Title: VASOCARE??? PREVENTS RENAL ISCHEMIA/REPERFUSION INJURY IN DOGS
Abstract: 445 The aim of this study was to evaluate the effect of Vasocare™ in prevention of ischemic reperfusion injury to the kidney in dogs. Male and female Beagle dogs were randomly assigned to two groups (n=18 each). In the treated group a sample of peripheral blood processed with heat, oxidation and ultraviolet irradiation (Vasocare™ therapy) was re-injected (5 ml) intramuscularly daily over 10 days in 2 courses with a 3-week rest. The control group received the same volume of 0.9% saline solution. The day after the last injection, the right kidney (control) was removed and the left kidney was submitted to 60 min ischemia followed by reperfusion. Renal function (serum creatinine) was tested daily for a period of 6 days. Mitochondrial membrane potential and liberation of Cytochrome C (Cyt C) from mitochondria were measured in proximal tubule cells isolated from the ischemic and control kidneys. The plasma creatinine levels remained below 200 μmol/L and decreased significantly (p=0.0325) in the treated as compared to the control group. There was no difference in the mitochondrial membrane potential in the contralateral control kidney of the two groups before ischemic reperfusion (1.26 ± 0.49 vs 1.56 ± 0.79 cps × 106; p=0.445). Ischemic reperfusion induced a fall of mitochondrial membrane potential from 1.56 ± 0.13 to 0.75 ± 0.16 (p=0.006) in the control group while in the treated group the fall was prevented (1.26 ± 0.49 vs 1.11 ± 0.3; p=0.224). Thus 6 days after, there was a significant difference in mitochondrial membrane potential between the two groups (p=0.006). Release of Cyt C from mitochondria was less in the contralateral control kidney of the treated group (2489 ± 255 vs 3694 ± 284 ng Cyt C/mg; p=0.0001) and remained lower 6 days post ischemic reperfusion compared with control group (1955 ± 242 vs 4539 ± 186; p=0.0001). In conclusion, Vasocare™ therapy effectively prevented acute renal failure induced by ischemia/reperfusion injury with a mechanism involving protection against apoptosis at the mitochondrial level.