Department of Surgery, Tufts University School of Veterinary Medicine, North Grafton, Massuchusetts 01536, USA.
Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. V. Microscopic observations
Article first published online: 23 APR 2010
© 1987 EVJ Ltd
Equine Veterinary Journal
Volume 19, Issue 5, pages 411–418, September 1987
How to Cite
O'CALLAGHAN, M. W., PASCOE, J. R., TYLER, W. S. and MASON, D. K. (1987), Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. V. Microscopic observations. Equine Veterinary Journal, 19: 411–418. doi: 10.1111/j.2042-3306.1987.tb02632.x
- Issue published online: 23 APR 2010
- Article first published online: 23 APR 2010
- Received for publication 28.1.87 Accepted 30.6.87
Lungs from 19 Thoroughbred racehorses with a history of exercise-induced pulmonary haemorrhage (EIPH) were studied using several forms of microscopy. Light microscopy of paraffin sections revealed three lesions in the caudodorsal region of the lungs from each horse. These correspond with the location of blue to brown stains seen at necropsy. These lesions include sequelae of bronchiolitis, hemosiderophages and increased connective tissue. Much of each of the lungs appeared normal, especially the more cranial or ventral portions. Foci of eosinophil infiltration were found in seven of the 19 lungs examined. With two exceptions, these eosinophilic foci had a different distribution to the three lesions. In areas of severe bronchiolar changes and fibrosis, vascular lesions typical of hypertension were found occasionally. Transmission electron microscopy was used to confirm cell types seen by light microscopy and to examine arterioles for changes characteristic of neovascularisation. Areas of enlarged airspaces from the vascular injected right lungs were examined by scanning electron microscopy. The balance of fibrosis and destruction varied in these areas, but none were as extensive as those seen in chronic obstructive pulmonary disease. The authors hypothesise that bronchiolitis and related neovascularisation are essential components of the aetiology of EIPH.