Results: 3

1.
Fig. 1.

Fig. 1. From: Soluble guanylate cyclase-?1 is required for the cardioprotective effects of inhaled nitric oxide.

Variations of coronary artery anatomy in wild-type (WT) mice and mice deficient in the sGC α1-subunit (sGCα1−/−). Representative photomicrographs of coronary arteries (red dye) in WT and sGCα1−/− mice (×16 magnification). * Bifurcation of the left anterior descending coronary artery (LAD) and the left circumflex coronary artery (LCx). In both WT and sGCα1−/− mice, low bifurcation and high bifurcation of the LAD-LCx was observed. In the photomicrographs, the left atrium (LA) is retracted cephalad. SB, septal branch.

Yasuko Nagasaka, et al. Am J Physiol Heart Circ Physiol. 2011 April;300(4):H1477-H1483.
2.
Fig. 3.

Fig. 3. From: Soluble guanylate cyclase-?1 is required for the cardioprotective effects of inhaled nitric oxide.

sGCα1 in bone marrow (BM)-derived cells mediates the cardioprotective effect of inhaled NO against ischemia-reperfusion injury. WT and sGCα1−/− mice were lethally irradiated and reconstituted with either WT or sGCα1−/− BM. Eight weeks after BM transplantation, mice underwent LAD occlusion for 60 min followed by 24 h of reperfusion. O2 or NO was administered during cardiac ischemia for 60 min, starting at 10 min after coronary occlusion until 10 min after reperfusion. Top: AAR/LV did not differ between groups. Numbers in each group are shown in the bottom of each bar. Bottom: NO inhalation decreased MI/AAR in WT or sGCα1−/− mice that received BM from WT mice [WT-WT and sGCα1−/− (knockout, KO)-WT, respectively], but breathing NO did not alter MI/AAR in WT or sGCα1-deficient mice that received BM from sGCα1−/− mice (KO-KO and WT-KO, respectively). * P = 0.012; †P = 0.024 vs. mice breathing O2; ‡P = 0.049 vs. WT-WT breathing O2. Data are presented as means ± SE.

Yasuko Nagasaka, et al. Am J Physiol Heart Circ Physiol. 2011 April;300(4):H1477-H1483.
3.
Fig. 2.

Fig. 2. From: Soluble guanylate cyclase-?1 is required for the cardioprotective effects of inhaled nitric oxide.

sGCα1 is required for inhaled nitric oxide (NO) to protect against cardiac ischemia-reperfusion injury. All mice received left coronary artery occlusion for 60 min, followed by 24 h of reperfusion. Mice received O2 or NO starting at 10 min after cardiac ischemia until 10 min after reperfusion for 60 min. A: representative cross sections after triphenyltetrazolium chloride staining of each group (×25 magnification). B, top: ratio of area at risk to left ventricle (AAR/LV) did not differ between groups. Numbers in each group are shown in the bottom of each bar. B, bottom: NO inhalation decreased ratio of myocardial infarction to AAR (MI/AAR) in WT mice but not in sGCα1−/− mice. * P < 0.001 vs. WT mice breathing O2. Data are presented as means ± SE.

Yasuko Nagasaka, et al. Am J Physiol Heart Circ Physiol. 2011 April;300(4):H1477-H1483.

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