peer reviewed

peer reviewed | OBJECTIVE: To characterize the cardiovascular response to i.v. administration of serotonin (5-hydroxytryptamine [5-HT]) in calves. ANIMALS: 5 healthy unsedated Friesian calves. PROCEDURE: 41 5-HT administrations were performed: II slow infusions (duration, 5 minutes) and 30 bolus infusions (duration, 5 seconds). Cardiovascular function values were recorded before, during, and after the infusion. RESULTS: Slow infusion of 5HT first resulted in a brief period of severe bradycardia, then in sustained tachycardia with a concomitant increase in cardiac output. Systemic initial hypotension concomitant with bradycardia, then a pressor phase associated with an increase in systemic vascular resistance, and finally, a long-lasting hypotensive phase associated with decreased systemic vascular resistance. Pulmonary hypertension was associated with increased pulmonary vascular resistance, reflecting intense pulmonary vasoconstriction. Bolus infusion at increasing dosages resulted in dose-dependent bradycardia and systemic hypotension, followed by dose-dependent systemic hypertension. Unlike with slow infusion, neither the second tachycardiac nor the third systemic hypotensive phases were evident. CONCLUSIONS: 5-HT induces dose-dependent cardiovascular responses, including a reflex response followed by pulmonary and systemic vasoconstriction, in healthy calves. CLINICAL RELEVANCE: Determining the type of serotonergic receptors responsible for these responses may help to determine whether 5-HT is involved in the mechanisms underlying brisket disease in cattle.

peer reviewed | OBJECTIVE--To characterize the hemodynamic effects of medetomidine (1 mg/m2 of body surface area; dosage, 39 to 46 micrograms/kg of body weight, IM) and midazolam (1 mg/kg of body weight, i.v.) combined with butorphanol (0.1 mg/kg, i.v.), buprenorphine (10 micrograms/kg, i.v.) or saline solution. Reversibility of these effects by atipamezole (2.5 mg/m2; dosage, 97.5 to 115 micrograms/kg, IM) was evaluated. DESIGN--2 treated groups and 1 control group, without repetition. ANIMALS--15 clinically normal dogs (3 groups of 5). PROCEDURE--Medetomidine was administered at time 0; midazolam and butorphanol, buprenorphine, or saline solution at time 20; and atipamezole at time 60. Heart rate, systemic and pulmonary arterial pressures, central venous pressure, body temperature, cardiac output, and arterial and mixed venous blood gas tensions and pH were measured. Cardiac index, stroke index, systemic and pulmonary vascular resistances, and left and right stroke work indexes were calculated. RESULTS--Body temperature, heart rate, cardiac index, and stroke index were significantly decrease below baseline values in some groups. Central venous pressure, pulmonary capillary wedge pressure, and systemic vascular resistance were significantly increased above baseline in all groups. Arterial and venous PO2 and pH decreased in all groups and PCO2 increased, but these changes were more pronounced when buprenorphine was administered. Arterial pressure decreased after atipamezole administration. CONCLUSION--The combinations seemed to result in cardiorespiratory depressant effects of similar importance and most of these effects, which are related to medetomidine, were reversed by atipamezole.

Healthy gilts and market-ready hogs were administered a single intramuscular (IM) injection of Borgal, a commercial formulation of trimethoprim-sulfadoxine (TMP-SDX), once or twice daily. The objectives were to determine if a newly-developed high-performance liquid chromatographic (HPLC) method would be suitable for measuring the residual concentrations of TMP in the plasma of these live animals, and to determine if the administration of this veterinary drug would leave measurable residues in their plasma and tissues at slaughter. Plasma and tissue concentrations of SDX and TMP from these animals were determined over a period of 14 d using thin-layer chromatography/densitometry (TLCD), and the newly-developed HPLC method, respectively. The lowest detectable limit (LDL) for SDX in plasma and tissue was 20 ppb by TLCD. The HPLC method had a LDL of 5 ppb for TMP in plasma and tissue. Both methods were then used to provide baseline data on the absorption and depletion of TMP and SDX from these healthy animals. It was observed that both TMP and SDX were readily absorbed into the blood and tissues, but TMP was eliminated much faster than SDX. No TMP residues were detected in the plasma of any of the gilts at and beyond 21 h after drug administration. Also, no TMP residues were detected in the plasma of any of the market-ready hogs 24 h after drug administration at either the label dose or twice the label dose. Sulfadoxine residues at concentrations above the maximum residue limit (MRL) of 100 ppb were, however, detected in the plasma, muscle, kidney, liver, and injection sites of hogs slaughtered 1 and 3 d after a single IM administration at the label dose. Although SDX residues were still detectable in the lungs, kidney, liver and plasma of some hogs 10 d after administration of the label dose and twice the label dose, these were below the MRL. Postmortem examination revealed necrosis and inflammation at the injection sites, but no visible deposits of the injected drug.

The impact of dietary sodium on the incidence of nursing sickness in mink dams and on the average litter biomass of 28 and 42 day old kits was studied. One group (n = 115 including 12 barren females) was given a standard feed mixture with a natural content of 0.53 g NaCl/MJ and another group (n = 115 including 8 barren females) was given the same feed mixture supplemented with NaCl to a final content of 1.00 g/MJ. The average dam weight at weaning was significantly lower (P < 0.001) and the incidence of nursing sickness during the last part of the lactation period 3 times higher in the nonsupplemented group. The average litter biomass at weaning did not differ between the 2 experimental groups. A number of biochemical markers of preclinical nursing sickness, e.g. plasma aldosterone and osmolality, Na+ and Cl concentrations in plasma and urine, were studied during the last part of the lactation period and at weaning in 20 dams of the nonsupplemented group, in 10 dams of the salt supplemented group and, for comparison, in 5 + 5 barren females on the day corresponding to day 34 after parturition in nursing mink. The nonsupplemented group had significantly lower concentrations of sodium and chloride in plasma and urine and a significantly higher concentration of plasma aldosterone as compared to the salt supplemented group. Distinct signs of relative salt deficiency and preclinical nursing sickness thus characterized the nonsupplemented group throughout this period, while more blurred hints of electrolyte imbalances were noticed in the sodium chloride supplemented group at weaning. A beneficial effect of salt supplementation on the incidence of nursing sickness was shown; however, it remains unclear whether salt deficiency can cause nursing sickness or whether salt acts as an appetite stimulant preventing inanition and the development of the disorder.