|1.||Mengozzi, G: 2 articles (09/2002 - 03/2001)|
|2.||Hansen, Marie N: 1 article (07/2015)|
|3.||Madsen, Steffen S: 1 article (07/2015)|
|4.||Jensen, Frank B: 1 article (07/2015)|
|5.||Gerber, Lucie: 1 article (07/2015)|
|6.||Urbanska, Krystyna: 1 article (11/2013)|
|7.||Łącki, Piotr: 1 article (11/2013)|
|8.||Krzykawska-Serda, Martyna: 1 article (11/2013)|
|9.||Susz, Anna: 1 article (11/2013)|
|10.||Jakubowska, Monika: 1 article (11/2013)|
04/01/1994 - "At the relatively low concentrations (5-80 ppm) that are effective in relieving experimental pulmonary hypertension induced by alveolar hypoxia, inhaled NO gas causes accumulation of NO2- + NO3- in plasma and a small increase in MetHb but no detectable nitrosylhemoglobin."
07/01/2015 - "Nitrite uptake was slightly higher in hypoxia than normoxia, and high internal nitrite levels extensively converted blood hemoglobin to methemoglobin and nitrosylhemoglobin. "
03/23/2004 - "RBC-induced relaxations during hypoxia correlated with S-nitrosohemoglobin (SNO-Hb) (R2=0.88) but not iron nitrosylhemoglobin (HbFeNO) content. "
06/02/2000 - "Our studies show that 1) increased O(2) affinity of SNO-Hb (which otherwise retains allosteric responsivity) restricts the hypoxia-induced allosteric transition that exchanges NO groups with ambient thiols for vasorelaxation; 2) some NO groups released from Cys(beta93) upon transition to T structure are autocaptured by the hemes, even in the presence of glutathione; and 3) an O(2)-dependent equilibrium between SNO-Hb and iron nitrosylhemoglobin acts to conserve NO. Thus, by sequestering a significant fraction of NO liberated upon transition to T structure, Hb can conserve NO groups that would otherwise be released in an untimely or deleterious manner."
|2.||Pulmonary Hypertension (Ayerza Syndrome)
|4.||Middle Cerebral Artery Infarction (Middle Cerebral Artery Syndrome)
03/01/1996 - "We investigated the levels of nitrosyl hemoglobin (HbNO) in rat jugular blood by electron spin resonance (ESR) spectroscopy during and after middle cerebral artery occlusion. "
12/06/1996 - "Both nitrosyl hemoglobin (HbNO) (2.5 +/- 0.4 microM) and plasma nitrite plus nitrate levels (61 +/- 5 microM) in rats under normothermia (approximately 37 degrees C) after 30 min of reperfusion following 2 h of left middle cerebral artery occlusion were significantly high, compared with sham operated rats (1.3 +/- 0.1 microM, 40 +/- 4 microM, respectively). "
11/17/1995 - "To assess the interaction of nitric oxide (NO) and superoxide during reperfusion after cerebral ischemia, we studied the dose effects of superoxide dismutase (SOD) on the levels of nitrosyl hemoglobin and plasma nitrite + nitrate which were increased at 30 min reperfusion after 2 h middle cerebral artery occlusion in rats. "
07/01/1996 - "Nitric oxide was detected as the nitrosyl-hemoglobin complex by electron paramagnetic resonance analysis of blood drawn from mice at different times of infection, and it was shown to increase with the evolution of the disease. "
06/01/1996 - "Nitric oxide was detected as the nitrosyl hemoglobin complex by EPR analysis of blood drawn from mice at 35, 64 and 148 days of infection. "
|2.||Sulfhydryl Compounds (Thiols)
|3.||Glutathione (Reduced Glutathione)
|4.||Nitric Oxide (Nitrogen Monoxide)
|6.||glycosylated-nitric oxide complex hemoglobin A