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Nitric Oxide Protects Kidneys During Cardiac Surgery

By HospiMedica International staff writers
Posted on 01 Dec 2015
Administering nitric oxide (NO) during prolonged cardiopulmonary bypass procedures may help protect the kidneys, according to a new study.

Researchers at Massachusetts General Hospital (MGH; Boston, MA, USA) conducted a double-blind, randomized study that enrolled 217 patients undergoing surgical replacement of multiple heart valves in procedures expected to take more than 90 minutes at a single center in China; average time on cardiopulmonary bypass was 132 minutes (placebo group) to 137 minutes (NO group). More...
Patients were randomized to NO, which was delivered via the oxygenator during cardiopulmonary bypass and via the ventilator for 24 hours after surgery, or to placebo.

The results showed that acute kidney injury—defined as a 50% increase in serum creatinine within 7 days of surgery, or a 0.3-mg/dL increase in serum creatinine within 2 days of surgery—was reduced by 22% among those who received NO; in all, acute kidney injury was observed in 63% of the 112 control patients and 50% of the 105 NO patients. No serious adverse events occurred in either group, but mortality rates trended lower with the intervention, as did need for dialysis after surgery. The study was presented at the annual American Heart Association (AHA) Scientific Sessions, held during November 2015 in Orlando (FL, USA).

“Acute kidney injury is the most common complication after cardiac surgery with prolonged cardiopulmonary bypass, and is associated with hemolysis and high levels of free hemoglobin that cause the depletion of NO which is associated with acute kidney injury,” said lead author and study presenter anesthesiologist Lorenzo Berra, MD. “The administration of exogenous NO causes the oxidation of ferrous oxyhemoglobin and would decrease the risk of kidney injury by reducing the plasma depletion of NO.”

NO has been identified as an important molecule with versatile roles in human physiology, including selective pulmonary vasodilation, bronchodilation, and pulmonary surfactant activities to improve ventilation-perfusion mismatch and hence oxygenation. The clinical effects of NO that have been reported include reduction of right heart load, reduction of ischemia, reduction of hypoxemia, inhibition of platelet aggregation, and anti-inflammatory, fungicidal, virocidal, and bactericidal effects.

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