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Background : Pulmonary damage resulting from lipid peroxidation is a principal effect of paraquat intoxication. The host-defense functions of surfactant are known to be mediated by the surfactant proteins A and D (SP-A and SP-D, respectively). The primary objective of this study was to evaluate the variations over time in levels of surfactant protein and lipid peroxidation (LPO) in lung tissue following free-radical-induced injury.Methods : 42 adult, male, Sprague-Dawley rats were administered intraperitoneal injections of paraquat (35 mg/kg body weight). SP-A and SP-D levels were determined via Western blot. LPO in the left lung homogenate was measured via analyses of the levels of thiobarbituric acid-reactive substances.Results : LPO levels peaked at 6 hours, with no associated histological changes. SP-D levels increased until hour 12 and declined until hour 48; SP-D levels subsequently began to increase again, peaking at hour 72. SP-A levels peaked at hour 6, declining thereafter.Conclusions : We suggest that in the early phase of paraquat injury, SP-D levels reflect alveolar damage and that de novo synthesis of SP-D takes 72 hours. Levels of SP-A, on the other hand, reflect abnormalities in the surfactant system in the late stage of paraquat intoxication. Surfactant proteins may play a role in protecting the lungs from reactive oxygen injury. A time-dependent variation has been observed in the levels of surfactant proteins A and D following paraquat injury, and it has been suggested that these proteins play a role in the protection of lung tissue against ROS-induced injuries.

Objectives: To examine whether exogenous pulmonary surfactants (exPS) substitute for or merely supplement endogenous pulmonary surfactants (enPS) by looking at sequential changes in the surfactant proteins (SP) SP-A and SP-D in alveolar pools. Methods: Fourteen preterm infants with RDS treated with an artificial surfactant were compared to five normalterm infants without RDS who were treated with artificial ventilation at birth. Results: Immediately after birth, SP-A and SP-D were essentially absent in the alveolar pools of the RDS group, but were present at normal levels in the controls. Treatment with exPS apparently stimulated enPS production. Conclusions: In infants who responded well to exPS therapy, the SP concentration reached essentially normal levels within 48-72 h after birth.

The stable microbubble test is an effective indirect method that tests the changes in surfactant quantity. In the in vitro experiment, we observed an inhibitory effect of meconium on the surfactant activity using the stable microbubble test.

Introduction We aimed to determine whether maximal exercise capacity, left ventricular function, and quality of life (QoL) scores are sustained in patients with atrial fibrillation (AF) after termination of training following exercise-based cardiac rehabilitation (ECR). Methods In a prospective study, 58 patients with AF (age, 62 ± 7 years) were randomized into an exercise training group for 12 months (ECR, n = 13), a group with 6-month detraining after a 6-month exercise training (DT, n = 15), and a medical treatment only group (MT, n = 30). For exercise training, cycling on a bicycle ergometer was performed in the DT and ECR groups 3 times a week for 6 and 12 months, respectively. Each session started with a 10-minute warm-up at 60%–70% of the maximal heart rate (HRpeak), followed by four 4-minute intervals at 80%–90% of the HRpeak, with 3 minutes of active recovery at 60%–70% of the HRpeak between intervals, ending with a 5-minute cool-down period. Peak exercise oxygen consumption (Vo2), left ventricular function, plasma lipid level, N-terminal pro B-type natriuretic peptide level, and QoL score were measured at baseline, after 6 months of training, and after additional 6 months of continuous training or detraining follow-up assessments. Results Six months of exercise training increased the peak Vo2 (ECR: 28.2 ± 7.0 ml/[kg·min] and DT: 28.0 ± 8.3 ml/[kg·min] vs. MT: 23.0 ± 5.2 ml/[kg·min], p= 0.047) and QoL scores (36-Item Short-form Health Survey) and decreased the total cholesterol level (ECR: 146.8 ± 43.8 mg/dl and DT: 140.6 ± 22.4 vs. MT: 182 ± 44.2 mg/dl, p = 0.008). Detraining resulted in an increase in QoL score and a decrease in total cholesterol level (ECR: 142.8 ± 21.4 mg/dl and DT: 151.8 ± 39.8 vs. MT: 176.8 ± 34.2 mg/dl, p = 0.017). However, the exercise training-induced increase in peak Vo2 reverted to the baseline level after detraining (ECR: 27.1 ± 5.1 ml/kg/min vs. DT: 24.4 ± 7.2 ml/[kg·min] and MT: 21.5 ± 4.86 ml/[kg·min], p = 0.017). The resting left ventricular systolic and diastolic functions were not significantly different, with no inter-group difference after 6 months of training and 6 months of continuous training or detraining. Conclusions As the QoL scores are maintained despite peak Vo2 being lowered by detraining after an exercise training period in patients with AF, physicians should encourage patients’ participation in a continuous exercise program to sustain the improvement in both the QoL score and peak Vo2 with exercise training. Further studies with larger sample sizes are needed to observe the long-term effects of exercise training and detraining.