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Articles in PresS, published online ahead of print December 18, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00329.2001
Submitted on October 30, 2001
Accepted on December 15, 2001
1 Departments of Medicine, Physiology and Biophysics and Program in Bioengineering, State University of New York, Stony Brook, NY, USA
2 Departments of Urology and Medical Engineering, Kawasaki Medical School, Okayama, Japan
3 Department of Electrical Engineering, Okayama University of Science, Okayama, Japan
4 Department of Cardiovascular Physiology, Okayama University School of Medicine and Dentistry, Okayama, Japan
* To whom correspondence should be addressed. E-mail: mgoligorsky{at}mail.som.sunysb.edu.
There is accumulating circumstantial evidence suggesting that endothelial cell dysfunction contributes to the "no-reflow" phenomenon in post-ischemic kidneys. Here, we demonstrated the vulnerability of in vitro, ex vivo and in vivo endothelial cells exposed to pathophysiologically relevant insults, such as oxidative and nitrosative stress, or ischemia. These stimuli all compromised the integrity of endothelial lining. Next, we performed minimally invasive intravital microscopy of blood flow in peritubular capillaries, which provided direct evidence of the existence of the "no-reflow" phenomenon, attributable at least in part to endothelial injury. In an attempt to ameliorate the hemodynamic consequences of the lost endothelial integrity, we transplanted endothelial cells or surrogate cells expressing endothelial nitric oxide synthase into rats subjected to renal artery clamping. Implantation of endothelial cells or their surrogates expressing the functional endothelial nitric oxide synthase in the renal microvasculature resulted in a dramatic functional protection of ischemic kidneys. These observations strongly suggest that endothelial cell dysfunction is the primary cause of the "no-reflow" phenomenon, which, when ameliorated, results in prevention of renal injury seen in acute renal failure.
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