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D J Pavlin

Publications and source records attributed to D J Pavlin.

22 records · Page 2Linked to original sources
PubMed1981

Increased pulmonary vascular permeability as a cause of re-expansion edema in rabbits.

In order to study the mechanism(s) underlying re-expansion edema, we measured the concentration of labeled albumin (RISA) in the extravascular, extracellular water (EVECW) of the lung as a measure of pulmonary vascular permeability. Re-expansion edema was first induced by rapid re-expansion of rabbit lungs that had been collapsed for 1 wk by pneumothorax. The RISA in EVECW was expressed as a fraction of its plasma concentration: (RISA)L/(RISA)PL. The volume of EVECW (ml/gm dry lung) was measured using a 24Na indicator. Results in re-expansion edema were compared with normal control lungs and with oleic acid edema as a model of permeability edema. In re-expanded lungs, EVECW (3.41 +/- SD 1.24 ml/g) and (RISA)L/(RISA)PL 0.84 +/- SD 0.15) were significantly increased when compared with normal control lungs (2.25 +/- 0.41 ml/g and 0.51 +/- 0.20, respectively). Results in oleic acid edema (5.66 +/- 2.23 ml/g and 0.84 +/- 0.23) were similar to re-expansion edema. This suggested that re-expansion edema is due to increased pulmonary vascular permeability caused by mechanical stresses applied to the lung during re-expansion.

Animals↗
PubMed1980

Pulmonary arteriovenous shunts during halothane anesthesia in dogs.

The fraction of cardiac output flowing through pulmonary arteriovenous anastomoses (Qav/Qt) was measured in dogs during halothane anesthesia and compared with results obtained in normal awake dogs. Flow through arteriovenous anastomoses was measured using 99mTc-labelled polystyrene microspheres (50 microns diameter). The fraction of cardiac output perfusing pulmonary arteriovenous anastomoses during halothane anaesthesia was 4.1% (+/- SD 1.75) compared with 4.6% (+/- SD 0.73) in air-breathing awake control dogs. In spite of variations in arteriovenous shunt fraction, no significant relationship between the Qav/Qt and Qs/Qt was detected. These results suggest that pulmonary arteriovenous anastomases do not contribute significantly to the physiological shunt observed during halothane anaesthesia.

Anesthesia, Inhalation↗
PubMedDate not supplied

Oxygen and resolution of lung injury.

We investigated the effects of varying inspired oxygen concentrations on the resolution of oleic acid-induced lung injury in rabbits. Rabbits were injected intravenously with oleic acid and maintained in room air, or exposed to 60, 70, or 80% oxygen for periods of 7 or 10 days. Oleic acid caused hemorrhagic pulmonary edema with hypoxemia. Hypoxemia was more profound in the oxygen-treated animals, a difference that was significant after 7 days' exposure to 60 and 70% oxygen, and after 4 days to 80% oxygen. Mortality was increased in the animals maintained in 80% oxygen. The data suggest that environmental oxygen concentrations greater than 60% interfere with the return to normal lung function following oleic acid injury in rabbits. The hypoxemia may be due to either mismatching of ventilation and perfusion or to a diffusion block resulting from the increased septal width. There was no evidence of massive pulmonary edema as a cause of the hypoxemia. It was not possible to distinguish between injury primarily caused by oxygen and its interference with the healing process.

Animals↗