Biomedical subjects

D Tighe

Publications and source records attributed to D Tighe.

22 records · Page 2Linked to original sources

PubMed1989

Multi-organ damage resulting from experimental faecal peritonitis.

1. Using specific-pathogen-free New Zealand White rabbits, we have compared the effects of faecal peritonitis over a period of 5 h in eight test animals with eight controls in which a sham operation was performed. 2. There was morphological damage to lungs, liver and spleen of test animals. Lung capillaries and sinusoids of the liver showed occlusion by cell debris and leucocytes, with endothelial damage. The lungs also showed alveolar epithelial disruption, basement membrane exposure and type II pneumocytes lacking lamellar bodies. In the liver there was fibrin deposition and swollen Kupffer cells. The spleen showed degranulating neutrophils, fibrin deposits, platelet aggregates and activated macrophages, with no damage to the endothelium. 3. There was no morphological damage to the kidney or heart of test animals or to any organs of sham-operated animals. 4. There were mixed anaerobes and aerobes in faecal material used to induce peritonitis. Cultures of liver, spleen and kidney isolated four different types of micro-organisms. Blood cultures showed two types of micro-organisms. Cultures of lung and heart showed one type of micro-organism. 5. The presence of micro-organisms in an organ could not be correlated with the degree of histological damage to that organ. 6. In test animals an early significant reduction in circulating leucocytes and platelets was sustained for the duration of the experiment with significant diffuse intravascular coagulation. 7. There was no change in test animal neutrophil adhesiveness until 120 min, when significant reduction was observed. 8. Serum phospholipase A2 (EC 3.1.1.4) activity in the test group showed a threefold increase at 300 min.

Animals↗

PubMed1989

Pentoxifylline reduces pulmonary leucostasis and improves capillary patency in a rabbit peritonitis model.

This study examines the changes in pulmonary leucostasis and capillary ultrastructure in 18 rabbits divided into three groups. Those in the first group were sham operated, and those in the second and third groups underwent peritonitis induction; those in the latter group were treated with pentoxifylline (PTF). White blood cells (WBC) were counted, and tissue area, total capillary area, and capillary patency were measured from electron micrographs of lung tissue. Pulmonary WBCs were 1.2 per unit field in the sham group, 9.7 in the test group (P less than 0.001 compared with sham), and 2.5 in the PTF group (P less than 0.001 compared with sham). Capillary patency was 53 +/- 5% in the sham group, 12 +/- 4% (P less than 0.001 compared with sham) in the test group, and 24 +/- 2% (P less than 0.001 compared with sham) in the PTF group. Pentoxifylline treatment attenuates pulmonary leucostasis, pulmonary capillary occlusion, and endothelial and epithelial damage associated with peritonitis in rabbits. This study shows that PTF warrants investigation into its potential protective effects on the lungs in clinical sepsis.

Animals↗

PubMed1987

A phospholipase inhibitor modifies the pulmonary damage associated with peritonitis in rabbits.

Peritonitis has been produced in rabbits by the spreading of 5 ml of caecal contents throughout the peritoneal cavity. After sacrifice at 5 h, electron microscopy revealed a increase of 600% in PMN and 1200% in lymphocytes in the pulmonary capillaries of the test animals when compared to the sham operated group. The pulmonary capillaries in the test group showed a 27% reduction in their luminal area, which was associated with a 73% reduction in their patency due to occlusion by WBC and cell debris. In addition there was endothelial and epithelial disruption with basement membrane exposure. The PMN were degranulated and adherent to the pulmonary endothelium. Pretreatment with the phospholipase inhibitor, mepacrine, significantly attenuated these responses, so that there was only an increase of 200% in PMN and 450% in lymphocytes in the lungs with no evidence of degranulation or adhesion to the pulmonary endothelium. Furthermore there was no change in capillary luminal area when compared to the sham operated group. In addition there was only slight damage to the endothelium and epithelium with no exposure of the basement membrane. Peripheral WBC in both the test and mepacrine groups showed a similar 62% and 75% reduction after 5 h when compared to baseline values. The sham group did not show this change. These results suggest that phospholipase inhibition plays an important role in attenuating the pulmonary response to faecal peritonitis and may be of potential benefit in treating clinical septicaemia.

Animals↗

PubMed1982

Abolition, by dopamine blockade, of the natriuretic response produced by lower-body positive pressure.

1. In a preliminary study, a positive pressure of 25 mmHg applied to the lower body raised right atrial pressure by a mean of 7 mmHg. 2. Sustained application of lower-body positive pressure (LBPP) in six normal adult males increased sodium excretion ([Na]V) from a control level of 126.5 +/- 10 mumol/min to 213 +/- 21 mumol/min (P = 0.003) and fractional sodium excretion (EfNa) from 0.7 +/- 0.1 to 1.2 +/- 0.1 (P = 0.001). 3. Urine flow (UF) increased from 0.85 +/- 0.07 ml/min to 4.1 +/- 0.8 ml/min (P = 0.002), osmolar clearance (Cosm) from 2.6 +/- 0.13 ml/min to 4.2 +/- 0.4 ml/min (P = 0.003) and free water clearance (CH2O) from -1.75 +/- 0.1 ml/min to -0.1 +/- 0.01 ml/min (P = 0.001). Creatinine clearance (Ccr) showed no significant change. 4. After dopamine blockade with domperidone, LBPP did not cause a rise in [Na]V or EfNa. However, urine flow, Cosm. and CH2O remained significantly above control values, implying persistent suppression of antidiuretic hormone. 5. Dopamine blockade without positive pressure did not affect basal sodium excretion.

Adolescent↗