an independent determinant of biological risk factors. Lifestyle variables, including body mass index, explained 9 to 19% of variance in cardiovascular risk factors, with relative weight being the strongest of the predictors related to behaviour. Entering age and sex into the regression models enhanced the predictive power of the equations to 16 to 26% explained risk factor variance. We conclude from this population-based, cross-sectional study that personal health habits such as diet, exercise, alcohol consumption and smoking, as well as body weight are significantly and independently related to blood lipid and blood pressure levels; the apparent size of effect of these behavioural traits on biological risk factors for cardiovascular diseases was only modest, but it may nevertheless be relevant to prevention.

Adult↗

Ventricular histamine concentrations and mast cell counts in the rat heart during acute ischaemia.

The ventricular histamine concentrations and mast cell counts of naive and disodium cromoglycate-treated rats subjected to acute left coronary artery ligation under pentobarbitone anaesthesia were examined. In naive animals, there was a significant increase in the right ventricular histamine level at 2 min following left coronary artery ligation. Left ventricular histamine concentrations tended to decrease, and were significantly lower than those of the right ventricle at 5 min. However there were no significant changes in mast cell counts of the right or left ventricles after left coronary artery ligation. Treatment with disodium cromoglycate did not significantly alter the ventricular mast cell counts, interfere with the changes in ventricular histamine concentrations, or the occurrence of early ventricular arrhythmias and haemodynamic changes in response to acute left coronary artery ligation. It is suggested that the increase in the right and decrease in the left ventricular histamine concentrations during acute myocardial ischaemia involves mainly the non-mast cell stores, instead of mast cell sources, of cardiac histamine.

Animals↗