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Abstract

Objective—To determine components of the increase in oxygen consumption (O2) and evaluate determinants of hemoglobin saturation (SO2) during incremental treadmill exercise in unfit horses.

Animals—7 unfit adult mares.

Procedures—Horses performed 1 preliminary exercise test (EXT) and 2 experimental EXT. Arterial and mixed venous blood samples and hemodynamic measurements were taken during the last 30 seconds of each step of the GXT to measure PO2, hemoglobin concentration ([Hb]), SO2, and determinants of acidbase state (protein, electrolytes, and PCO2).

Results—Increased O2 during exercise was facilitated by significant increases in cardiac output (CO), [Hb], and widening of the arteriovenous difference in O2. Arterial and venous pH, PaO2, and PvO2 decreased during exercise. Arterial PCO2, bicarbonate ([HCO3])a, and [HCO3]v decreased significantly, whereas PvCO2 and increased. Arterial and venous sodium concentration, potassium concentration, strong ion difference, and venous lactate concentration all increased significantly during exercise.

Conclusions and Clinical Relevance—Increases in CO, [Hb], and O2 extraction contributed equally to increased O2 during exercise. Higher PCO2 did not provide an independent contribution to shift in the oxyhemoglobin dissociation curve (OCD) in venous blood. However, lower PaCO2 shifted the curve leftward, facilitating O2 loading. The shift of ODC resulted in minimal effect on O2 extraction because of convergence of the ODC at lower values of PO2. Decreased pH appeared responsible for the rightward shift of the ODC, which may be necessary to allow maximal O2 extraction at high blood flows achieved during exercise. (Am J Vet Res 2000;61:1325–1332)

Full access
in American Journal of Veterinary Research

Objective—

To determine the clinical findings, course of treatment, and long-term outcome of horses on a farm in central Kentucky during an epizootic of equine protozoal myeloencephalitis (EPM).

Design—

Cohort study.

Animals—

21 horses on a farm in central Kentucky, 12 of which developed clinical signs of EPM.

Procedure—

Horses on the farm were serially examined for signs of neurologic disease and serum and CSF antibodies to Sarcocystis neurona. Horses were considered to have EPM if they had neurologic signs and positive test results for antibodies to S neurona in CSF. Blood values were monitored for evidence of abnormalities resulting from long-term pyrimethamine and trimethoprim-sulfamethoxazole administration. Physical, neurologic, and fetal necropsy examinations were performed as needed. Horses were treated for EPM until they had negative test results for CSF antibodies to S neurona.

Results—

Of 21 horses on the farm, 12 had EPM over the course of 6 months. The duration of treatment ranged from 45 to 211 days, excluding 1 horse that persistently had CSF antibodies to S neurona. Adverse effects from pyrimethamine and trimethoprim-sulfamethoxazole administration included transient fever, anorexia, and depression (n = 2); acute worsening of ataxia (2); mild anemia (4); and abortions (3).

Clinical Implications—

EPM may develop as an epizootic. In the horses of this report, subtle clinical signs that were originally considered unimportant ultimately progressed to obvious neurologic signs. Adverse effects associated with EPM treatment included worsening of neurologic signs, anemia, abortion, and leukopenic and febrile episodes. (J Am Vet Med Assoc 1997;210:923–927)

Free access
in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association