Superoxide anion release (O2-) after ischemia and reperfusion

Julie A. Freischlag, Dinah Hanna

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Neutrophils have been implicated as mediators of the reperfusion injury following ischemia. In order to measure neutrophil activation, O2- was determined after 2 hr of ischemia followed by 1 hr of reperfusion (no clinical reperfusion injury) and 3 hr of ischemia followed by 1 hr of reperfusion (significant clinical reperfusion injury). Using New Zealand white rabbits, baseline blood samples were drawn from an ear artery. The right iliac and femoral arteries were exposed and clamped. Just prior to clamp release, blood was obtained from the right iliac vein (ischemia). After 1 hr of reperfusion, blood was again taken from the right iliac vein (reperfusion). Neutrophils were isolated from the blood samples. O2- was determined by the reduction of cytochrome e using a spectrophotometer. In the 2-hr group, results (expressed as μmole O2-/min/2 × 106 cells) were: baseline, 0.337 ± 0.025; ischemia, 0.512 ± 0.039;* and reperfusion, 0.634 ± 0.064*. (*P < .05 as compared to baseline). In the 3-hr group, results were: baseline, 0.391 ± 0.038; ischemia, 0.413 ± 0.051; and reperfusion, 0.258 ± 0.043** (**P < 0.05 as compared to 2 hr reperfusion). A significant increase in O2- was seen after 2 hr of ischemia followed by 1 hr of reperfusion. However, little O2- increase was seen after 3 hr of ischemia and a significant O2- decrease was seen after 1 hr of reperfusion. We conclude: (1) Neutrophil O2 is stimulated early in ischemia followed by reperfusion; (2) after reperfusion injury occurs (3 hr), neutrophils have been activated and O2- can no longer be stimulated; and (3) O2- in this model may be involved in the clinical reperfusion injury seen.

Original languageEnglish (US)
Pages (from-to)565-568
Number of pages4
JournalJournal of Surgical Research
Volume50
Issue number6
DOIs
StatePublished - 1991

Fingerprint

Superoxides
Reperfusion
Ischemia
Reperfusion Injury
Neutrophils
Iliac Vein
Neutrophil Activation
Iliac Artery
Femoral Artery
Cytochromes
Ear
Arteries
Rabbits

ASJC Scopus subject areas

  • Surgery

Cite this

Superoxide anion release (O2-) after ischemia and reperfusion. / Freischlag, Julie A.; Hanna, Dinah.

In: Journal of Surgical Research, Vol. 50, No. 6, 1991, p. 565-568.

Research output: Contribution to journalArticle

Freischlag, Julie A. ; Hanna, Dinah. / Superoxide anion release (O2-) after ischemia and reperfusion. In: Journal of Surgical Research. 1991 ; Vol. 50, No. 6. pp. 565-568.
@article{fe0aebb7b0be4771b237e1879dec271d,
title = "Superoxide anion release (O2-) after ischemia and reperfusion",
abstract = "Neutrophils have been implicated as mediators of the reperfusion injury following ischemia. In order to measure neutrophil activation, O2- was determined after 2 hr of ischemia followed by 1 hr of reperfusion (no clinical reperfusion injury) and 3 hr of ischemia followed by 1 hr of reperfusion (significant clinical reperfusion injury). Using New Zealand white rabbits, baseline blood samples were drawn from an ear artery. The right iliac and femoral arteries were exposed and clamped. Just prior to clamp release, blood was obtained from the right iliac vein (ischemia). After 1 hr of reperfusion, blood was again taken from the right iliac vein (reperfusion). Neutrophils were isolated from the blood samples. O2- was determined by the reduction of cytochrome e using a spectrophotometer. In the 2-hr group, results (expressed as μmole O2-/min/2 × 106 cells) were: baseline, 0.337 ± 0.025; ischemia, 0.512 ± 0.039;* and reperfusion, 0.634 ± 0.064*. (*P < .05 as compared to baseline). In the 3-hr group, results were: baseline, 0.391 ± 0.038; ischemia, 0.413 ± 0.051; and reperfusion, 0.258 ± 0.043** (**P < 0.05 as compared to 2 hr reperfusion). A significant increase in O2- was seen after 2 hr of ischemia followed by 1 hr of reperfusion. However, little O2- increase was seen after 3 hr of ischemia and a significant O2- decrease was seen after 1 hr of reperfusion. We conclude: (1) Neutrophil O2 is stimulated early in ischemia followed by reperfusion; (2) after reperfusion injury occurs (3 hr), neutrophils have been activated and O2- can no longer be stimulated; and (3) O2- in this model may be involved in the clinical reperfusion injury seen.",
author = "Freischlag, {Julie A.} and Dinah Hanna",
year = "1991",
doi = "10.1016/0022-4804(91)90042-K",
language = "English (US)",
volume = "50",
pages = "565--568",
journal = "Journal of Surgical Research",
issn = "0022-4804",
publisher = "Academic Press Inc.",
number = "6",

}

TY - JOUR

T1 - Superoxide anion release (O2-) after ischemia and reperfusion

AU - Freischlag, Julie A.

AU - Hanna, Dinah

PY - 1991

Y1 - 1991

N2 - Neutrophils have been implicated as mediators of the reperfusion injury following ischemia. In order to measure neutrophil activation, O2- was determined after 2 hr of ischemia followed by 1 hr of reperfusion (no clinical reperfusion injury) and 3 hr of ischemia followed by 1 hr of reperfusion (significant clinical reperfusion injury). Using New Zealand white rabbits, baseline blood samples were drawn from an ear artery. The right iliac and femoral arteries were exposed and clamped. Just prior to clamp release, blood was obtained from the right iliac vein (ischemia). After 1 hr of reperfusion, blood was again taken from the right iliac vein (reperfusion). Neutrophils were isolated from the blood samples. O2- was determined by the reduction of cytochrome e using a spectrophotometer. In the 2-hr group, results (expressed as μmole O2-/min/2 × 106 cells) were: baseline, 0.337 ± 0.025; ischemia, 0.512 ± 0.039;* and reperfusion, 0.634 ± 0.064*. (*P < .05 as compared to baseline). In the 3-hr group, results were: baseline, 0.391 ± 0.038; ischemia, 0.413 ± 0.051; and reperfusion, 0.258 ± 0.043** (**P < 0.05 as compared to 2 hr reperfusion). A significant increase in O2- was seen after 2 hr of ischemia followed by 1 hr of reperfusion. However, little O2- increase was seen after 3 hr of ischemia and a significant O2- decrease was seen after 1 hr of reperfusion. We conclude: (1) Neutrophil O2 is stimulated early in ischemia followed by reperfusion; (2) after reperfusion injury occurs (3 hr), neutrophils have been activated and O2- can no longer be stimulated; and (3) O2- in this model may be involved in the clinical reperfusion injury seen.

AB - Neutrophils have been implicated as mediators of the reperfusion injury following ischemia. In order to measure neutrophil activation, O2- was determined after 2 hr of ischemia followed by 1 hr of reperfusion (no clinical reperfusion injury) and 3 hr of ischemia followed by 1 hr of reperfusion (significant clinical reperfusion injury). Using New Zealand white rabbits, baseline blood samples were drawn from an ear artery. The right iliac and femoral arteries were exposed and clamped. Just prior to clamp release, blood was obtained from the right iliac vein (ischemia). After 1 hr of reperfusion, blood was again taken from the right iliac vein (reperfusion). Neutrophils were isolated from the blood samples. O2- was determined by the reduction of cytochrome e using a spectrophotometer. In the 2-hr group, results (expressed as μmole O2-/min/2 × 106 cells) were: baseline, 0.337 ± 0.025; ischemia, 0.512 ± 0.039;* and reperfusion, 0.634 ± 0.064*. (*P < .05 as compared to baseline). In the 3-hr group, results were: baseline, 0.391 ± 0.038; ischemia, 0.413 ± 0.051; and reperfusion, 0.258 ± 0.043** (**P < 0.05 as compared to 2 hr reperfusion). A significant increase in O2- was seen after 2 hr of ischemia followed by 1 hr of reperfusion. However, little O2- increase was seen after 3 hr of ischemia and a significant O2- decrease was seen after 1 hr of reperfusion. We conclude: (1) Neutrophil O2 is stimulated early in ischemia followed by reperfusion; (2) after reperfusion injury occurs (3 hr), neutrophils have been activated and O2- can no longer be stimulated; and (3) O2- in this model may be involved in the clinical reperfusion injury seen.

UR - http://www.scopus.com/inward/record.url?scp=0025835205&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025835205&partnerID=8YFLogxK

U2 - 10.1016/0022-4804(91)90042-K

DO - 10.1016/0022-4804(91)90042-K

M3 - Article

VL - 50

SP - 565

EP - 568

JO - Journal of Surgical Research

JF - Journal of Surgical Research

SN - 0022-4804

IS - 6

ER -