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Kidney oxygenation in the subacute phase of ischemia‐reperfusion injury (890.1)
Author(s) -
Evans Roger,
Ow Connie,
Abdelkader Amany,
Hilliard Lucinda,
Malpas Simon,
Koeners Maarten
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.890.1
Subject(s) - ischemia , medicine , renal ischemia , medullary cavity , kidney , anesthesia , hypoxia (environmental) , urology , reperfusion injury , chemistry , oxygen , organic chemistry
We determined the status of kidney tissue oxygenation during the subacute phase of renal ischemia reperfusion injury in 10‐12 week old male Sprague‐Dawley rats. Inner medullary oxygen tension (PO 2 ) was determined using a carbon paste electrode attached to a telemetry transmitter, for 24 hours before and for 5 days after 60 min of bilateral renal ischemia (n=4) or sham (n=4) surgery. In a second protocol, renal tissue PO 2 was measured by Clark electrode under thiobutabarbital anesthesia, either 1 or 5 days after recovery from renal ischemia (n = 6 and 3 respectively) or sham surgery (n = 5 and 3 respectively). Inner medullary tissue PO 2 measured by telemetry was increased by 45 ± 15% 24 h after reperfusion, but then progressively fell over the next 5 days. Tissue PO 2 measured by Clark electrode was well maintained 24 h after ischemia. However, outer medullary PO 2 was 69% less 5 days after ischemia than after sham surgery. Our observations suggest that widespread renal hypoxia may not be obligatory in the subacute phase of renal ischemia‐reperfusion injury. However, medullary hypoxia may evolve over a period of days following reperfusion. Grant Funding Source : Supported by the National Health and Medical Research Council of Australia