Introduction:

Decreased blood flow disrupts the endothelium, changes the nitric oxide/endothelin -1 ratio, narrows the capillaries and results in microcirculatory dysfunction. Secondary anoxia leads to mitochondrial energy imbalance, depletion of adenosine-triphosphate and disruption of the intracellular hydrogen, sodium and calcium homeostasis. If the flow is restored, the reperfusion stimulates the endothelial expression of adhesion molecules attracting polymorphic nucleotides and platelets, with sub endothelial infiltration of these cells and their entrapment in the microvasculature, as well as vasoconstriction, endothelial edema and reduced flexibility of the cellular membrane. Ischemia/reperfusion may result in inflammation and organ failure.

Objective:

To determine whether hypertonic saline solution reduces the ischemic/reperfusion injury in the liver, the kidney, and the ileum.

Materials and methods:

Experimental trial in pigs. Aortic blood flow suppression (15 min) and reperfusion (60 min). The experimental group was pretreated with 7.5% hypertonic saline and the control group received normal 0.9% saline solution. Hemodynamic, gasometric, and biochemical measurements were taken, and the serum and tissue levels of ET-1, TNF-alpha, IL-10, and IL-2 were determined.

Results:

There were no significant differences in the tissue expression of ET-1, TNF-alpha, IL-10, and IL-2 between the two groups. The hemodynamic behavior was similar in both groups. The group treated with hypertonic solution showed an increasing post-perfusion systolic rate up to the basal values, while the systolic rate in the control group dropped significantly (p = 0.015).

Conclusion:

Hypertonic solution prior to the ischemic insult improves the ventricular function after reperfusion.

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