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Biomedical subjects

S F Duan

Publications and source records attributed to S F Duan.

At least 19 recordsLinked to original sources
PubMed1992

Effects of sustained ligustrazine on hemorrheology in patients with chronic pulmonary heart disease.

Before and after oral administration of sustained Ligustrazine, changes of hemorrheology and TXA2/PGI2 were evaluated in 16 patients with advanced chronic pulmonary heart disease. A decrease in whole blood and plasma viscosity, and reductions in hematocrit and fibrinogen were found after one course of treatment with sustained Ligustrazine. The mechanism of these effects may be related to improved modulation of imbalance of TXA2/PGI2 in patients with advanced chronic pulmonary heart disease.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Effects of exercise on pulmonary gas exchange and oxygen transport in chronic obstructive pulmonary diseases.

The effect of exercise on pulmonary gas exchange, arterial oxygenation, oxygen transport and delivery, and hemodynamics are studied in 100 patients with chronic obstructive pulmonary diseases. According to the change of PaO2 or PaCO2 induced by exercise, patients were divided into two groups. Group A (n = 52) had significantly increased of PaO2 with little change in PaCO2. Mixed venous PO2, oxygen transport and coefficient of oxygen delivery decreased while the alveolar-arterial PO2 gradients and venous admixture increased significantly in Group B as compared with these parameters in Group A during exercise. Our data imply that exercise may lead to marked deterioration of pulmonary gas exchange, arterial oxygenation, oxygen transport and hemodynamic abnormalities in patients in whom PaO2 is decreased during exercise.

Blood Gas Analysis↗
PubMed1991

Effects of ligustrazine controlled release capsule in chronic pulmonary heart disease.

Before and after oral administration of ligustrazine controlled release capsule, pulmonary hemodynamics, right cardiac function, arterial blood gas and TXB2/6-keto-PGF1 alpha were studied in 16 patients with advanced cor pulmonale. The decrease of pulmonary arterial pressure and pulmonary vascular resistance, increase of cardiac output, improvement of right cardiac function and arterial blood gas were demonstrated after one course of treatment. The mechanism of these effects may be related to improvement of imbalance of TXB2/6-keto-PGF1 alpha. These results were in agreement with those of intravenous administration of ligustrazine, but no adverse reactions were found.

Administration, Oral↗
PubMed1991

Noninvasive diagnosis of latent pulmonary hypertension in COPD by exercise-load impedance rheopneumogram: a comparative study with right heart catheterization.

Impedance rheopneumogram (IRP) and right heart Swan-Ganz catheter examinations were simultaneously carried out in 63 patients. Two equations for calculating after-exercise-pulmonary-pressure (PAPm) were obtained by stepwise regression analysis: 1) PAPm (kPa) = -1.40-0.88.InHs+8.30.(B-F)+5.78.Q-B/B-Y (r = 0.730, IRP is measured at rest); 2) PAPm(kPa) = 6.46-5.04.Hs/square root of R-R +4.35.Q-B/B-Y-19.34.(Q-C) (r = 0.648, IRP is measured after exercise). This is a new method for diagnosing latent pulmonary hypertension noninvasively.

Cardiac Catheterization↗
PubMed1991

[Changes of thromboxane A2 (TXA2) and prostacyclin (PGI2) in COPD patients with pulmonary hypertension].

We measured the pulmonary arterial pressure and the level of Thromboxane A2 (TXA2), and Prostacyclin (PGI2) in 30 stable COPD patients and the level of TXA2 and PGI2 in 10 normal subjects so as to investigate the changes of TXA2 and PGI2 in COPD patients with pulmonary hypertension. The results showed that the level of TXA2 increased significantly in COPD patients with dominant and latent pulmonary hypertension when compared with that in normal subjects (P less than 0.001, less than 0.01), and the level of TXA2 in COPD patients with dominant pulmonary hypertension was also higher than that in COPD patients with latent pulmonary hypertension (P less than 0.02), but there was no difference in the level of PGI2 among normal subjects and COPD patients with or without pulmonary hypertension. This indicates that TXA2 plays an important role in causing pulmonary hypertension in COPD patients.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

[Pulmonary artery compliance and its relation with pulmonary hemodynamics in patients with chronic obstructive pulmonary disease].

In order to investigate pulmonary artery compliance (Cpa) and its relation with the clinical conditions and the other parameters of pulmonary hemodynamics in patients with chronic obstructive pulmonary disease (COPD), we performed right heart Swan-Ganz catheterization in 146 COPD patients and measured their Cpa with Engelberg's method. The results showed that Cpa of BB type patients was lower than that of PP type ones; patients with pulmonary hypertension or cor pulmonale had lower Cpa than those without. These results suggest that Cpa in COPD patients decreases as their clinical condition worsens. Cpa had close relation with other pulmonary hemodynamic parameters. It had significant negative correlation with pulmonary arterial mean pressure, pulmonary vascular resistance and right ventricular stroke work index and significant positive correlation with cardiac index and stroke volume index. Using Engelberg's method as the standard, we also compared Reuben's, Wang's and Zhong's methods which are all simpler than Engelberg's method for measuring Cpa clinically. The results showed that Cpa measured with Wang's method was the closest to that measured with Engelberg's method.

Aged↗
PubMed1991

[Investigation of the relation of impedance rheopneumogram with pulmonary hemodynamics and right ventricular function in patients with chronic obstructive pulmonary disease].

In order to investigate the relation of impedance rheopneumogram with pulmonary hemodynamics and right ventricular function in patients with chronic obstructive pulmonary disease (COPD), we measured impedance rheopneumogram and did right heart catheterization in 150 COPD patients simultaneously both at rest and after exercise. The results showed that impedance rheopneumogram was mainly influenced by right ventricular after-load, while the influences of right ventricular pre-load, right ventricular contraction, right ventricular stroke work index and cardiac output were rather small, suggesting that in COPD patients impedance rheopneumogram is valuable in predicting pulmonary arterial pressure noninvasively, but not so use in judging the right ventricular function.

Cardiac Catheterization↗
PubMed1990

Investigation on the relation of impedance rheopneumogram with pulmonary hemodynamics and right ventricular function in patients with chronic obstructive pulmonary disease.

In order to investigate the relation of impedance rheopneumogram with pulmonary hemodynamics and right ventricular function in patients with chronic obstructive pulmonary disease (COPD), we measured impedance rheopneumogram and performed right heart catheterization on 150 COPD patients simultaneously both at rest and during exercise test. The results showed that impedance rheopneumogram was mainly influenced by right ventricular after-load while the influences of right ventricular pre-load, right ventricular contractivity, right ventricular work index and cardiac output were rather slight. These results also suggest that in COPD patients impedance rheopneumogram is of great value when used to predict pulmonary arterial pressure but of little value when used to measure the right ventricular function.

Aged↗
PubMed1990

[Renin-angiotensin-aldosterone system and pulmonary hemodynamics in patients with pulmonary artery hypertension].

To investigate the relationship between renin-angiotensin-aldosterone system and pulmonary hemodynamic parameters in patients with chronic pulmonary artery hypertension, we measured plasma levels of renin activity, angiotensin II and aldosterone in 11 patients during right heart catheterization. All patients had chronic obstructive pulmonary disease. At rest, plasma concentration of angiotensin II positively correlated with mean pulmonary artery pressure (r = 0.76, P less than 0.01) and pulmonary vascular resistance (r = 0.64, P less than 0.05). During exercise, plasma level of angiotensin II increased from 70 +/- 21 to 81 +/- 24 pg/ml (P less than 0.01) and plasma renin activity from 0.66 +/- 0.54 to 1.28 +/- 1.2 ng/ml/h (P less than 0.05), whereas mean pulmonary artery pressure increased from 3.73 +/- 0.85 to 6.27 +/- 1.81 kPa (28 +/- 6.4 to 47 +/- 13.6 mmHg). Increase of angiotensin II correlated with changes in mean pulmonary artery pressure (r = 0.69, P less than 0.05) but not with systemic artery pressure. The results of present study suggest that angiotensin II might play a role in the development of pulmonary artery hypertension in patients with chronic obstructive pulmonary disease.

Aged↗
PubMed1989

The acute effects of ligustrazini on hemodynamics and right cardiac function in pulmonary arterial hypertension secondary to chronic obstructive pulmonary disease.

We studied 20 patients with pulmonary arterial hypertension secondary to chronic obstructive pulmonary disease (COPD) to investigate the acute effect of Ligustrazini on hemodynamics and right cardiac function. The results suggested that Ligustrazini had the effects of dilating pulmonary vessel, decreasing mean pulmonary arterial pressure and pulmonary vascular resistance, increasing cardiac output, and improving right cardiac function. The maximum effects of Ligustrazini occurred at 30 min after starting administration of the drug, but its effects disappeared 1 h after its withdrawal. From the above we are led to conclude that Ligustrazini as a vasodilator works rapidly, but its effects do not persist long.

Adult↗
PubMed1989

Ultrastructural investigation of changes of pulmonary surfactant system in experimental emphysema produced by intratracheal elastase instillation.

In this study the dynamic changes of the pulmonary surfactant system in guinea pigs were observed by scanning electron microscopy, transmission electron microscopy and special electron stain for surfactant. The results showed that in the early stage of instillation of elastase, the pulmonary surfactant decreased. After one week, it increased gradually. Type II epithelial cells proliferated and their secretion increased. By the 25th day, the pulmonary surfactant system tended to return to normal, indicating that the changes of the pulmonary surfactant system may have some effect during the developing process of emphysema.

Animals↗
PubMed1989

[Evaluation of the immediate effect of ligustrazine in chronic cor pulmonale].

Twenty patients with chronic cor pulmonale were studied to assess the immediate effect of Ligustrazini on hemodynamic and right cardiac function. After intravenous administration of Ligustrazini at rest, there was statistically significant decrease in pulmonary arterial pressure, pulmonary vascular resistance and heart rate, increase in cardiac output and improvement in right cardiac function. Maximal effect was observed half an hour after treatment. But the effect disappeared after discontinuing the treatment of Ligustrazini for one hour. It is suggested that the effect of Ligustrazini appears early but does not last long.

Adult↗
PubMed1989

[Role of the renin-angiotensin-aldosterone system in the pathogenesis of edema formation in chronic obstructive pulmonary disease].

The pathogenesis of edema in COPD patients is poorly understood. In 50 COPD patients without cor pulmonale, we measured water sodium and potassium excretion in 24 hours, concentration of sodium and potassium in plasma as well as PRA, ATII and aldosterone levels. We found that PRA, ATII, and aldosterone levels in COPD patients with edema are much higher than those in patients without edema and sodium and water excretion decreased significantly in edematous COPD patients. Elevation of PRA, ATII, and aldosterone correlated with inability to excrete sodium and water. These data suggest that, in conjunction with hypercapnia-hypoxia-mediated disturbance in renal function, stimulation of RAAS, especially the resulting increase of aldosterone may contribute to edema formation in COPD patients.

Adult↗