Medical Journals

Inhaled Nitric Oxide Decreases Infarction Size and Improves Left Ventricular Function in a Murine Model of Myocardial Ischemia-reperfusion Injury.

Authors:
  • Hataishi Ryuji
  • Rodrigues Ana Clara
  • Neilan Tomas G
  • Morgan John G
  • Buys Emmanuel
  • Shiva Sruti
  • Tambouret Rosemary
  • Jassal Davinder S
  • Raher Michael J
  • Furutani Elissa
  • Ichinose Fumito
  • Gladwin Mark T
  • Rosenzweig Anthony
  • Zapol Warren M
  • Picard Michael H
  • Bloch Kenneth D
  • Scherrer-Crosbie Marielle

From: Department of Anesthesia and Critical Care, Massachusetts General Hospital and Havard Medical School, Boston, MA 02114, USA.

American journal of physiology. Heart and circulatory physiology

  • Publish Date: Jul 2006
  • ISSN: 0363-6135
  • Volume: 291
  • Issue: 1
  • Pages: H379-84
  • Medium: Print
  • Language: English
  • Citation (JAMA): Hataishi Ryuji, Rodrigues Ana Clara, Neilan Tomas G, et al. Inhaled Nitric Oxide Decreases Infarction Size and Improves Left Ventricular Function in a Murine Model of Myocardial Ischemia-reperfusion Injury.. Am. J. Physiol. Heart Circ. Physiol. Jul 2006;291:H379-84

Abstract

To learn whether nitric oxide (NO) inhalation 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 min followed by reperfusion. Mice breathed NO beginning 20 min before reperfusion and continuing thereafter for 24 h. MI size and area at risk were measured, and left ventricular (LV) function was evaluated using echocardiography and invasive hemodynamic measurements. Inhalation of 40 or 80 ppm, but not 20 ppm, NO decreased the ratio of MI size to area at risk. NO inhalation improved LV systolic function, as assessed by echocardiography 24 h after reperfusion, and systolic and diastolic function, as evaluated by hemodynamic measurements 72 h 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 NO markedly and significantly decreased MI size and improved LV function after ischemia and reperfusion in mice. NO inhalation may represent a novel method to salvage myocardium at risk of I/R injury.

Mesh Headings (Keywords): Administration, Inhalation, Animals, Disease Models, Animal, Male, Mice, Mice, Inbred C57BL, Myocardial Reperfusion Injury, Nitric Oxide, Severity of Illness Index, Treatment Outcome, Ventricular Dysfunction, Left


Check for Full Text / PubMed Unique Identifier (PMID): 16443673


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