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  • Author or Editor: Kenneth H. McKeever x
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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)

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in American Journal of Veterinary Research


Objective—To describe neuroendocrine responses that develop in dogs subjected to prolonged periods of ventricular pacing.

Animals—14 adult male hound-type dogs.

Procedure—Samples were obtained and neuroendocrine responses measured before (baseline) and after 3 periods of ventricular pacing. A pacemaker was used to induce heart rates of 180, 200, and 220 beats/min (BPM). Each heart rate was maintained for 3 weeks before increasing to the next rate. Atrial natriuretic peptide, antidiuretic hormone, aldosterone, norepinephrine, epinephrine, and dopamine concentrations and plasma renin activity were measured. Severity of left ventricular compromise was estimated.

Results—Shortening fraction decreased significantly with increasing heart rates (mean ± SE, 35.5 ± 1.4, 25.0 ± 1.4, 19.5 ± 1.9, and 12.2 ± 2.3 for baseline, 180 BPM, 200 BPM, and 220 BPM, respectively). Atrial natriuretic peptide concentrations increased significantly at 180 BPM (44.1 ± 3.0 pg/mL) and 200 BPM (54.8 ± 5.5 pg/mL), compared with baseline concentration (36.8 ± 2.6 pg/mL). Dopamine concentration increased significantly at 200 BPM (70.4 ± 10.4 pg/mL), compared with baseline concentration (44.2 ± 7.3 pg/mL). Norepinephrine concentrations increased significantly from baseline concentration (451 ± 46.2 pg/mL) to 678 ± 69.8, 856 ± 99.6, and 1,003 ± 267.6 pg/mL at 180, 200, and 220 BPM, respectively.

Conclusions and Clinical Relevance—Dogs subjected to ventricular pacing for 9 weeks developed neuroendocrine responses similar to those that develop in humans with more chronic heart failure and, except for epinephrine concentrations, similar to those for dogs subjected to ventricular pacing for < 6 weeks. (Am J Vet Res 2002;63:1413–1417)

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in American Journal of Veterinary Research