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  Discussion on Research Study: EIPH pathogenesis?
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DrO

Posted on Thursday, Oct 16, 2008 - 8:46 am:

Here is one of the best attempts at identifying the cause of EIPH I have seen. These researchers found remodeling of the vasculature to some areas of the lung that lead to occlusion of the venules, the small veins that drain the lung. This would be equivalent to stopping up a hose and having the pressure "split the hose" and spouting leaks. Around these areas signs of hemorrhage and the changes associated with hemorrhage were common. So it does leave us the question of what caused the original venous occlusion.
DrO

Regional pulmonary veno-occlusion: a newly identified lesion of equine exercise-induced pulmonary hemorrhage.

Williams KJ, Eriksson FJ, de Feijter-Rupp H, Pannirselvam RR, Steel CM, Robinson NE.

Department of Pathobiology and Diagnostic Investigation, College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824, USA.

Exercise-induced pulmonary hemorrhage (EIPH) is common in horses following intense exertion, occurring in up to 75% of racing Thoroughbreds and Standardbreds. In spite of this, the pathogenesis of EIPH is poorly understood. In 7 racing Thoroughbred horses with EIPH, 6 sections were collected from the left and right lung, representing the cranial, middle, and caudal region of the dorsal and ventral lung (84 sites total). Grossly, both right and left lungs had numerous dark brown to blue-black foci along the caudodorsal visceral pleura. Tissue sections were stained with hematoxylin-eosin, Masson's trichrome, and Prussian blue. Verhoeff Van Gieson and immunohistochemistry for alpha-smooth muscle actin were used to assess the pulmonary vasculature. Histologic scores (HS = 0-3) were assigned to each region/slide for the presence and severity of 5 findings: interstitial fibrosis, hemosiderin accumulation, pleural/interlobular septal thickness, arterial and venous wall thickness, and evidence of angiogenesis (maximum cumulative HS = 15). Thirty-nine of the 84 (46%) sections were histologically normal (HS = 0); 33/84 (39%) were mildly to moderately affected, with small amounts of hemosiderin and fibrosis (HS = 1-9) while 12/84 (14%), primarily from the dorsocaudal lung, had severe vascular remodeling, fibrosis, and hemosiderin accumulation (HS = 10-15). In the latter, veno-occlusive remodeling of the interlobular veins colocalized with hemosiderosis, fibrosis, hypertrophy of vessels within the pleura, and interlobular septa and bronchial neovascularization. We propose that regional veno-occlusive remodeling, especially within the caudodorsal lung fields, contributes to the pathogenesis of EIPH, with the venous remodeling leading to regional vascular congestion and hemorrhage, hemosiderin accumulation, fibrosis, and bronchial angiogenesis.
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