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  • Author or Editor: Neil C. Olson x
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SUMMARY

We evaluated the biochemical and hemodynamic response to hypertonic saline solution plus dextran in isoflurane-anesthetized pigs infused IV with Escherichia coli endotoxin (5 μg/kg of body weight for 0 to 1 hour + 2 μg/kg for 1 to 4 hours). After 120 minutes of endotoxemia, pigs were treated with a bolus (4 ml/kg over 3 minutes) of either normal saline solution (NSS; 0.9% NaCI), or hypertonic saline solution plus dextran (HSSD; 7.5% NaCI + 6% dextran-70). Administration of HSSD significantly (P < 0.05) increased serum osmolality and concentrations of sodium and chloride for approximately 2 hours during endotoxemia. Plasma total protein concentration decreased significantly (P < 0.05) for 2 hours after treatment with HSSD, indicating hemodilution and increased plasma volume. Although HSSD transiently increased cardiac index (CI) for approximately 15 minutes, this effect was not sustained; however, the endotoxin-induced decrease in CI was ameliorated from 120 to 180 minutes. In pigs of the endotoxin + NSS group from 180 to 240 minutes, CI decreased significantly (P < 0.05), compared with baseline and control values. The endotoxin-induced increases in mean pulmonary arterial pressure and pulmonary vascular resistance were not attenuated by HSSD. At 135 minutes, total peripheral vascular resistance was transiently lower (for approx 15 minutes) in pigs treated with HSSD, compared with control pigs. The endotoxin-induced increase in plasma lactate concentration was not attenuated by HSSD, indicating continued peripheral O2 debt. We conclude that, despite sustained increases in serum osmolality and concentrations of sodium and chloride, HSSD has only transiently beneficial cardiopulmonary effects during endotoxemia in pigs.

Free access
in American Journal of Veterinary Research

Summary

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.

Free access
in American Journal of Veterinary Research