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G Niehaus

Publications and source records attributed to G Niehaus.

7 recordsLinked 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↗
PubMed1986

Etiology of the pulmonary pathophysiology associated with inhalation injury.

This study describes an experimental model of smoke inhalation injury in sheep in which the same pathophysiologic alterations occur as with clinical inhalation injury in man. Diffuse pulmonary mucosal sloughing with atelectasis and emphysema with concomitant development of pulmonary edema results in a decrease in arterial oxygen and progressive pulmonary deterioration which results in a substantial mortality. Increased pulmonary edema fluid is shown to be caused by an increased microvascular permeability to protein with pulmonary lymph and tracheobronchial fluid, a filtrate of plasma. Concomitant with this increase in microvascular permeability is an influx of neutrophils, release of proteolytic enzymes and an identified presence of the metabolite of the prostanoid thromboxane A2 which are postulated as contributors to the progressive pulmonary dysfunction post inhalation injury.

Animals↗
PubMed1979

Pulmonary microvascular response to hemorrhagic shock, resuscitation, and recovery.

We studied the effect of hemorrhagic shock, resuscitation, and recovery on the pulmonary microcirculation. We used lung lymph flow (QL) and lymph-to-plasma protein ratio as sensitive indices of transvascular fluid filtration rate and protein permeability. We measured pulmonary vascular pressures, cardiac output, blood gases, lymph flow, and lymph and plasma proteins before and during a 2-h period of shock, a 3-h period of resuscitation, and a 72-h period of recovery, in nine unanesthetized sheep with chronic lung lymph fistula. We found a 30% decrease in QL during early shock as animals were bled into bags containing an acetate citrate dextrose solution until aortic pressure was 50 Torr. QL gradually increased to or exceeded base line in five of nine animals during late shock as pulmonary vascula resistance increased by 250%. During the 3-h resuscitation period, mean QL increased by 110%, with the lymph-to-plasma protein ratio being significantly decreased, indicating no protein permeability change. In five of nine studies, lymph became visible bloody. The increased QL and lymph RBCs were felt to be secondary to an elevation in microvascular pressure. During the recovery period, pressures and QL returned to base line.

Animals↗
PubMed1979

Lactic dehydrogenase activity in lung lymph during hemorrhagic shock, resuscitation and recovery.

Lactic dehydrogenase activity was determined in lung lymph before, during and after hemorrhagic shock to determine if this insult produced pulmonary cellular damage. Lung lymph flow and lymph protein content, reliable indices of fluids filtration rate and microvascular protein permeability were also monitored. The experiment was performed in unanesthetized sheep with a chronic lung lymph fistula. Lymph flow, lymph LDH and protein content did not change during the period of shock. Lymph flow increased significantly during resuscitation but lymph LDH and protein content decreased in relation to plasma values indicating the sieving effect of the microvascular membrane for protein to be intact. The increased flow was most likely caused by an increase in microvascular hydrostatic pressure. Plasma LDH was significantly increased during the 72 hour recovery period with lymph flow, lymph protein and lymph LDH being normal. We therefore found that hemorrhagic shock produced a systemic cellular injury reflected in an increased plasma LDH activity. No pulmonary cellular damage was noted.

Animals↗