Replacement of chloride deficit by use of 1.8% NaCl to correct experimentally induced hypochloremic metabolic alkalosis in sheep

S. L. Fubini From the Department of Clinical Sciences, New York State College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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D. F. Smith From the Department of Clinical Sciences, New York State College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Y. T. Grohn From the Department of Clinical Sciences, New York State College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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S. A. Levine From the Department of Clinical Sciences, New York State College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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D. M. Deuel From the Department of Clinical Sciences, New York State College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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SUMMARY

Five adult 40- to 50-kg female sheep were surgically fitted with a reentrant cannulae placed in the proximal part of the duodenum just distal to the pylorus. By diversion of abomasal outflow, this model has been shown to produce hypochloremic metabolic alkalosis accompanied by dehydration, hypokalemia, and hyponatremia. Each sheep was subjected to 3 separate, 12-hour iv treatment trials, in each case preceded by a control period of 48 hours, and a diversion period of 36 to 96 hours, during which a hypochloremic (Cl ≤ 60 ± 2 mEq/L) metabolic alkalosis with hypokalemia and hyponatremia was produced.

Treatment 1, consisting of 6 L of isotonic Na gluconate, was designed to replace volume without replenishing the Cl deficit. Although hydration improved, plasma Cl decreased further, and the sheep became increasingly weak and depressed. Treatment 2, consisting of 2 L of 1.8% NaCl, was designed to replace the Cl deficit without replacing total volume. Plasma Na+ and Cl concentrations returned to normal during the 12 hours of treatment; acid-base balance and plasma K+ concentrations returned to normal within 36 hours of treatment. During treatment 3 (control, no treatment), measured metabolic values changed minimally. We concluded that the iv replacement of Cl without K+ is effective in the correction of experimentally induced hypochloremic metabolic alkalosis in sheep.

SUMMARY

Five adult 40- to 50-kg female sheep were surgically fitted with a reentrant cannulae placed in the proximal part of the duodenum just distal to the pylorus. By diversion of abomasal outflow, this model has been shown to produce hypochloremic metabolic alkalosis accompanied by dehydration, hypokalemia, and hyponatremia. Each sheep was subjected to 3 separate, 12-hour iv treatment trials, in each case preceded by a control period of 48 hours, and a diversion period of 36 to 96 hours, during which a hypochloremic (Cl ≤ 60 ± 2 mEq/L) metabolic alkalosis with hypokalemia and hyponatremia was produced.

Treatment 1, consisting of 6 L of isotonic Na gluconate, was designed to replace volume without replenishing the Cl deficit. Although hydration improved, plasma Cl decreased further, and the sheep became increasingly weak and depressed. Treatment 2, consisting of 2 L of 1.8% NaCl, was designed to replace the Cl deficit without replacing total volume. Plasma Na+ and Cl concentrations returned to normal during the 12 hours of treatment; acid-base balance and plasma K+ concentrations returned to normal within 36 hours of treatment. During treatment 3 (control, no treatment), measured metabolic values changed minimally. We concluded that the iv replacement of Cl without K+ is effective in the correction of experimentally induced hypochloremic metabolic alkalosis in sheep.

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