Hyperoxic reperfusion exacerbates postischemic renal dysfunction

Charles F. Zwemer, James L. Shoemaker, Sprague W. Hazard, Rachel E. Davis, Alessandro G. Bartoletti, Carrie Phillips

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Background. Hyperoxic reperfusion from global ischemia worsens functional outcome because of oxygen radical-mediated injury. This study tested the hypothesis that hyperoxic reperfusion would exacerbate postischemic renal dysfunction. Methods. Twenty-nine healthy, uninephrectomized, male mongrel rabbits (Oryctolagus cuniculus) in 3 groups were subjected to 30 minutes of complete normothermic renal ischemia followed by reperfusion under hyperoxic or normoxic conditions. The groups were: hyperoxically reperfused (n = 8), normoxically reperfused (n = 8), hyperoxic sham (no ischemia, n = 5), and allopurinol-pretreated (50 mg/kg, intravenously), hyperoxically reperfused animals (n = 8). Plasma concentrations of creatinine, urea nitrogen and electrolytes were measured at 0, 24, 48, and 72 hours after ischemia and served as functional outcome markers. Histopathologic analysis of kidneys for injury was performed by an expert who was blinded to the procedures. Results. Plasma creatinine in hyperoxically reperfused rabbits was significantly elevated above normoxic (P = .02) and sham (P = .003) animals by 48 hours and remained elevated to 72 hours. Plasma urea nitrogen in hyperoxically reperfused rabbits was significantly elevated above the normoxic group (P = .01), the sham group (P = .02), and the allopurinol group (P = .04) by 72 hours. These coincided with a significantly elevated histopathologic injury score in hyperoxically reperfused rabbits compared with sham (P = .019), normoxic (P = .035), and allopurinol-pretreated hyperoxically reperfused animals (P = .037). Conclusions. Hyperoxic reperfusion exacerbates renal dysfunction after 30 minutes of complete normothermic ischemia. This dysfunction may be mediated by oxygen radical-related injury.

Original languageEnglish
Pages (from-to)815-821
Number of pages7
JournalSurgery
Volume128
Issue number5
DOIs
StatePublished - 2000

Fingerprint

Reperfusion
Ischemia
Allopurinol
Rabbits
Kidney
Wounds and Injuries
Urea
Reactive Oxygen Species
Creatinine
Nitrogen
Electrolytes

ASJC Scopus subject areas

  • Surgery

Cite this

Zwemer, C. F., Shoemaker, J. L., Hazard, S. W., Davis, R. E., Bartoletti, A. G., & Phillips, C. (2000). Hyperoxic reperfusion exacerbates postischemic renal dysfunction. Surgery, 128(5), 815-821. https://doi.org/10.1067/msy.2000.109117

Hyperoxic reperfusion exacerbates postischemic renal dysfunction. / Zwemer, Charles F.; Shoemaker, James L.; Hazard, Sprague W.; Davis, Rachel E.; Bartoletti, Alessandro G.; Phillips, Carrie.

In: Surgery, Vol. 128, No. 5, 2000, p. 815-821.

Research output: Contribution to journalArticle

Zwemer, CF, Shoemaker, JL, Hazard, SW, Davis, RE, Bartoletti, AG & Phillips, C 2000, 'Hyperoxic reperfusion exacerbates postischemic renal dysfunction', Surgery, vol. 128, no. 5, pp. 815-821. https://doi.org/10.1067/msy.2000.109117
Zwemer CF, Shoemaker JL, Hazard SW, Davis RE, Bartoletti AG, Phillips C. Hyperoxic reperfusion exacerbates postischemic renal dysfunction. Surgery. 2000;128(5):815-821. https://doi.org/10.1067/msy.2000.109117
Zwemer, Charles F. ; Shoemaker, James L. ; Hazard, Sprague W. ; Davis, Rachel E. ; Bartoletti, Alessandro G. ; Phillips, Carrie. / Hyperoxic reperfusion exacerbates postischemic renal dysfunction. In: Surgery. 2000 ; Vol. 128, No. 5. pp. 815-821.
@article{ce42bcb9caf945caa3f7fcb08c3fb17a,
title = "Hyperoxic reperfusion exacerbates postischemic renal dysfunction",
abstract = "Background. Hyperoxic reperfusion from global ischemia worsens functional outcome because of oxygen radical-mediated injury. This study tested the hypothesis that hyperoxic reperfusion would exacerbate postischemic renal dysfunction. Methods. Twenty-nine healthy, uninephrectomized, male mongrel rabbits (Oryctolagus cuniculus) in 3 groups were subjected to 30 minutes of complete normothermic renal ischemia followed by reperfusion under hyperoxic or normoxic conditions. The groups were: hyperoxically reperfused (n = 8), normoxically reperfused (n = 8), hyperoxic sham (no ischemia, n = 5), and allopurinol-pretreated (50 mg/kg, intravenously), hyperoxically reperfused animals (n = 8). Plasma concentrations of creatinine, urea nitrogen and electrolytes were measured at 0, 24, 48, and 72 hours after ischemia and served as functional outcome markers. Histopathologic analysis of kidneys for injury was performed by an expert who was blinded to the procedures. Results. Plasma creatinine in hyperoxically reperfused rabbits was significantly elevated above normoxic (P = .02) and sham (P = .003) animals by 48 hours and remained elevated to 72 hours. Plasma urea nitrogen in hyperoxically reperfused rabbits was significantly elevated above the normoxic group (P = .01), the sham group (P = .02), and the allopurinol group (P = .04) by 72 hours. These coincided with a significantly elevated histopathologic injury score in hyperoxically reperfused rabbits compared with sham (P = .019), normoxic (P = .035), and allopurinol-pretreated hyperoxically reperfused animals (P = .037). Conclusions. Hyperoxic reperfusion exacerbates renal dysfunction after 30 minutes of complete normothermic ischemia. This dysfunction may be mediated by oxygen radical-related injury.",
author = "Zwemer, {Charles F.} and Shoemaker, {James L.} and Hazard, {Sprague W.} and Davis, {Rachel E.} and Bartoletti, {Alessandro G.} and Carrie Phillips",
year = "2000",
doi = "10.1067/msy.2000.109117",
language = "English",
volume = "128",
pages = "815--821",
journal = "Surgery",
issn = "0039-6060",
publisher = "Mosby Inc.",
number = "5",

}

TY - JOUR

T1 - Hyperoxic reperfusion exacerbates postischemic renal dysfunction

AU - Zwemer, Charles F.

AU - Shoemaker, James L.

AU - Hazard, Sprague W.

AU - Davis, Rachel E.

AU - Bartoletti, Alessandro G.

AU - Phillips, Carrie

PY - 2000

Y1 - 2000

N2 - Background. Hyperoxic reperfusion from global ischemia worsens functional outcome because of oxygen radical-mediated injury. This study tested the hypothesis that hyperoxic reperfusion would exacerbate postischemic renal dysfunction. Methods. Twenty-nine healthy, uninephrectomized, male mongrel rabbits (Oryctolagus cuniculus) in 3 groups were subjected to 30 minutes of complete normothermic renal ischemia followed by reperfusion under hyperoxic or normoxic conditions. The groups were: hyperoxically reperfused (n = 8), normoxically reperfused (n = 8), hyperoxic sham (no ischemia, n = 5), and allopurinol-pretreated (50 mg/kg, intravenously), hyperoxically reperfused animals (n = 8). Plasma concentrations of creatinine, urea nitrogen and electrolytes were measured at 0, 24, 48, and 72 hours after ischemia and served as functional outcome markers. Histopathologic analysis of kidneys for injury was performed by an expert who was blinded to the procedures. Results. Plasma creatinine in hyperoxically reperfused rabbits was significantly elevated above normoxic (P = .02) and sham (P = .003) animals by 48 hours and remained elevated to 72 hours. Plasma urea nitrogen in hyperoxically reperfused rabbits was significantly elevated above the normoxic group (P = .01), the sham group (P = .02), and the allopurinol group (P = .04) by 72 hours. These coincided with a significantly elevated histopathologic injury score in hyperoxically reperfused rabbits compared with sham (P = .019), normoxic (P = .035), and allopurinol-pretreated hyperoxically reperfused animals (P = .037). Conclusions. Hyperoxic reperfusion exacerbates renal dysfunction after 30 minutes of complete normothermic ischemia. This dysfunction may be mediated by oxygen radical-related injury.

AB - Background. Hyperoxic reperfusion from global ischemia worsens functional outcome because of oxygen radical-mediated injury. This study tested the hypothesis that hyperoxic reperfusion would exacerbate postischemic renal dysfunction. Methods. Twenty-nine healthy, uninephrectomized, male mongrel rabbits (Oryctolagus cuniculus) in 3 groups were subjected to 30 minutes of complete normothermic renal ischemia followed by reperfusion under hyperoxic or normoxic conditions. The groups were: hyperoxically reperfused (n = 8), normoxically reperfused (n = 8), hyperoxic sham (no ischemia, n = 5), and allopurinol-pretreated (50 mg/kg, intravenously), hyperoxically reperfused animals (n = 8). Plasma concentrations of creatinine, urea nitrogen and electrolytes were measured at 0, 24, 48, and 72 hours after ischemia and served as functional outcome markers. Histopathologic analysis of kidneys for injury was performed by an expert who was blinded to the procedures. Results. Plasma creatinine in hyperoxically reperfused rabbits was significantly elevated above normoxic (P = .02) and sham (P = .003) animals by 48 hours and remained elevated to 72 hours. Plasma urea nitrogen in hyperoxically reperfused rabbits was significantly elevated above the normoxic group (P = .01), the sham group (P = .02), and the allopurinol group (P = .04) by 72 hours. These coincided with a significantly elevated histopathologic injury score in hyperoxically reperfused rabbits compared with sham (P = .019), normoxic (P = .035), and allopurinol-pretreated hyperoxically reperfused animals (P = .037). Conclusions. Hyperoxic reperfusion exacerbates renal dysfunction after 30 minutes of complete normothermic ischemia. This dysfunction may be mediated by oxygen radical-related injury.

UR - http://www.scopus.com/inward/record.url?scp=0033763506&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033763506&partnerID=8YFLogxK

U2 - 10.1067/msy.2000.109117

DO - 10.1067/msy.2000.109117

M3 - Article

VL - 128

SP - 815

EP - 821

JO - Surgery

JF - Surgery

SN - 0039-6060

IS - 5

ER -