Lymphocytic interstitial pneumonitis in a patient with systemic lupus erythematosus.

A 34-year-old woman with stable systemic lupus erythematosus (SLE) treated with low-dose prednisone and hydroxychloroquine developed multiple bilateral pulmonary nodules. Open lung biopsy documented lymphocytic interstitial pneumonitis (LIP). LIP should be considered in the differential diagnosis of nodular pulmonary lesions in patients with SLE.

Effect of aerosol heparin on the development of hypoxic pulmonary hypertension in the guinea pig.

Chronic hypoxia produces pulmonary artery hypertension through vasoconstriction and structural remodeling of the pulmonary vascular bed. The present study was designed to test the effect of heparin administered via aerosol on the development of hypoxic pulmonary hypertension. Anesthetized, intubated, and mechanically ventilated guinea pigs received an aerosol of either 2 ml normal saline (hypoxic control, HC) or 4,500 units of heparin diluted in 2 ml normal saline via an ultrasonic nebulizer (hypoxic heparin, HH). After 24 h of recovery, the animals were placed in a hypoxic chamber (10% O2) for 10 days. Animals kept in room air served as normoxic controls (NC). Hypoxia increased mean pulmonary artery pressure from 11 +/- 1 (SEM) mm Hg in NC to 24 +/- 1 mm Hg in HC (p < 0.05). Pulmonary artery pressure was significantly lower in HH-treated animals (20 +/- 1 mm Hg, p < 0.05 versus HC) as was the total pulmonary vascular resistance (0.15 +/- 0.01 in HH versus 0.20 +/- 0.01 mm Hg/ml/min in HC, p < 0.05). There was no difference in cardiac output (146 +/- 12 in HH versus 126 +/- 7 ml/min in HC), hematocrit (57 +/- 2 in HH versus 56 +/- 2% in HC), partial thromboplastin time (30 +/- 2 in HH versus 32 +/- 3 s in HC), prothrombin time (46 +/- 1 in HH versus 48 +/- 4 s in HC) or room air arterial blood gas values after 10 days of hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic hypoxic pulmonary hypertension in the guinea pig: effect of three levels of hypoxia.

Chronic hypoxia [inspiratory PO2 (PIO2) = 76 Torr for 10 days] produces pulmonary hypertension and vascular remodeling in the guinea pig. Increasing the duration of hypoxia from 10 to 21 days does not increase further pulmonary arterial pressure or medial thickening. To see if increasing severity of hypoxia affects the magnitude of pulmonary hypertension and remodeling, we exposed three groups of male Hartley guinea pigs to three levels of normobaric hypoxia for 10 days: PIO2 = 90 (n = 6), 78 (n = 6), and 65 Torr (n = 5). Pulmonary arterial pressure increased from 14 +/- 1 (+/- SE, n = 7) in room air to 23 +/- 3 mmHg when PIO2 = 90 Torr (P < 0.05). Pulmonary arterial pressure was slightly higher when PIO2 = 78 or 65 Torr (25 +/- 1 and 26 +/- 1 mmHg, respectively) but did not reach statistical significance vs. PIO2 = 90 Torr. Total pulmonary vascular resistance increased from 0.049 +/- 0.004 in room air to between 0.084 +/- 0.006 and 0.101 +/- 0.003 mmHg.min.kg.ml-1 (P < 0.05) in the three hypoxic groups; again there was no difference in total pulmonary vascular resistance among hypoxic groups. Medial thickness of alveolar duct and terminal bronchiole arteries increased with hypoxia, but there was no significant difference among the hypoxic groups. The percentage of intra-acinar vessels with thick walls (a measure of muscular extension) increased when PIO2 = 78 Torr and nearly doubled when PIO2 = 65 Torr in comparison to control.(ABSTRACT TRUNCATED AT 250 WORDS)