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Carroll, G. L., Matthews, N. S., Hartsfield, S. M., Slater, M. R., Champney, T. H., & Erickson, S. W. (1997). The effect of detomidine and its antagonism with tolazoline on stress-related hormones, metabolites, physiologic responses, and behavior in awake ponies. Vet Surg, 26(1), 69–77.
Abstract: Six ponies were used to investigate the effect of tolazoline antagonism of detomidine on physiological responses, behavior, epinephrine, norepinephrine, cortisol, glucose, and free fatty acids in awake ponies. Each pony had a catheter inserted into a jugular vein 1 hour before beginning the study. Awake ponies were administered detomidine (0.04 mg/kg intravenously [i.v.]) followed 20 minutes later by either tolazoline (4.0 mg/kg i.v.) or saline. Blood samples were drawn from the catheter 5 minutes before detomidine administration (baseline), 5 minutes after detomidine administration, 20 minutes before detomidine administration which was immediately before the administration of tolazoline or saline (time [T] = 0), and at 5, 30, and 60 minutes after injections of tolazoline or saline (T = 5, 30, and 60 minutes, respectively). Compared with heart rate at T = 0, tolazoline antagonism increased heart rate 45% at 5 minutes. There was no difference in heart rate between treatments at 30 minutes. Blood pressure remained stable after tolazoline, while it decreased over time after saline. Compared with concentrations at T = 0, tolazoline antagonism of detomidine in awake ponies resulted in a 55% increase in cortisol at 30 minutes and a 52% increase in glucose at 5 minutes. The change in free fatty acids was different for tolazoline and saline over time. Free fatty acids decreased after detomidine administration. Free fatty acids did not change after saline administration. After tolazoline administration, free fatty acids increased transiently. Tolazoline tended to decrease sedation and analgesia at 15 and 60 minutes postantagonism. Antagonism of detomidine-induced physiological and behavioral effects with tolazoline in awake ponies that were not experiencing pain appears to precipitate a stress response as measured by cortisol, glucose, and free fatty acids. If antagonism of an alpha-agonist is contemplated, the potential effect on hormones and metabolites should be considered.
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Pere, M. C. (1995). Maternal and fetal blood levels of glucose, lactate, fructose, and insulin in the conscious pig. J. Anim Sci., 73(10), 2994–2999.
Abstract: To study nutrition and metabolism in the fetal pig, a chronic catheterization method was developed that allows blood sampling in arteries and veins, at both the umbilical and uterine sources, in the conscious, unstressed animal. A catheter was inserted in the fetal aorta through a femoral artery, and another one was introduced in the umbilical vein. A catheter was put in a femoral artery of the sow so that its end was in the abdominal aorta. A fourth catheter was placed in a uterine vein draining the fetoplacental unit studied. This procedure was applied to 18 Large White primiparous sows at 99 d of gestation. Blood samples were drawn simultaneously using the four catheters before a meal at 103 d of pregnancy, and glucose, insulin, lactate, and fructose were determinated. Glycemia was 2.5 times higher in the sow than in the fetus. The extraction coefficient of glucose by the fetus amounted to 14% of the umbilical supply. The insulin level in the fetal pig was very low ( < 5 microU/mL). Lactate and fructose seemed to originate from the placenta. Blood lactate was 2.6 times lower in the sow than in the fetus, and its extraction coefficient by the fetus amounted to 8%. Fructose in the fetal blood was 2.3 times higher than that of glucose. Fructose was not utilized by the pig fetus. The present results obtained in the fetal pig are comparable to the conclusions drawn from studies with other species.
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