Lung surfactant in subacute pulmonary disease

Pulmonary surfactant is a surface active material composed of both lipids and proteins that is produced by alveolar type II pneumocytes. Abnormalities of surfactant in the immature lung or in the acutely inflamed mature lung are well described. However, in a variety of subacute diseases of the mature lung, abnormalities of lung surfactant may also be of importance. These diseases include chronic obstructive pulmonary disease, asthma, cystic fibrosis, interstitial lung disease, pneumonia, and alveolar proteinosis. Understanding of the mechanisms that disturb the lung surfactant system may lead to novel rational therapies for these diseases

A comparison of the hemodynamic and respiratory effects of surfactant instillation during interrupted ventilation versus noninterrupted ventilation in rabbits with severe respiratory failure

The purpose of this study was to evaluate whether avoiding interruption of ventilation during surfactant instillation improves the effects on lung function and surfactant distribution and whether it prevents the adverse effects on blood pressure and cerebral blood flow. The study was performed using rabbits with severe respiratory failure induced by lung lavages. These rabbits were randomized to Tc-99m-Nanocoll labeled surfactant instillation through a side lumen of the endotracheal tube without interrupting ventilation or instillation during a short interruption of ventilation. After surfactant instillation with interruption of ventilation, Pao, rose from 8.7 +/- 1.3 to 24.9 +/- 6.4 kPa (mean +/- SEM). Without interruption, Pao, rose from 8.4 +/- 0.8 to 32.4 +/- 4.3 kPa, Pace, decreased with interruption from 4.69 +/- 0.51 to 3.61 +/- 0.26 kPa and without interruption from 5.06 +/- 0.41 to 4.13 +/- 0.23 kPa. Dynamic and static compliance indites were not statistically different after both procedures. Surfactant distribution tended to be less nonuniform after instillation without interrupting ventilation. In contrast, avoidance of interruption of ventilation resulted in less uniform lobar distribution and less peripheral deposition of surfactant. By instillation with interruption, blood pressure increased quickly (28 +/- 6.6%), followed by a 22 +/- 5.3% decrease. Blood pressure increased quickly (16 +/- 4.2%), followed by a 40 +/- 10% decrease by surfactant instillation without interruption. Cerebral blood flow, measured by an ultrasonic transit time flow probe on the carotid artery, increased quickly (45 +/- 14%), followed by a 64 +/- 11% decrease with interruption, whereas it increased 15 +/- 4.9% (p = 0.06 versus with interruption) and decreased 61 +/- 13% without interruption of ventilation. Therefore, avoiding interruption of ventilation during surfactant instillation tends to prevent the potential adverse effects of a rapid rise in cerebral blood flow, and furthermore, tends to improve uniformity of surfactant distribution, whereas having no detrimental effect on respiratory function

Number and activation of circulating polymorphonuclear leukocytes and platelets are associated with neonatal respiratory distress syndrome severity

Objective. To determine whether number and activation of circulating polymorphonuclear leukocytes (PMNs) and platelets are associated with disease severity in neonatal respiratory distress syndrome (RDS). Design. Prospective study. Setting. Tertiary neonatal intensive care unit. Patients. Preterm infants with, severe (n = 18) or mild tee moderate (n = 18) RDS who were consecutively admitted. Interventions. FMN and platelet counts and plasma concentrations of elastase-alpha(1)-proteinase inhibitor (E-alpha(1)-PI) and thromboxane B-2 (TxB(2)) were recorded each day during the first 5 days of life. E-alpha(1)-PI-to PMN and TxB(2)-to-platelet ratios were calculated to correct for the influence of the PMN and platelet count on elastase and thromboxane release. Results. From day 2, the severe RDS group had lower median PMN counts (1.5 vs 4.5 x 10(9)/L), lower mean platelet counts (136 vs 230 x 10(9)/L), and more elastase and thromboxane release, indicated by higher median E-alpha(1)-PI-to-PMN (39.2 vs 13.0 ng/10(6) PMNs on day 2) and TxB(2)-to-platelet (2.61 vs 0.52 pg/10(6) platelets on day 3) ratios than the mild-to-moderate group. Lower PMN and platelet counts and higher elastase and thromboxane release were correlated with birth asphyxia (lower 5-minute Apgar scores and umbilical arterial PH values), higher respiratory requirements (fraction of inspired oxygen and peak inspiratory pressure), and decreased values for continuous measures of RDS severity (ventilatory efficiency index and PaO2-to-alveolar oxygen tension ratio). Conclusion. Decreased PMN and platelet counts and increased elastase and thromboxane release are correlated with increased RDS severity. Birth asphyxia (hypoxia and acidosis) and tissue injury caused by high-pressure ventilation and hyperoxia may promote this activation process