Over a 54-hour period, blood was removed from 8 adult sheep (body weight, 38.1 +/- 0.5 kg mean +/- SEM) in 9 episodes, 5 on day 1, 3 on day 2, and 1 on day 3. Cumulative blood loss was 1,630 +/- 63, 2,380 +/- 71, and 2,693 +/- 69 ml on days 1, 2, and 3, respectively. Blood samples (20 ml) were collected from 5 control ewes (33.8 +/- 2.8 kg) at equivalent times. Over the first day, mean arterial blood pressure decreased in the hemorrhaged sheep from 101 +/- 2 mm of Hg to 76 +/- 5 mm of Hg, but returned to control values by the beginning of the second day and, thereafter, was not different from control values. Heart rate was increased after the first hemorrhage episode and remained high throughout the entire protocol. Over the entire period, there were statistically significant decreases in hematocrit, plasma osmolality, sodium, total calcium (P < 0.001), potassium, and chloride values (P < 0.05). There was no change in plasma phosphate, bicarbonate, creatinine, or magnesium concentrations and an increase in plasma urea nitrogen (P < 0.001) concentrations. Plasma arginine vasopressin concentration was increased significantly (P < 0.001) over the entire period. Plasma ACTH concentration was significantly (P < 0.05) increased over time, but only some values on day 1 were significantly outside the normal range of the control group data. Because of wide variation between sheep, the group data for aldosterone were not significantly different from control values. Blood volume was restored on day 1 with fluid of osmolality, Na, and Cl composition equivalent to that of plasma. The effects of arginine vasopressin were apparent by day 2, when the major decrease in osmolality and Na and Cl concentrations were observed The sheep has good capacity to withstand severe, prolonged hemorrhage, most likely because of a large reserve of RBC in the spleen; hematocrit remained at 31% of control values when an estimated 100% of initial circulating blood volume had been removed.

Effects of dietary ochratoxin A (OA) and T-2 toxin, fed singly and in combination, were evaluated in growing crossbred pigs. Thirty-six barrows (3 replicates of 3 for each of 4 treatment groups, mean body weight, 18.0 kg) were fed: 0 mg of OA and 0 mg of T-2/kg of feed (control); 2.5 mg of OA/kg of feed; 8.0 mg of T-2/kg of feed; or 2.5 mg of OA plus 8.0 mg of T-2/kg of feed for 30 days. Production performance, serum biochemical, hematologic, immunologic, and pathologic evaluations were made. Body weight and body weight gain were decreased by all toxin treatments, but the combination toxin treatment reduced weight gain more than did either of the toxins administered singly and could be considered additive. Liver weight was decreased by combination treatment, whereas kidney weight was increased by OA treatment. Ochratoxin decreased serum cholesterol, inorganic phosphorus, and alkaline phosphatase values; reduced mean cell volume, hemoglobin concentration, and macrophage phagocytosis; and increased creatinine and total protein values. Consumption of T-2 toxin reduced hemoglobin and serum alkaline phosphatase values. The combination treatment decreased serum cholesterol, gamma-glutamyltransferase, alkaline phosphatase, mean cell volume, hematocrit, and hemoglobin values, as well as lymphoblastogenesis and phagocytosis, and increased serum nine concentration. We concluded that OA and T-2, singly or in combination, can affect clinical performance, serum biochemical, hematologic, and immunologic values, and organ weights of growing barrows. Although some analytes were affected more by the combination than by either toxin alone, the interactions could best be described as additive, not synergistic.

In this preliminary investigation, various hematologic variables potentially influential in determining the degree of blood viscosity were evaluated in 10 Thoroughbred horses subjected to competitive acute running exercise. Following completion of sprints over a distance of 1.25 miles, mean percent (+/- SD) increases in PCV (38.3 +/- 12.9%), RBC (47.8 +/- 15.3%), and rouleaux index (232.7 +/- 176.8%) were recognized. Simultaneous increases in total plasma protein (28.3 +/- 5.31%), serum albumin (26.7 +/- 6.80%), alpha 1-globulin (60.0 +/- 49.0%), alpha 2-globulin(25.5 +/- 27.9%), beta 1-globulin (46.7 +/- 21.1%), beta 2-globulin (35.0 +/- 50.6%), gamma 1- and 2-globulins (38.7 +/- 29.6%), and plasma fibrinogen (12.5 +/- 10.4%) concentrations increased simultaneously. Horses also had consistent decreases in albumin:globulin ratio (- 10.0 +/- 7.43%). Alterations in these hematologic values after acute running exercise in Thoroughbred horses accompanied increases in serum (69.3 +/- 39.7%), plasma (39.7 +/- 11.9%), and blood (134.7 +/- 55.3%) viscosity.

L-lactic acid and D,L-lactic acid infusion in ponies resulted in metabolic acidosis with high anion gap (AG). Increased AG was explained entirely by increased blood L- and D-lactate concentrations. Hydrochloric acid infusion caused metabolic acidosis with decreased AG. Saline (NaCl) infusion caused mild metabolic acidosis, with no significant change in AG. Plasma K+ concentration was decreased by all types of infusions, with a maximum of 0.50, 0.25, 0.40, 0.50 mmol/L below baseline at the end of infusion in the L-lactic acid-, D,L-lactic acid-, HCl-, and NaCl-infused ponies, respectively. Only hydrochloric acid had a tendency to increase plasma K+ concentration. Hypophosphatemia developed in NaCl- and HCl-infused ponies, but not in the D,L-lactic acid-infused ponies. Serum inorganic phosphate concentration in L-lactic acid-infused ponies increased initially, but was significantly (P < 0.05) lower than values in the other ponies at 4 hours after onset of infusion. In ponies, the effect of acidemia on plasma K+ and serum inorganic phosphate concentrations was similar to that reported for other species. Changes were small in magnitude and depended on the nature of the acid anion. Results indicate that large changes in plasma K+ and serum inorganic phosphate concentrations during acidosis are probably not a direct result of acidemia.

We compared the ability of 2 alpha2-adrenergic receptor antagonists, atipamezole and yohimbine, to reverse medetomidine-induced CNS depression and cardiorespiratory changes in lambs. Twenty lambs (7.8 +/- 2.6 kg) were randomly allotted to 4 treatment groups (n = 5). Each lamb was given medetomidine (30 micrograms/kg of body weight, IV), followed in 15 minutes by IV administration of atipamezole (30 or 60 micrograms/kg), yohimbine (1 mg/kg), or 0.9% NaCl (saline) solution. Medetomidine caused lateral recumbency in 1 to 2 minutes in all treated lambs. Medetomidine significantly (P < 0.05) decreased heart rate at 5 and 10 minutes after its administration. Heart rate remained above 120 beats/min, and severe bradycardia (< 70 beats/min) and other arrhythmias did not occur throughout the study. Medetomidine also induced tachypnea in all treated lambs. The tachypnea was abolished by atipamezole and yohimbine, but not by saline solution administration. The medetomidine-induced tachypnea did not significantly affect arterial pH and PaCO2. Arterial oxygen tension was within acceptable range (PaO2 = 71 to 62 mm of Hg), but was lower than expected. Administration of atipamezole, yohimbine, or saline solution did not change PaO2 significantly. Lambs treated with 30 or 60 micrograms of atipamezole/kg were able to walk unassisted in 2.4 +/- 0.4 and 2.3 +/- 0.7 minutes, respectively, whereas yohimbine-and saline-treated lambs did not walk unassisted until 15.6 +/- 2.7 and 73.0 +/- 6.8 minutes later, respectively. Results of this study indicated that medetomidine is a potent CNS depressant in lambs. Atipamezole at dosage of 30 or 60 micrograms/kg was equally effective, and was more effective in antagonizing medetomidine-induced CNS depression than was yohimbine.