Summary
Developmental changes of the gastrointestinal tract were probably responsible for the changes in faecal composition during the first week of the foals' life, which resembled small intestinal ingesta of adult horses, suggesting a minimal colonic modification. Faecal composition at the time of foal heat diarrhoea was suggestive of a secretory‐type diarrhoea, in that the electrolyte concentration accounted for most of faecal osmolality and the faecal pH was alkaline. After foal heat diarrhoea faecal composition slowly approached that of adult horses. These data suggest that foal heat diarrhoea is most likely caused by hypersecretion in the small intestinal mucosa, which may overwhelm an immature colon that is unable to compensate by increased fluid and electrolyte absorption.
Summary
Plasma volume (PV) decreased by 13 per cent following the completion of 1,000 m of maximal exercise in the horse. This study demonstrated that the critical reduction in PV following maximal exercise occurred within 10 mins of completion of exercise, as previously reported in man. Total plasma protein (TPP) increased by 23 per cent at 2 and 5 mins, and by 21 per cent at 10 mins post exercise. Therefore, it does not appear to be an accurate measurement to assess the degree of PV contraction in the horse. Protein was apparently added to the intravascular space either during or following exercise. The changes in osmolality correlated strongly with those in sodium, which is the primary determinant of alterations in plasma tonicity. The increase in osmolality (12 per cent) was similar to the reduction in PV (13 per cent) concluding that a transient hypotonic fluid loss had occurred. The increase in plasma renin activity (PRA) following maximal exercise was followed by an increase in aldosterone (ALD) concentration in both magnitude and time course. Alterations in PV should be considered when interpreting electrolyte and serum enzyme activity data collected following maximal exercise.
Chronic laminitis is a disabling condition that affects the laminar corium of the horse’s hooves. Commonly, it develops as a collateral injury of numerous primary systemic diseases. It is believed that the critical physiopathological event that renders a hoof laminitic is the loss of mesenchymal stem cells. This loss greatly impairs the ability of the laminar corium to regenerate. Although previous work provides credibility to this notion, there remain unsettled issues that must be addressed before accepting it as a well-founded fact. Here, it was reexamined the central tenet of the physiopathological model of laminitis by infusing allogeneic bone marrow-derived mesenchymal stem cells (ABM-MSCs), through the digital palmar vein, into the hooves of horses afflicted by chronic laminitis. Horses were clinically monitored during 6 mo by evaluating them monthly using the lameness-modified Obel-Glasgow’s scale and hooves thermography. Venograms and lamellar biopsies were taken at the beginning and at the end of the study period to gathered evidence on vascular remodeling and laminar corium regeneration. The results showed that ABM-MSCs infusion promotes vascular remodeling and laminar corium regeneration, further supporting that the loss of stem cells is the critical event leading to chronic laminitis. This work also demonstrated that the infusion of ABM-MSCs is safe since the treated horses did not develop local or systemic, negative clinical manifestations attuned with rejection reactions, at least during the 6-mo period they were follow up and under the therapeutic scheme proposed.
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