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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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Grubb, T. L., Foreman, J. H., Benson, G. J., Thurmon, J. C., Tranquilli, W. J., Constable, P. D., et al. (1996). Hemodynamic effects of calcium gluconate administered to conscious horses. J Vet Intern Med, 10(6), 401–404.
Abstract: Calcium gluconate was administered to conscious horses at 3 different rates (0.1, 0.2, and 0.4 mg/kg/min for 15 minutes each). Serum calcium concentrations and parameters of cardiovascular function were evaluated. All 3 calcium administration rates caused marked increases in both ionized and total calcium concentrations, cardiac index, stroke index, and cardiac contractility (dP/dtmax). Mean arterial pressure and right atrial pressure were unchanged; heart rate decreased markedly during calcium administration. Ionized calcium concentration remained between 54% and 57% of total calcium concentration throughout the study. We conclude that calcium gluconate can safely be administered to conscious horses at 0.1 to 0.4 mg/kg/min and that administration will result in improved cardiac function.
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Trim, C. M., Moore, J. N., & Clark, E. S. (1989). Renal effects of dopamine infusion in conscious horses. Equine Vet J Suppl, (7), 124–128.
Abstract: An ultrasonic flow probe was implanted around a branch of the left renal artery in five horses. The effects of dopamine were studied in the unsedated horses 10 days after surgery. Three experiments, separated by at least two days, were performed in random order on each horse. In two experiments, dopamine was infused intravenously for 60 mins at either 2.5 and 5.0 micrograms/kg bodyweight (bwt)/min. Saline was infused for 60 mins before and after each infusion, and for 180 mins in the third experiment as a control. Renal blood flow increased during administration of dopamine at both dose rates (P = 0.0001). Urine volume increased (P = 0.055), and osmolality decreased (P < 0.05), with infusion of dopamine at 5.0 micrograms/kg bwt/min. Arterial blood pressure and heart rate were not significantly affected. Fractional excretions of sodium and potassium were not significantly changed with dopamine infusion. The higher dopamine dose rate was accompanied by dysrhythmias in some horses.
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Alexander, F., & Collett, R. A. (1974). Pethidine in the horse. Res Vet Sci, 17(1), 136–137.
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Alexander, F., & Nicholson, J. D. (1968). The blood and saliva clearances of phenobarbitone and pentobarbitone in the horse. Biochem Pharmacol, 17(2), 203–210.
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de Waal, F. B. M. (2005). How animals do business. Sci Am, 292(4), 54–61.
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de Waal, F. B. M. (2004). Peace lessons from an unlikely source. PLoS. Biol., 2(4), E101.
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Preston, S. D., & de Waal, F. B. M. (2002). Empathy: Its ultimate and proximate bases. Behav Brain Sci, 25(1), 1–20; discussion 20–71.
Abstract: There is disagreement in the literature about the exact nature of the phenomenon of empathy. There are emotional, cognitive, and conditioning views, applying in varying degrees across species. An adequate description of the ultimate and proximate mechanism can integrate these views. Proximately, the perception of an object's state activates the subject's corresponding representations, which in turn activate somatic and autonomic responses. This mechanism supports basic behaviors (e.g., alarm, social facilitation, vicariousness of emotions, mother-infant responsiveness, and the modeling of competitors and predators) that are crucial for the reproductive success of animals living in groups. The Perception-Action Model (PAM), together with an understanding of how representations change with experience, can explain the major empirical effects in the literature (similarity, familiarity, past experience, explicit teaching, and salience). It can also predict a variety of empathy disorders. The interaction between the PAM and prefrontal functioning can also explain different levels of empathy across species and age groups. This view can advance our evolutionary understanding of empathy beyond inclusive fitness and reciprocal altruism and can explain different levels of empathy across individuals, species, stages of development, and situations.
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de Waal, F. B., Aureli, F., & Judge, P. G. (2000). Coping with crowding. Sci Am, 282(5), 76–81.
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Parish, A. R., & De Waal, F. B. (2000). The other “closest living relative”. How bonobos (Pan paniscus) challenge traditional assumptions about females, dominance, intra- and intersexual interactions, and hominid evolution. Ann N Y Acad Sci, 907, 97–113.
Abstract: Chimpanzee (Pan troglodytes) societies are typically characterized as physically aggressive, male-bonded and male-dominated. Their close relatives, the bonobos (Pan paniscus), differ in startling and significant ways. For instance, female bonobos bond with one another, form coalitions, and dominate males. A pattern of reluctance to consider, let alone acknowledge, female dominance in bonobos exists, however. Because both species are equally “man's” closest relative, the bonobo social system complicates models of human evolution that have historically been based upon referents that are male and chimpanzee-like. The bonobo evidence suggests that models of human evolution must be reformulated such that they also accommodate: real and meaningful female bonds; the possibility of systematic female dominance over males; female mating strategies which encompass extra-group paternities; hunting and meat distribution by females; the importance of the sharing of plant foods; affinitive inter-community interactions; males that do not stalk and attack and are not territorial; and flexible social relationships in which philopatry does not necessarily predict bonding pattern.
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