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  • Author or Editor: Richard E. Moon x
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We evaluated the effects of clenbuterol HCl (0.8 μg/kg, of body weight, iv), a β2, agonist, on ventilation-perfusion matching and hemodynamic variables in anesthetized (by iv route), laterally recumbent horses. The multiple inert gas elimination technique was used to assess pulmonary gas exchange. Clenbuterol HCl induced a decrease in arterial oxygen tension (from 57.0 ± 1.8 to 49.3 ± 1.2 mm of Hg; mean ± sem) as a result of increased shunt fraction (from 6.6 ± 2.1 to 14.4 ± 3.1%) and ventilation to regions with high ventilation-perfusion ratios. In contrast, no changes in these variables were found in horses given sterile water. In horses given clenbuterol HCl, O2 consumption increased from 2.23 ± 0.18 to 2.70 ± 0.14 ml · min-1 · kg-1, and respiratory exchange ratio decreased from 0.80 ± 0.02 to 0.72 ± 0.01. Respiratory exchange ratio and O, consumption were not significantly modified in sterile water-treated (control) horses. Clenbuterol HCl administration was associated with increased cardiac index (from 57.4 ± 4.0 to 84.2 ± 6.3 ml. min-1 · kg-1), decreased total peripheral vascular resistance (from 108.3 ± 9.3 to 47.6 ± 2.8 mm of Hg · s · kg · ml-1), and decreased pulmonary vascular resistance (from 31.3 ± 3.8 to 13.6 ± 0.7 mm of Hg · s · kg · ml-1). Our findings indicated that clenbuterol HCl may potentiate hypoxemia as a result of increased shunt fraction in horses anesthetized by the iv route, and caused changes in hemodynamic variables that were consistent with its ability to stimulate β2-adrenergic receptors.

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in American Journal of Veterinary Research


Eighteen healthy dogs were allotted to 3 groups (n = 6 dogs each). All dogs were evaluated at the beginning of the study by complete physical examination; total and differential WBC counts; serum biochemical analysis (alanine transaminase and alkaline phosphatase activities and bilirubin and albumin concentrations); sulfobromophthalein excretion, ammonia tolerance, and glucagon response testing; portal and intraparenchymal pressure determinations; operative mesenteric portography; and histologic assessment of hepatic biopsy specimens.

The left hepatic vein was ligated completely in dogs of groups 1 and 2. Group-3 (control) dogs had a ligature placed loosely around the left hepatic vein. Dogs of groups 1 and 3 were reevaluated 24 hours after surgery by use of the aforementioned hematologic and biochemical tests. Group-1 dogs were reevaluated by use of portal and intraparenchymal pressure determinations, jejunal vein portography, and complete necropsy at 48 hours after surgery. At 4 weeks after surgery, dogs of groups 2 and 3 were reevaluated by use of all aforementioned tests.

Results indicated transient hepatic congestion, which resolved by the fourth postoperative week. Longstanding effect on hepatic structure, circulation, or function was not found. We concluded that left hepatic vein ligation in clinically normal dogs does not cause severe or permanent liver damage.

Free access
in American Journal of Veterinary Research