Effects of ischemic and hypoxic preconditioning on the state of mitochondria and function of ischemic kidneys

Laser confocal microscopy showed that fluorescence of tetramethylrhodamine ethyl ether probe specifically accumulating in energized mitochondria significantly decreased in renal tubular epithelium after 40-min thermal ischemia, while fluorescence of dichlorodihydrofluorescein and diaminofluorescein...

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Bibliographic Details
Published in:Bulletin of experimental biology and medicine 2007-01, Vol.143 (1), p.105-109
Main Authors: Kirpatovskii, V I, Kazachenko, A V, Plotnikov, E Yu, Kon'kova, T A, Drozhzheva, V V, Zorov, D B
Format: Article
Language:English
Subjects:
Animals
Hypoxia - metabolism
Hypoxia - physiopathology
Ischemia - metabolism
Ischemia - physiopathology
Ischemia - prevention & control
Ischemic Preconditioning
Kidney - blood supply
Kidney - physiopathology
Kidney - ultrastructure
Kidney Tubules - metabolism
Kidney Tubules - ultrastructure
Male
Microscopy, Confocal
Mitochondria - metabolism
Nitric Oxide - metabolism
Rats
Reactive Oxygen Species - metabolism
Urothelium - metabolism
Urothelium - ultrastructure
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Summary:Laser confocal microscopy showed that fluorescence of tetramethylrhodamine ethyl ether probe specifically accumulating in energized mitochondria significantly decreased in renal tubular epithelium after 40-min thermal ischemia, while fluorescence of dichlorodihydrofluorescein and diaminofluorescein probes in the same structures increased under these conditions, which attests to increased generation of ROS and NO, respectively. These forms were generated predominantly in mitochondria of tubular epitheliocytes. Hypoxic preconditioning (a series of sessions of breathing hypoxic mixture) preserved functional activity of mitochondria and prevented activation of ROS and NO generation. Ischemic preconditioning of the kidney consisting of three preliminary episodes of vascular clamping (5 min with 5 min reperfusion periods) also increased the percentage of functionally active mitochondria and prevented activation of NO synthesis without appreciably modifying ROS production. Both protective methods significantly reduced the severity of postischemic dysfunction of the kidney.
ISSN:0007-4888
1573-8221
DOI:10.1007/s10517-007-0028-8