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Erythrocytes decrease myocardial hydrogen peroxide levels and reperfusion injury.

J M Brown¹, M A Grosso, L S Terada

¹Department of Surgery, University of Colorado Health Sciences Center, Denver 80262.

The American Journal of Physiology

|February 1, 1989

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Red blood cells (RBCs) containing catalase and glutathione protect ischemic hearts during reperfusion. These components in RBCs reduce hydrogen peroxide (H2O2) levels, mitigating reperfusion injury and improving heart function.

Area of Science:

Cardiovascular Physiology
Biochemistry
Red Blood Cell Biology

Background:

Reperfusion injury is a significant complication following ischemic events, characterized by oxidative stress.
Hydrogen peroxide (H2O2) is a key mediator of oxidative damage during myocardial reperfusion.
The role of endogenous antioxidants within transfused red blood cells (RBCs) in mitigating this injury is not fully understood.

Purpose of the Study:

To investigate the protective mechanisms of intact human red blood cells (RBCs) during myocardial reperfusion.
To determine the specific contributions of catalase and glutathione within RBCs to reducing oxidative stress and improving cardiac function post-ischemia.
To elucidate the role of RBCs in managing endogenous hydrogen peroxide (H2O2) levels in ischemic hearts.

Main Methods:

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Isolated rat hearts underwent a period of ischemia followed by reperfusion with various preparations of human RBCs.
RBCs were modified to deplete or inhibit key antioxidant enzymes (catalase, glutathione) or anion channels.
Ventricular function was assessed, and myocardial H2O2 levels were quantified using H2O2-dependent aminotriazole (AMT) inactivation of catalase activity.

Main Results:

Reperfusion with untreated, carbon monoxide-treated, or glutaraldehyde-fixed RBCs significantly improved ventricular function and reduced myocardial H2O2 levels.
RBCs lacking functional catalase or glutathione showed diminished protective effects on ventricular function and H2O2 reduction.
RBCs with inhibited anion channels or depleted superoxide dismutase exhibited protective effects comparable to untreated RBCs.

Conclusions:

Intact red blood cells (RBCs) possess intrinsic protective capabilities against myocardial reperfusion injury.
The presence of functional catalase and/or glutathione within RBCs is crucial for mitigating oxidative stress by reducing endogenous H2O2.
RBCs can serve as a therapeutic vehicle to deliver antioxidant capacity, thereby reducing reperfusion injury in ischemic hearts.