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Biomedical subjects

M E Goad

Publications and source records attributed to M E Goad.

22 records · Page 2Linked to original sources
PubMed1986

Surfactant alterations following acute bleomycin and hyperoxia-induced lung damage.

Hamsters treated with 0.5 U/kg intratracheal bleomycin and exposed for 24 h to 80% O2 develop acute respiratory failure 72 h after treatment. To examine indirectly the lung epithelial type II cell changes, alterations in pulmonary surfactant was measured. Presence and amount of dipalmitoyl phosphatidyl choline (DDPC) and sphingomyelin (SM) were measured, and the DPPC/SM ratio was determined in brochoalveolar lavage samples from treated and control animals 24, 48, 72, and 96 h after treatment. Hamsters treated with bleomycin and O2 had a significantly decreased DPPC/SM ratio at 72 h, which is the time of onset of respiratory failure. The decreased DPPC/SM ratio may reflect type II cell damage and inhibition of surfactant function by the edema fluid.

1,2-Dipalmitoylphosphatidylcholine↗
PubMedDate not supplied

Establishment and validation of an isolated rat lung model for pulmonary metabolism studies.

An isolated rat lung model was established and validated for use in pulmonary metabolism studies. During the establishment phase of the study, several problems were encountered and overcome in order to maintain the lungs in physiological condition. In the validation phase of the study, the lungs were removed, ventilated and perfused from 34 male Fischer 344 rats. After an equilibration period, lungs were ventilated and perfused for up to 4 h. Morphological, biochemical and functional parameters were evaluated to validate the physiological condition of the lungs. Morphological parameters included wet/dry lung weight ratios and gross and histological scoring for edema. Biochemical parameters included assays for tissue ATP and reduced glutathione content, glutathione reductase activity and glucose utilization. Functional parameters included changes in lung tidal volume, dynamic compliance and airway resistance. Results indicated that edema formation was only detected histologically, that lungs remained nearly biochemically normal for 210 min and that pulmonary function declined to about 80-90% of normal. Overall, these findings indicated that the isolated, perfused rat lung remained in acceptable physiological condition for ca. 210 min. This period of time should be adequate for conducting pulmonary metabolism studies with a variety of exogenous compounds.

Adenosine Triphosphate↗
PubMedDate not supplied

Hepatic toxicity and recovery of Fischer 344 rats following exposure to 2-aminoanthracene by intraperitoneal injection.

Humans may be exposed to 2-aminoanthracene (2-AA), a substituted polycyclic aromatic hydrocarbon, and a recognized mutagen and carcinogen, through oral and respiratory routes from contact with a variety of environmental sources. For the present study, we sought to evaluate hepatic damage and recovery in Fischer 344 rats following multiple i.p. injections of 5 mg of 2-AA. Rats were injected weekly for up to 5 weeks. Subgroups were then allowed to recover for 1, 5, or 9 weeks, and biochemical and pathologic changes were evaluated. We observed that weight gains were reduced relative to controls for all groups receiving > or = 2 injections. Serum enzyme levels indicative of liver damage were evident and included alterations in serum aspartate aminotransferase, alkaline phosphatase, total protein, albumin, and globulin. These alterations usually returned to normal by 5 weeks following cessation of 2-AA administration. In contrast, histologic liver changes, including hepatocyte hypertrophy, biliary hyperplasia with oval cell proliferation, altered foci, nodular hyperplasia, and one hepatocellular adenoma became more severe with time. This experiment demonstrates patterns of hepatic damage and recovery in rats exposed to 2-AA.

Adenoma↗