Effects of diagnostic cardiac ultrasound on oxygen free radical production and microvascular perfusion during ischemia reperfusion.

Diagnostic ultrasound (US) is reported to increase intracellular oxidative stress in vitro. Increased oxidative stress mediated ischemia-reperfusion injury in the microcirculation. To examine the effects of US in hamster cheek pouch microcirculation during baseline and ischemia and reperfusion (I/R), I/R injury was provoked in the cheek pouch under "sham" (transducer off, group 1) and active US irradiation (group 2) at baseline (15 min) and at the beginning (15 min) of the reperfusion after ischemia (30 min). US transmission was delivered in the harmonic mode (2.5 MHz) with 1.3 mechanical index (MI) and 2.0 peak negative pressure. Microvascular damage was evaluated by measuring arterial diameter, red blood cell velocity, wall shear stress, permeability, perfused capillary length and adherent leukocytes in venules. Lipid peroxides were determined in the systemic blood. US increased permeability (baseline: 0.04 +/- 0.02; after US 0.30 +/- 0.04, p < 0.01) and slightly decreased capillary perfusion by 7% during baseline (p < 0.01). Arteriolar diameter (35 +/- 7 microm vs. 20 +/- 5 microm, p < 0.05), RBC velocity (2.8 +/- 0.4 mm s(-1) vs. 0.75 +/- 0.05 mm s(-1), p < 0.05) and shear stress ( 0.76 +/- 0.09 Pa vs. 0.36 +/- 0.05 Pa, p < 0.05) decreased significantly after reperfusion. These parameters increased by 40, 64 and 33%, respectively after US. Leukocyte adhesion decreased by 31 % (p < 0.05) after US and lipid peroxides decreased by 26% and 51% during baseline and 15 min of reperfusion after US, respectively. In conclusion, diagnostic US increased microvascular permeability during baseline and reperfusion. Moreover, US enhanced wall shear stress and reduced oxidative stress during postischemic reperfusion; thus, increasing capillary perfusion.