Beschreibung:
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<jats:bold>Introduction:</jats:bold>
We have previously documented in a rat model of VF and closed-chest resuscitation that administration of erythropoietin (EPO) preserves left ventricular distensibility - yielding hemodynamically more effective CPR - and attenuates post-resuscitation myocardial dysfunction.
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<jats:bold>Hypothesis:</jats:bold>
Given that similar functional myocardial benefits can be elicited by preservation of mitochondrial bioenergetic function, we hypothesized that EPO could mediate the aforementioned myocardial effects in part by preserving activity of electron transport complexes I, III, IV and V (FoF1 ATPase).
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<jats:bold>Methods:</jats:bold>
VF was electrically induced in 10 Sprague-Dawley male rats and left untreated for 8 minutes before attempting resuscitation by closed-chest resuscitation and delivery of electrical shocks. Rats were randomized to receive 5,000 U/kg of EPO (n=5) or NaCl 0.9% vehicle (n=5) into the right atrium immediately before starting closed-chest resuscitation, with the investigators blind to the assignment. All rats were resuscitated and survived 120 minutes, time at which hearts were removed storing the left ventricles at -80°C. Mitochondria were isolated from frozen tissue and activity of electron transport complexes I, I & III, IV and V measured spectrophotometrically
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dichloro indophenol reduction, cytochrome
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reduction, cytochrome
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oxidation, and phosphate estimation, respectively.
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<jats:bold>Results:</jats:bold>
Only complex IV activity was significantly higher in EPO compared with NaCl 0.9% treated rats with the levels in EPO rats comparable to the reference levels (Table).
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<jats:bold>Conclusions:</jats:bold>
EPO ameliorated reductions in complex IV activity prompted by cardiac arrest and resuscitation, an effect that could mediate the favorable myocardial effect of EPO observed during resuscitation from cardiac arrest.
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