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1 Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA, USA; Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA
2 Cardiac Ultrasound Laboratory, Massachusetts General Hospital, Boston, MA, USA
3 Cardiac Ultrasound Laboratory, Massachusetts General Hospital, Boston, MA, USA; Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA
4 Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA
5 Cardiovascular Branch, National Heart Lung and Blood Institutes, National Institutes of Health, Bethesda, MD, USA
6 Department of Pathology, Massachusetts General Hospital, Boston, MA, USA
7 Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA; Cardiac Ultrasound Laboratory, Massachusetts General Hospital, Boston, MA, USA; Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA, USA
8 Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: marielle{at}crosbie.com.
To learn if the inhalation of nitric oxide (NO) can decrease myocardial ischemia-reperfusion (I/R) injury, we studied a murine model of myocardial infarction (MI). Anesthetized mice underwent left anterior descending coronary artery ligation for 30, 60, or 120 minutes (min), followed by reperfusion. Mice breathed NO beginning 20 min before reperfusion and continuing thereafter for 24 hours. MI and area at risk (AAR) were measured, and left ventricular (LV) function was evaluated using echocardiography and invasive hemodynamic measurements. Inhalation of 40 or 80 ppm NO decreased the ratio of MI to AAR whereas breathing 20 ppm did not. NO inhalation improved LV systolic function, as assessed by echocardiography 24 hours after reperfusion, and systolic and diastolic function evaluated by hemodynamic measurements 72 hrs after reperfusion. Myocardial neutrophil infiltration was reduced in mice breathing NO, and neutrophil depletion prevented inhaled NO from reducing myocardial I/R injury. NO inhalation increased arterial nitrite levels but did not change myocardial cGMP levels. Breathing 40 or 80 ppm of NO markedly and significantly decreases MI size and improves LV function following ischemia and reperfusion in mice. NO inhalation may represent a novel method to salvage myocardium at risk of I/R injury.
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