What is a possible explanation for the relationship among antioxidant injection, edema, and tissue damage?

When blood flow to human tissue is interrupted, the lack of sufficient blood supply is called ischemia. If ischemia is not restored quickly, the affected tissue may undergo a process called infarction, which involves a series of chemical changes that damage the tissue. The lack of blood supply results in lack of oxygen, and thus lactic acidosis. Mitochondrial dysfunction results. Microscopic examination and chemical analysis of ischemic cells reveal membrane degeneration, excessive calcium (Ca+) inside the cell, and free radical formation, accompanied by a reactive inflammation and free fatty acid formation. A research experiment is designed to evaluate the response of infarcted tissue to intra-arterial administration of an antioxidant. Preliminary results demonstrate that follow-up evaluation of tissue exposed to intra-arterial antioxidant injection resulted, on average, in a smaller area of infarcted tissue after seven days when compared to controls without exposure to the antioxidant. It was noted that 70% of the patients who demonstrated smaller areas of infarction also had a notable decease in edema of the ischemic tissue lasting about 6 to 10 hours after injection.

What is a possible explanation for the relationship among antioxidant injection, edema, and tissue damage?
A . Antioxidants produce anti-infarction biochemical reactions that decrease the size of the infarct.
B . Antioxidants decrease tissue damage by decreasing edema.
C . The prevention of tissue damage may be produced by a combination of the effect of decreased edema and the injection of antioxidants.
D . Increased blood flow causes paradoxical tissue damage due to ischemia.

View Answer

Answer: C

Explanation:

The experimental results do not demonstrate or prove that the antioxidant is responsible for the decrease in edema or that edema is the cause of tissue damage. However, because patients exposed to the antioxidant had a smaller area of infarcted tissue, it appears that the antioxidant has a beneficial effect. Most, but not all, of the patients with smaller areas of infarct also had decreased edema, suggesting that edema may also play a role. This suggests that some type of combination of the presence of edema and antioxidants was at play when decreased tissue damage was observed. There was no measured relationship to blood flow. It is unclear exactly why the antioxidant injected samples showed deceased damage, and it is a leap to suggest that the antioxidants themselves produce chemicals or biochemical reactions that decreased the size of the infarct or the edema.