Intestinal ischemia and reperfusion (intestinal I/R) causes acute lung inflammation that is characterized by leukocyte migration, increased lung microvascular permeability, and, in severe forms, noncardiogenic pulmonary edema and acute respiratory distress syndrome. Female sex hormones interfere with immune response, and experimental and clinical evidence shows that females are more resistant than males to organ injury caused by gut trauma. To reduce the lung inflammation caused by intestinal I/R, we have acutely treated male rats with estradiol. Intestinal I/R was performed by the clamping (45 min) of the superior mesenteric artery (SMA), followed by 2 h of intestinal reperfusion (unclamping SMA). Groups of rats received 17β estradiol (E2, 280 µg/kg, i.v., single dose) 30 min after the SMA occlusion (ischemia period) or 1 h after the unclamping of SMA (reperfusion period). Leukocytes influx into the lung and microvascular leakage were assessed by lung myeloperoxidase activity and Evans blue dye extravasation, respectively. The lung expression of adhesion molecules (intercellular adhesion molecule 1, platelet endothelial cell adhesion molecule 1, and vascular cell adhesion molecule [VCAM]) was evaluated by immunohistochemistry. Interleukin 1β (IL-1β), IL-10, and NOx concentrations were quantified in supernatants of cultured lung tissue. We have found that intestinal I/R increased the lung myeloperoxidase activity and Evans blue dye extravasation, which were reduced by treatment of rats with E2. Intestinal I/R increased ICAM-1 expression only, and it was decreased by E2 treatment. However, E2 treatment reduced the basal expression of platelet endothelial cell adhesion molecule 1. E2 treatment during intestinal ischemia was effective to reduce the levels of IL-10 and IL-1β in explant supernatant, but only IL-10 levels were reduced by E2 at reperfusion phase. The treatment with E2 did not affect NOx concentration. Taken together, our data suggest that estradiol modulates the lung inflammatory response induced by lung injury, likely by acute effects. Thus, acute estradiol treatment could be considered as a potential therapeutic agent in ischemic events.

The prophylactic treatment with 17β-estradiol showed better overall repercussions and was able to prevent any fatal occurrence, increase eNOS expression, thus preserving mesenteric perfusion and intestinal integrity, and reduce inflammation.

RESUMO Os biomarcadores ou marcadores biológicos são substâncias produzidas e liberadas de um órgão ou tecido, que indicam a ocorrência de uma determinada função, seja ela normal ou patológica. São substâncias que podem ser mensuradas por meio de fluidos corporais e permite a avaliação de certas alterações provocadas a um órgão ou tecido, sendo que o biomarcador ideal deve fornecer informações sobre diagnóstico, prognóstico ou resposta ao tratamento já realizado ao paciente. Este artigo de revisão descreverá sobre a utilidade dos biomarcadores cardíacos de estresse e lesão miocárdica como auxiliares para o diagnóstico e prognóstico das cardiopatias em cães e gatos. PALAVRAS-CHAVE: biomarcadores, cardiomiócitos, doenças cardíacas.

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Background/Introduction Acute mesenteric ischemia is a life-threatening emergency with overall mortality ranging from 60% to 80%, and this survival rate has not improved substantially in recent decades. In surgical aortic reconstruction, occlusion of the aorta affects various organs through the ischemia reperfusion injury. Among these organs, the intestine is probably the most affected one. Several studies have proposed that oestradiol has a beneficial effect in the course of the inflammatory lesion.