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.
Background-Tissue Doppler imaging (TDI) is a novel echocardiographic method to quantify regional myocardial function. The objective of this study was to assess whether myocardial velocities and strain rate (SR) could be obtained by TDI in mice and whether these indices accurately quantified alterations in left ventricular (LV) systolic function. Methods and Results-TDI was performed in 10 healthy mice to measure endocardial (v endo ) and epicardial systolic velocities and SR. In further experiments, TDI indices were compared with dP/dt max and with sonomicrometer-derived regional velocities, at rest and after administration of dobutamine or esmolol. TDI indices were also studied serially in 8 mice before and 4 and 7 hours after endotoxin challenge.
First, AFV occurs in 14% of patients at rest after valve replacement for aortic stenosis and can be provoked or worsened by ventricular unloading or inotropic stimulation. Second, AFV is related more frequently to cavity squeezing than to systolic anterior motion of the mitral valve apparatus. Third, a typical pattern (small, hyperdynamic, and asymmetrically hypertrophied ventricle) is predictive for postoperative AFV and should be taken into account for the postoperative management. Finally, the presence of AFV at rest is associated with high in-hospital morbidity but good long-term prognosis.
1) The magnitude of wall motion abnormalities induced by dobutamine infusion correlates with angiographic and, more closely, with functional indexes of stenosis severity, even though a wide scatter is observed. 2) In patients with a functionally significant stenosis, the amount of myocardium at risk is a critical determinant of the accuracy of dobutamine echocardiography.
Echographic image quality significantly influences the accuracy of Doppler echocardiographic determination of aortic valve area and, to a lesser extent, of transvalvular pressure gradient. Therefore, the mere noninvasive approach is not suitable to every consecutive patient with aortic stenosis. Qualifications concerning overall image quality should identify patients most likely to benefit from catheterization.
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