Mmol/ml, respectively) compared to N (7.99±0.60 Amol/ml).Phosphatidylcholine was decreased in A (62.64±2.20% PL) compared to N (76.27±2.05% PL). Phosphatidylglycerol was 11.58±1.21% PL in N and was decreased to 6.48±1.43% PL in A. SP-A was 123.64±20.66 zg/ml in N and was decreased to 49.28±21.68 jg/ml in AR and to 29.88±8.49 jg/ml in A. SP-B was 1.28±0.33 jig/ml in N and was decreased to 0.57±0.24 ,ug/ml in A. ST,,. was increased in AR (15.1±2.53 dyn/cm) and A (29.04±2.05 dyn/cm) compared to N (7.44±1.61 dyn/cm).

Lung surfactant is deficient in patients with acute respiratory distress syndrome (ARDS). We performed a randomized, prospective, controlled, open-label clinical study of administration of a bovine surfactant to patients with ARDS to obtain preliminary information about its safety and efficacy. Patients received either surfactant by endotracheal instillation in addition to standard therapy or standard therapy only. Three different groups of patients receiving surfactant were studied: patients receiving up to eight doses of 50 mg phospholipids/kg, those receiving up to eight doses of 100 mg phospholipids/kg, and those receiving up to four doses of 100 mg phospholipids/kg. Outcome measures included ventilatory support parameters, arterial blood gases, organ system failures, bronchoalveolar lavage (BAL) analyses, immunologic analyses, survival, and adverse events during the 28-d study period. Fifty-nine study patients were evaluable; 43 in the surfactant group and 16 in the control group. The FI(O2) at 120 h after treatment began was significantly decreased only for patients who received up to four doses of 100 mg phospholipids/kg surfactant as compared with control patients (p = 0.011). Mortality in the same group of patients was 18.8%, as compared with 43.8% in the control group (p = 0.075). The surfactant instillation was generally well tolerated, and no safety concerns were identified. This pilot study presents preliminary evidence that surfactant might have therapeutic benefit for patients with ARDS, and provides rationale for further clinical study of this agent.

Background:We have demonstrated effectiveness of an aerosolized, peptide-containing, synthetic surfactant (KL 4 surfactant), in spontaneously breathing CPAP-supported preterm lambs. Dose-ranging studies are required to define the dose that produces optimal physiologic and biomarker responses.

Immunoreactive and bioassayable plasma fibronectin (opsonic α 2 surface-binding (SB) glycoprotein) was measured during experimental Sarcoma-180 tumour growth in mice. Male C57BL/6 mice were challenged s.c. with 2 × 10 6 viable Sarcoma-180 tumour cells and evaluated sequentially in parallel with saline-injected controls over a 21-day experimental period. Before challenge, immunoreactive plasma fibronectin was 1050-1150 μg/ml. Minimal tumour growth occurred until 6 days after tumour challenge. There was then a rapid increase in primary tumour size, especially over the 7-14-day interval, with a plateau of growth over the 18-21-day interval. Immunoreactive plasma fibronectin was significantly ( P < 0·05) raised at 3 and 7 days after tumour challenge. A rapid rise ( P < 0·001) to 2816·6 ± 158·9 μg/ml was observed at 14 days followed by a modest decline at 21 days. Bioassayable opsonic activity increased ( P < 0·5) with the rise in immunoreactive fibronectin 3 and 7 days after tumour challenge, but the rapid rise in immunoreactive fibronectin over the 7-14-day interval was associated with a significant ( P < 0·5) fall in bioassayable opsonic activity. Thus, the rapid rise in immunoreactive plasma fibronectin parallels the rapid rate of tumour growth, but is associated with a fall in opsonically active plasma fibronectin. Dissociation between immunoreactive and opsonically active plasma fibronectin may be mediated by inhibition and/or alteration of circulating fibronectin during rapid tumour growth. Alternatively, it may reflect increased release of antigenically related protein (i.e. cell-surface fibronectin) during rapid tumour growth, which may have limited biological opsonic activity. Images Fig. 2

AbstractsResults Physical exam, cyanosis in the first 12 hours, tachypnea and/or a severe respiratory distress, systolic murmur on the left border of sternum. ECG: diastolic dysfunction of left ventricular (LV). Chest X ray: cardiomegaly (all cases). PaO 2 : low values-all patients. ECHO aspects: enlargement of the right chambers; severe tricuspid regurgitation with the peak velocity 3-4 m/sec; mitral regurgitation (12/41 of cases), left-to-right shunt across foramen ovale and/or ductus arteriosus (30/41 of cases), enlargement of the pulmonary artery and severe pulmonary regurgitation, septal hypertrophy (11/41 of cases); impaired LV relaxation with normal systolic function; congenital heart diseases (7). Repeated ECHO revealed in most of the cases diminished or no right-to left shunt across ductus arteriosus or foramen ovalae correlate with clinical improvement and disappearance of cyanosis. Conclusions Echocardiographic exam, beside clinical exam and history of the disease, is un important element for the diagnosis and follow up of evolution by the specific treatment applied for PPHN in the newborn with cyanosis and this investigation must be performed early after birth.