These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Injury versus inflammatory response in the lungs of rats intratracheally inoculated with bacterial lipopolysaccharide.
    Author: Lopez A, Yong S.
    Journal: Am J Vet Res; 1986 Jun; 47(6):1287-92. PubMed ID: 3729129.
    Abstract:
    The relationship between acute pulmonary cell injury and inflammatory response was investigated in rats killed 1, 3, and 7 days after intratracheal inoculation with bacterial lipopolysaccharide (LPS). Activities of lactate dehydrogenase (LDH) and alkaline phosphatase (AP) in bronchoalveolar lavage (BAL) fluid and bronchoalveolar cell (BAC) lysate supernatants were used as indicators of cell injury in the lung. Concentrations of protein in BAL fluid and the number and types of BAC were used as indicators of pulmonary inflammatory response. The magnitude of inflammation and cell injury was calculated as the percentage difference of cellular and biochemical values, compared with values of nontreated controls. Inoculation with LPS induced a significant and dramatic (greater than 18,000%) influx of polymorphonuclear leukocytes (PMN) and a mild (approx 250%) increase in pulmonary alveolar macrophages. A moderate, significant and time-dependent increase in LDH (up to approx 260%) and AP (up to approx 220%) was detected in BAL fluid and BAC lysate supernatants after LPS inoculations. Inoculation with saline solution alone resulted in increased PMN (approx 975%), but did not alter LDH and AP values. In all rats evaluated, protein concentrations did not change. Numbers of PMN significantly and positively correlated with activities of LDH and AP. Protein concentrations and PMN counts had a negative nonsignificant association. Evidence of further cell injury was not detected after massive influx of PMN into the bronchoalveolar space. Therefore, the cellular influx of PMN induced by LPS probably was disproportionate to the magnitude of pulmonary cell injury.
    [Abstract] [Full Text] [Related] [New Search]