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1.
Braz. J. Anesth. (Impr.) ; 73(2): 186-197, March-Apr. 2023. tab, graf
Artículo en Inglés | LILACS | ID: biblio-1439585

RESUMEN

Abstract Anemia is associated with increased risk of Acute Kidney Injury (AKI), stroke and mortality in perioperative patients. We sought to understand the mechanism(s) by assessing the integrative physiological responses to anemia (kidney, brain), the degrees of anemia-induced tissue hypoxia, and associated biomarkers and physiological parameters. Experimental measurements demonstrate a linear relationship between blood Oxygen Content (CaO2) and renal microvascular PO2 (y = 0.30x + 6.9, r2= 0.75), demonstrating that renal hypoxia is proportional to the degree of anemia. This defines the kidney as a potential oxygen sensor during anemia. Further evidence of renal oxygen sensing is demonstrated by proportional increase in serum Erythropoietin (EPO) during anemia (y = 93.806*10−0.02, r2= 0.82). This data implicates systemic EPO levels as a biomarker of anemia-induced renal tissue hypoxia. By contrast, cerebral Oxygen Delivery (DO2) is defended by a profound proportional increase in Cerebral Blood Flow (CBF), minimizing tissue hypoxia in the brain, until more severe levels of anemia occur. We hypothesize that the kidney experiences profound early anemia-induced tissue hypoxia which contributes to adaptive mechanisms to preserve cerebral perfusion. At severe levels of anemia, renal hypoxia intensifies, and cerebral hypoxia occurs, possibly contributing to the mechanism(s) of AKI and stroke when adaptive mechanisms to preserve organ perfusion are overwhelmed. Clinical methods to detect renal tissue hypoxia (an early warning signal) and cerebral hypoxia (a later consequence of severe anemia) may inform clinical practice and support the assessment of clinical biomarkers (i.e., EPO) and physiological parameters (i.e., urinary PO2) of anemia-induced tissue hypoxia. This information may direct targeted treatment strategies to prevent adverse outcomes associated with anemia.


Asunto(s)
Humanos , Hipoxia Encefálica/complicaciones , Accidente Cerebrovascular , Lesión Renal Aguda/etiología , Anemia/complicaciones , Oxígeno , Biomarcadores , Riñón , Hipoxia/complicaciones
2.
Mem. Inst. Oswaldo Cruz ; 95(4): 445-52, July-Aug. 2000.
Artículo en Inglés | LILACS | ID: lil-264223

RESUMEN

Wild golden lion tamarins (Leontopithecus rosalia) -- endangered primates that are native to the Brazilian Atlantic coastal forest -- were surveyed for the presence of Trypanosoma cruzi with the use of Giemsa-stained blood smears, hemocultures and an indirect immunofluorescence assay (IFAT). Positive IFAT with titers ranging from 1:20 to 1:1280 were observed in 52 per cent of the 118 wild tamarins examined and the parasite was isolated from 38 tamarins. No patent parasitemia was observed among the tamarins from which T. cruzi was isolated. Serum conversion and positive hemoculture was observed for three animals that had yielded negative results some months earlier, which indicates that T. cruzi is actively transmitted among tamarins. In contrast to observations with other sylvatic isolates, those from the tamarins were significantly more virulent and most of them produced mortality in experimentally infected Swiss mice. Some variation in the kDNA restriction profiles among the isolates was observed. Electrophoresis with GPI, G6PDH, IDH, MDH and ME enzymes showed a Z2 profile.


Asunto(s)
Animales , Ratones , Callitrichinae/parasitología , Enfermedad de Chagas/veterinaria , Enfermedades de los Monos/parasitología , Trypanosoma cruzi , Brasil/epidemiología , Cebidae/parasitología , Enfermedad de Chagas/epidemiología , Enfermedad de Chagas/transmisión , Técnica del Anticuerpo Fluorescente Indirecta , Estudios de Seguimiento , Transmisión Vertical de Enfermedad Infecciosa , Enfermedades de los Monos/epidemiología , Enfermedades de los Monos/transmisión , Parasitemia , Trypanosoma cruzi/genética , Trypanosoma cruzi/aislamiento & purificación , Trypanosoma cruzi/patogenicidad
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