What question did this study set out to answer?

To determine whether human recombinant superoxide dismutase produces a sustained reduction in myocardial infarct size and improves functional recovery after coronary occlusion and reperfusion.

February 1, 1990AJP Heart and Circulatory Physiology

Effect of human recombinant superoxide dismutase on canine myocardial infarction

View Full Paper

Ask AI

Bookmark

Why the study?

Does human recombinant superoxide dismutase reduce infarct size in a canine model of myocardial infarction with reperfusion?

Population

Anesthetized dogs undergoing a 2-h coronary occlusion followed by either 48 or 4 h of reperfusion

Comparison

Intravenous human recombinant superoxide… vs Equivalent volumes of intravenous saline

Design

Preclinical, Randomized to three intravenous treatments or two treatments…

Follow-up

4 hours or 48 hours of reperfusion

Authors

BPBrijeshkumar S. PatelMayo Clinic in Arizona MJMohamed O. JeroudiTexas Medical Center POPadraig Gearoid O’NeillMercy General Hospital

Discussion

Member takes

Implication

h-SOD failed to limit infarct size in this canine reperfusion model; leaves open whether antioxidant strategies reduce human MI size.

Key Points

To determine whether human recombinant superoxide dismutase produces a sustained reduction in myocardial infarct size and improves functional recovery after coronary occlusion and reperfusion.
Anesthetized dogs underwent a 2-hour coronary occlusion followed by either 48 hours or 4 hours of reperfusion.
In the 48-hour protocol, dogs were randomized to low-dose h-SOD, high-dose h-SOD, or saline; in the 4-hour protocol, dogs were randomized to high-dose h-SOD or saline.
Investigators were blinded to treatment assignments, and infarct size was quantified relative to the occluded bed size using triphenyl tetrazolium chloride staining and planimetry.
In the 48-hour reperfusion study, infarct size was 41.3 ± 7.6% of the occluded bed in the control group, 37.1 ± 7.2% in the low-dose h-SOD group, and 48.0 ± 7.1% in the high-dose h-SOD group.
In the 4-hour reperfusion study, infarct size was 30.6 ± 4.9% in the control group and 31.5 ± 9.6% in the high-dose h-SOD group.
Treatment with h-SOD did not alter flow-infarct relationships across any collateral blood flow level and failed to enhance the recovery of regional myocardial function in either cohort.

Structured PICO

Does human recombinant superoxide dismutase reduce infarct size in a canine model of myocardial infarction with reperfusion?

Population

Anesthetized dogs undergoing a 2-h coronary occlusion followed by either 48 or 4 h of reperfusion

Intervention

Intravenous human recombinant superoxide dismutase (h-SOD) given as a low-dose (2 mg/kg bolus 2 min before reperfusion followed by 4 mg/kg over 45 min) or high-dose (8 mg/kg bolus 2 min before reperfusion followed by 8 mg/kg over 45 min)

Comparator

Equivalent volumes of intravenous saline

Outcome

Infarct size expressed as percent of occluded bed sizesurrogate

Large doses of human recombinant superoxide dismutase given at the time of reperfusion failed to limit infarct size or enhance recovery of function in a canine model of myocardial infarction.

Cite This Study

Patel et al. (1990) studied this question.

synapsesocial.com/papers/6a7be651c2a640f0bcdf8751 https://doi.org/10.1152/ajpheart.1990.258.2.h369

View Full Paper

Ask AI

Bookmark

Effect of human recombinant superoxide dismutase on canine myocardial infarction

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Effect of human recombinant superoxide dismutase on canine myocardial infarction

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider