Hypoproteinemia does not alter plasma volume expansion (PVE) in response to 0.9% saline infusion in sheep

K. I. Brauer, Donald Prough, L. D. Traber, D. L. Traber

Research output: Contribution to journalArticle

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Abstract

Introduction: Hypoproteinemia is associated with systemic and pulmonary edema during crystalloid infusion1. Although Stahle et al.2 have developed pharmacokinetic models to describe PVE in response to intravenous infusions, no data describe the influence on the distribution of infused crystalloid of hypoproteinemia, which we hypothesized would decrease the fraction of crystalloid remaining intravascularly. We addressed this hypothesis in conscious, chronically instrumented sheep. Methods: Halothane-anesthetized ewes (n=5, 37±3 kg) were surgically prepared with cardiopulmonary catheters. After a 5-day recovery period, each ewe was subjected to a 5-day test period. On days 1 and 5, we infused one liter of 0.9% saline (50 mL/min for 20 min). Plasmapheresis on days 2, 3 and 4 reduced serum protein concentration. PVE was kinetically analyzed from decreases in hemoglobin. Data from days 1 and 5 were compared via repeated measures analysis of variance, with P<0.05 considered significant. Results: Total plasma protein concentrations and colloid osmotic (oncotic) pressures decreased from 5.7±0.4 g/dL and 20.0±1.4 mmHg to 2.6±0.5 g/dL and 9.6±1.4 mmHg (p<0.05), respectively, after plasma-pheresis. However, the response of PVE was not different. PVE was 22.1±9.6% and 24.2±7.4% (p<0.05 vs baseline) at the end of the infusion and then decreased over 30 to 40 min to remain at 15.9±6.0% and 16.7±7.7%, in the eu-and hypoproteinemic states, repectively. Urinary output was not different. Discussion: Hypoproteinemia did not decrease the fraction of crystalloid remaining intravascularly in this conscious, large animal model. Because hypoproteinemia produced by plasmapheresis may not be equivalent to hypoproteinemia associated with critical illness, further studies are necessary in experimental models such as sepsis.

Original languageEnglish (US)
JournalCritical Care Medicine
Volume27
Issue number1 SUPPL.
StatePublished - 1999

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Hypoproteinemia
Plasma Volume
Sheep
Plasmapheresis
Blood Proteins
Blood Component Removal
Osmotic Pressure
Colloids
Halothane
Pulmonary Edema
Intravenous Infusions
Critical Illness
Sepsis
Analysis of Variance
Hemoglobins
Theoretical Models
Catheters
Animal Models
Pharmacokinetics
crystalloid solutions

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Hypoproteinemia does not alter plasma volume expansion (PVE) in response to 0.9% saline infusion in sheep. / Brauer, K. I.; Prough, Donald; Traber, L. D.; Traber, D. L.

In: Critical Care Medicine, Vol. 27, No. 1 SUPPL., 1999.

Research output: Contribution to journalArticle

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title = "Hypoproteinemia does not alter plasma volume expansion (PVE) in response to 0.9{\%} saline infusion in sheep",
abstract = "Introduction: Hypoproteinemia is associated with systemic and pulmonary edema during crystalloid infusion1. Although Stahle et al.2 have developed pharmacokinetic models to describe PVE in response to intravenous infusions, no data describe the influence on the distribution of infused crystalloid of hypoproteinemia, which we hypothesized would decrease the fraction of crystalloid remaining intravascularly. We addressed this hypothesis in conscious, chronically instrumented sheep. Methods: Halothane-anesthetized ewes (n=5, 37±3 kg) were surgically prepared with cardiopulmonary catheters. After a 5-day recovery period, each ewe was subjected to a 5-day test period. On days 1 and 5, we infused one liter of 0.9{\%} saline (50 mL/min for 20 min). Plasmapheresis on days 2, 3 and 4 reduced serum protein concentration. PVE was kinetically analyzed from decreases in hemoglobin. Data from days 1 and 5 were compared via repeated measures analysis of variance, with P<0.05 considered significant. Results: Total plasma protein concentrations and colloid osmotic (oncotic) pressures decreased from 5.7±0.4 g/dL and 20.0±1.4 mmHg to 2.6±0.5 g/dL and 9.6±1.4 mmHg (p<0.05), respectively, after plasma-pheresis. However, the response of PVE was not different. PVE was 22.1±9.6{\%} and 24.2±7.4{\%} (p<0.05 vs baseline) at the end of the infusion and then decreased over 30 to 40 min to remain at 15.9±6.0{\%} and 16.7±7.7{\%}, in the eu-and hypoproteinemic states, repectively. Urinary output was not different. Discussion: Hypoproteinemia did not decrease the fraction of crystalloid remaining intravascularly in this conscious, large animal model. Because hypoproteinemia produced by plasmapheresis may not be equivalent to hypoproteinemia associated with critical illness, further studies are necessary in experimental models such as sepsis.",
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AB - Introduction: Hypoproteinemia is associated with systemic and pulmonary edema during crystalloid infusion1. Although Stahle et al.2 have developed pharmacokinetic models to describe PVE in response to intravenous infusions, no data describe the influence on the distribution of infused crystalloid of hypoproteinemia, which we hypothesized would decrease the fraction of crystalloid remaining intravascularly. We addressed this hypothesis in conscious, chronically instrumented sheep. Methods: Halothane-anesthetized ewes (n=5, 37±3 kg) were surgically prepared with cardiopulmonary catheters. After a 5-day recovery period, each ewe was subjected to a 5-day test period. On days 1 and 5, we infused one liter of 0.9% saline (50 mL/min for 20 min). Plasmapheresis on days 2, 3 and 4 reduced serum protein concentration. PVE was kinetically analyzed from decreases in hemoglobin. Data from days 1 and 5 were compared via repeated measures analysis of variance, with P<0.05 considered significant. Results: Total plasma protein concentrations and colloid osmotic (oncotic) pressures decreased from 5.7±0.4 g/dL and 20.0±1.4 mmHg to 2.6±0.5 g/dL and 9.6±1.4 mmHg (p<0.05), respectively, after plasma-pheresis. However, the response of PVE was not different. PVE was 22.1±9.6% and 24.2±7.4% (p<0.05 vs baseline) at the end of the infusion and then decreased over 30 to 40 min to remain at 15.9±6.0% and 16.7±7.7%, in the eu-and hypoproteinemic states, repectively. Urinary output was not different. Discussion: Hypoproteinemia did not decrease the fraction of crystalloid remaining intravascularly in this conscious, large animal model. Because hypoproteinemia produced by plasmapheresis may not be equivalent to hypoproteinemia associated with critical illness, further studies are necessary in experimental models such as sepsis.

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