Ectopic Origin of the Left Anterior Descending Artery from the Proximal Right Coronary Artery: An Imaging Report.

Anomalies of the coronary arteries represent rare congenital disorders, which are characterized by a wide spectrum of clinical manifestations. Usually, they are asymptomatic, but sometimes they cause myocardial ischemia or sudden cardiac death. Here, we describe the case of a patient who suffered from angina. Coronary angiography revealed an ectopic origin of the left anterior descending coronary artery from the proximal trait of the right coronary artery and the left circumflex artery, originating from the left sinus; the whole coronary tree was free of atherosclerosis. To better define the coronary anatomy, we performed computed tomography angiography with a three-dimensional reconstruction. The patient was discharged from the clinic after 48 h under optimal medical treatment.

Interspecific variation and plasticity in hemoglobin nitrite reductase activity and its correlation with oxygen affinity in vertebrates.

Deoxygenated hemoglobin (Hb) is a nitrite reductase that reduces naturally occurring nitrite to nitric oxide (NO), supplying physiological relevant NO under hypoxic conditions. The nitrite reductase activity is modulated by the allosteric equilibrium between the R and T structures of Hb that also determines oxygen affinity. In the present study we investigated nitrite reductase activity and O2 affinity in Hbs from ten different vertebrate species under identical conditions to disclose interspecific variations and allow an extended test for a correlation between the rate constant for nitrite reduction and O2 affinity. We also tested plastic changes in Hb properties via addition of T-structure-stabilizing organic phosphates (ATP and GTP). The decay in deoxyHb during its reaction with nitrite was exponential-like in ectotherms (Atlantic hagfish, carp, crucian carp, brown trout, rainbow trout, cane toad, Indian python and red-eared slider turtle), while it was sigmoid in mammals (harbor porpoise and rabbit). Typically, hypoxia-tolerant species showed a faster reaction than intolerant species. Addition of ATP and GTP decreased O2 affinity and slowed the rate of nitrite reduction in a concentration-dependent manner. The initial second order rate constant of the deoxyHb-mediated nitrite reduction showed a strong curvilinear correlation with oxygen affinity among all ectothermic vertebrates, and the relationship also applied to plastic variations of Hb properties via organic phosphates. The relationship predicts high nitrite reductase activity in hypoxic tolerant species with high Hb-O2 affinity and reveals that the decrease in erythrocyte ATP and/or GTP during acclimation to hypoxia in ectotherms increases the erythrocyte NO generating capacity.

Nitric oxide metabolites during anoxia and reoxygenation in the anoxia-tolerant vertebrate Trachemys scripta.

Moderate elevations of nitrite and nitric oxide (NO) protect mammalian tissues against ischemia (anoxia)-reperfusion damage by inhibiting mitochondrial electron transport complexes and reducing the formation of reactive oxygen species (ROS) upon reoxygenation. Crucian carp appear to exploit this mechanism by upregulating nitrite and other nitrite/NO metabolites (S-nitroso and iron-nitrosyl compounds) in several tissues when exposed to anoxia. We investigated whether this is a common strategy amongst anoxia-tolerant vertebrates by evaluating NO metabolites in red-eared slider turtles during long-term (9 days) anoxia and subsequent reoxygenation at low temperature, a situation naturally encountered by turtles in ice-covered ponds. We also measured glutathione in selected tissues and assessed the impact of anoxia on electrolyte status. Anoxia induced major increases in [nitrite] in the heart, pectoral muscle and red blood cells, while [nitrite] was maintained unaltered in brain and liver. Concomitantly, the concentrations of S-nitroso and iron-nitrosyl compounds increased, showing that nitrite was used to produce NO and to S-nitrosate cellular molecules during anoxia. The changes were gradually reversed during reoxygenation (1 h and 24 h), testifying that the processes were reversible. The increased NO bioavailability occurred in the absence of NO synthase activity (due to global anoxia) and may involve mobilization of internal/external nitrite reservoirs. Our data support the theory that anoxic upregulation of nitrite and other NO metabolites could be a general cytoprotective strategy amongst anoxia-tolerant vertebrates. The possible mechanisms of nitrite-derived NO and S-nitrosation in protecting cells from destructive Ca(2+) influx during anoxia and in limiting ROS formation during reoxygenation are discussed.

Nitrite as Direct S-Nitrosylating Agent of Kir2.1 Channels.

Nitrite, a physiological nitric oxide (NO) storage form and an alternative way for NO generation, affects numerous biological processes through NO-dependent and independent pathways, including the S-nitrosylation of thiol-containing proteins. Mechanisms underlying these phenomena are not fully understood. The purpose of this study was to analyse in the rat heart (as prototype of mammalian heart) whether nitrite affects S-nitrosylation of cardiac proteins and the potential targets for S-nitrosylation. Rat hearts, perfused according to Langendorff, were exposed to nitrite. By Biotin Switch Method, we showed that nitrite treatment increased the degree of S-nitrosylation of a broad range of membrane proteins. Further analysis, conducted on subfractioned proteins, allowed us to identify a high level of nitrosylation in a small range of plasmalemmal proteins characterized by using an anti-Kir2.1 rabbit polyclonal antibody. We also verified that this effect of nitrite is preserved in the presence of the NO scavenger PTIO (2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide). Our results suggest, for the first time, that nitrite represents a direct S-nitrosylating agent in cardiac tissues and that inward-rectifier potassium ion channels (Kir2.1) are one of the targets. These observations are of relevance since they support the growing evidence that nitrite is not only a NO reserve but also a direct modulator of important functional cardiac proteins.