Effect of hypertonic vs isotonic saline solution on responses to sublethal Escherichia coli endotoxemia in horses

Joseph J. Bertone From the Department of Veterinary Clinical Sciences (J. Bertone, Shoemaker, A. Bertone, Schneiter) and Department of Clinical Pathology (Gossett), Louisiana State University School of Veterinary Medicine, Baton Rouge, LA 70803.

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Kent A. Gossett From the Department of Veterinary Clinical Sciences (J. Bertone, Shoemaker, A. Bertone, Schneiter) and Department of Clinical Pathology (Gossett), Louisiana State University School of Veterinary Medicine, Baton Rouge, LA 70803.

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Katherine E. Shoemaker From the Department of Veterinary Clinical Sciences (J. Bertone, Shoemaker, A. Bertone, Schneiter) and Department of Clinical Pathology (Gossett), Louisiana State University School of Veterinary Medicine, Baton Rouge, LA 70803.

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Alicia L. Bertone From the Department of Veterinary Clinical Sciences (J. Bertone, Shoemaker, A. Bertone, Schneiter) and Department of Clinical Pathology (Gossett), Louisiana State University School of Veterinary Medicine, Baton Rouge, LA 70803.

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Harvey L. Schneiter From the Department of Veterinary Clinical Sciences (J. Bertone, Shoemaker, A. Bertone, Schneiter) and Department of Clinical Pathology (Gossett), Louisiana State University School of Veterinary Medicine, Baton Rouge, LA 70803.

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SUMMARY

Cardiovascular responses to sublethal endotoxin infusion (Escherichia coli, 50 μg/ml in lactated Ringer solution at 100 ml/h until pulmonary arterial pressure increased by 10 mm of Hg) were measured 2 times in 5 standing horses. In a 2-period crossover experimental design, horses were either administered hypertonic (2,400 mosm/kg of body weight, iv) or isotonic (300 mosm/kg, iv) NaCl solution after endotoxin challenges. Each solution was administered at a dose of 5 ml/kg (infusion rate, 80 ml/min). Complete data sets (mean arterial, central venous, and pulmonary arterial pressures, pulmonary arterial blood temperature, cardiac output, total peripheral vascular resistance, heart rate, plasma osmolality, plasma concentration of Na, K, Cl, and total protein, blood lactate concentration, and pcv) were collected at 0 (baseline, before endotoxin infusion), 0.25, 1, 1.5, 2, 2.5, 3, 3.5, 4, and 4.5 hours after initiation of the endotoxin infusion. Blood constituents alone were measured at 0.5 hour and cardiovascular variables alone were evaluated at 0.75 hour. By 0.25 hour, endotoxin infusion was completed, a data set was collected, and saline infusion was initiated. By 0.75 hour, saline solutions had been completely administered.

Mean (± sem) cardiac output decreased (99.76 ± 3.66 to 72.7 ± 2.35 ml/min/kg) and total peripheral resistance (1.0 ± 0.047 to 1.37 ± 0.049 mm of Hg/ml/min/kg) and pulmonary arterial pressure (33.4 ± 0.86 to 58.3 ± 1.18 mm of Hg) increased for both trials by 0.25 hour after initiation of the endotoxin infusion and prior to fluid administration. For the remainder of the protocol, cardiac output was increased and total peripheral resistance was decreased during the hypertonic, compared with the isotonic, saline trial. Cardiac output was decreased and total peripheral resistance was increased during the isotonic saline trial, compared with baseline values. Both trials were associated with increased blood lactate concentration, but lactate values during the isotonic saline trial were greater and remained increased above baseline values for a longer period (4 hours) than during the hypertonic saline trial (2.5 hours). It was concluded for this model of endotoxemia, that iv administered hypertonic saline solution was associated with more-desirable cardiovascular and metabolic responses than was an equal volume of isotonic saline solution.

SUMMARY

Cardiovascular responses to sublethal endotoxin infusion (Escherichia coli, 50 μg/ml in lactated Ringer solution at 100 ml/h until pulmonary arterial pressure increased by 10 mm of Hg) were measured 2 times in 5 standing horses. In a 2-period crossover experimental design, horses were either administered hypertonic (2,400 mosm/kg of body weight, iv) or isotonic (300 mosm/kg, iv) NaCl solution after endotoxin challenges. Each solution was administered at a dose of 5 ml/kg (infusion rate, 80 ml/min). Complete data sets (mean arterial, central venous, and pulmonary arterial pressures, pulmonary arterial blood temperature, cardiac output, total peripheral vascular resistance, heart rate, plasma osmolality, plasma concentration of Na, K, Cl, and total protein, blood lactate concentration, and pcv) were collected at 0 (baseline, before endotoxin infusion), 0.25, 1, 1.5, 2, 2.5, 3, 3.5, 4, and 4.5 hours after initiation of the endotoxin infusion. Blood constituents alone were measured at 0.5 hour and cardiovascular variables alone were evaluated at 0.75 hour. By 0.25 hour, endotoxin infusion was completed, a data set was collected, and saline infusion was initiated. By 0.75 hour, saline solutions had been completely administered.

Mean (± sem) cardiac output decreased (99.76 ± 3.66 to 72.7 ± 2.35 ml/min/kg) and total peripheral resistance (1.0 ± 0.047 to 1.37 ± 0.049 mm of Hg/ml/min/kg) and pulmonary arterial pressure (33.4 ± 0.86 to 58.3 ± 1.18 mm of Hg) increased for both trials by 0.25 hour after initiation of the endotoxin infusion and prior to fluid administration. For the remainder of the protocol, cardiac output was increased and total peripheral resistance was decreased during the hypertonic, compared with the isotonic, saline trial. Cardiac output was decreased and total peripheral resistance was increased during the isotonic saline trial, compared with baseline values. Both trials were associated with increased blood lactate concentration, but lactate values during the isotonic saline trial were greater and remained increased above baseline values for a longer period (4 hours) than during the hypertonic saline trial (2.5 hours). It was concluded for this model of endotoxemia, that iv administered hypertonic saline solution was associated with more-desirable cardiovascular and metabolic responses than was an equal volume of isotonic saline solution.

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