Hemorrhagic shock and surgical stress alter distribution of labile zinc within high- and low-molecular-weight plasma fractions

Zinc ions (Zn) are essential for tissue repair following injury or stress. We hypothesize that during such stresses Zn is redistributed to labile pools in plasma components. Here we tested this hypothesis using a novel assay to monitor labile Zn in plasma in hemorrhagic shock. Adult rats in the shoc...

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Published inShock (Augusta, Ga.) Vol. 38; no. 3; p. 314
Main Authors Kelly, Edward, Mathew, Jeff, Kohler, Jonathan E, Blass, Amy L, Soybel, And David I
Format Journal Article
LanguageEnglish
Published United States 01.08.2012
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Abstract Zinc ions (Zn) are essential for tissue repair following injury or stress. We hypothesize that during such stresses Zn is redistributed to labile pools in plasma components. Here we tested this hypothesis using a novel assay to monitor labile Zn in plasma in hemorrhagic shock. Adult rats in the shock group (S group) underwent hemorrhage and resuscitation. Blood samples were drawn at baseline and at 1, 4, and 24 h. The surgical control group (SC group) was anesthetized and instrumented, but not bled. Albumin, total Zn, and labile Zn levels were assayed in plasma. Binding capacity for Zn was assessed in high- and low-molecular-weight pools. Significant decreases in total Zn were observed by 24 h, in both S and SC groups. Albumin levels were significantly reduced in the S group at 1 and 4 h but restored at 24 h; significant changes were not observed in other groups. In whole plasma, labile Zn levels were stable initially in the S and SC groups, but declined at 24 h. In the high-molecular-weight pool, marked and significant impairment of binding was noted throughout all time periods following the shock period in the S group. Such changes were observed in the SC group of less intensity and duration. These experiments suggest that shock alters affinity of plasma proteins for Zn, promoting delivery to peripheral tissues during periods of increased Zn utilization.
AbstractList Zinc ions (Zn) are essential for tissue repair following injury or stress. We hypothesize that during such stresses Zn is redistributed to labile pools in plasma components. Here we tested this hypothesis using a novel assay to monitor labile Zn in plasma in hemorrhagic shock. Adult rats in the shock group (S group) underwent hemorrhage and resuscitation. Blood samples were drawn at baseline and at 1, 4, and 24 h. The surgical control group (SC group) was anesthetized and instrumented, but not bled. Albumin, total Zn, and labile Zn levels were assayed in plasma. Binding capacity for Zn was assessed in high- and low-molecular-weight pools. Significant decreases in total Zn were observed by 24 h, in both S and SC groups. Albumin levels were significantly reduced in the S group at 1 and 4 h but restored at 24 h; significant changes were not observed in other groups. In whole plasma, labile Zn levels were stable initially in the S and SC groups, but declined at 24 h. In the high-molecular-weight pool, marked and significant impairment of binding was noted throughout all time periods following the shock period in the S group. Such changes were observed in the SC group of less intensity and duration. These experiments suggest that shock alters affinity of plasma proteins for Zn, promoting delivery to peripheral tissues during periods of increased Zn utilization.
Author Kohler, Jonathan E
Mathew, Jeff
Blass, Amy L
Kelly, Edward
Soybel, And David I
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Snippet Zinc ions (Zn) are essential for tissue repair following injury or stress. We hypothesize that during such stresses Zn is redistributed to labile pools in...
SourceID pubmed
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StartPage 314
SubjectTerms Animals
Blood Proteins - metabolism
Ions - metabolism
Male
Molecular Weight
Protein Binding - physiology
Rats
Rats, Sprague-Dawley
Resuscitation
Serum Albumin - metabolism
Shock, Hemorrhagic - blood
Stress, Physiological - physiology
Zinc - blood
Title Hemorrhagic shock and surgical stress alter distribution of labile zinc within high- and low-molecular-weight plasma fractions
URI https://www.ncbi.nlm.nih.gov/pubmed/22744307
Volume 38
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