Biomedical subjects

L Traber

Publications and source records attributed to L Traber.

21 records · Page 2Linked to original sources

PubMed1988

Ibuprofen reduces the lung lymph flow changes associated with inhalation injury.

Inhalation injury was produced in sheep which were chronically prepared for study. The injury was induced by insufflating them with smoke from burning cotton cloth. One group of animals was treated with the cyclooxygenase inhibitor ibuprofen and another group was untreated. Eight hr following the administration of smoke, there was an elevation of lung lymph flow in both groups. These changes were not as severe in the animals which were treated with ibuprofen. The pulmonary changes which occur following smoke inhalation injury are associated with elevations of the metabolites of arachidonic acid, especially those generated by the cyclooxygenase pathway. These metabolites in some way contribute to the pathophysiological changes induced by the inhalation of smoke, since they are reduced by the administration of a cyclooxygenase inhibitor.

Animals↗

PubMed1985

Potentiation of lung vascular response to endotoxin by superoxide dismutase.

We studied the effects of superoxide dismutase (SOD), an enzyme that converts superoxide into peroxide, on the cardiopulmonary response to endotoxin in sheep. Sheep (n = 18) were prepared for chronic measurement of cardiopulmonary variables, including lung lymph flow, by surgically implanting catheters under halothane anesthesia. Nine of the animals were studied before and after the administration of endotoxin (0.75 microgram/kg) with and without SOD. An additional nine animals received SOD without the lipopolysaccharide. Endotoxin produced an increase in lung lymph flow that was initially associated with a marked pulmonary arterial (PA) hypertension and reduced lymph-to-plasma protein ratio (L/P). The lymph flow remained elevated later in the response, but there was only a mild increase in PA pressure, and the L/P was normal. There was also a fall in blood neutrophils and in cardiac index. SOD increased this secondary elevation in lung lymph flow, and the corresponding L/P was greater than the preendotoxin value. The fall in neutrophil count, cardiac output, and the elevation in PA pressure seen with endotoxin were not affected by SOD. When administered in the absence of endotoxin, SOD produced no perceptible change in the cardiopulmonary and lymph values. We conclude that peroxide, hydroxyl ion, and/or other free radicals formed by the action of SOD must be responsible for a portion of the endotoxin response rather than superoxide itself.

Animals↗

PubMedDate not supplied

Time course of alterations in lung lymph and bronchial blood flows after inhalation injury.

The effects of inhalation injury on the pulmonary microvascular fluid flux and bronchial blood flow were examined in a long-term study of sheep (N = 13). They were insufflated with either 48 breaths of cotton smoke (n = 8) or air (n = 5) while they were deeply anesthetized with halothane. After injury, anesthesia was discontinued and the animals were mechanically ventilated throughout the experimental period (24 hours). Bronchial blood flow increased significantly at all time points recorded and reached its peak 20 minutes after the inhalation trauma (11 +/- 1 ml/hr to 106 +/- 18 ml/hr; p less than 0.05). Thereafter, bronchial blood flow decreased to a value that was six to eight times above the baseline measurement for the remainder of the study period. With these changes in blood flow, there was a concomitant increase in lung lymph flow. This variable gradually increased and was 633% of the baseline value (6 +/- 1 ml/hr to 44 +/- 8 ml/hr) 24 hours after the challenge with smoke. The control animals showed little or no change in cardiopulmonary function during the experimental period. There is no correlation between the increase in bronchial blood flow and lung lymph flow patterns after cotton smoke inhalation injury.

Animals↗