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- Author or Editor: Kenneth H. McKeever x
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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)
Abstract
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)