No abstract

PGE1 suppressed the production of IL-6 and IL-8 but not IL-10, IL-1ra, sTNF RI, or sTNF RII. The change in the balance between pro-and anti-inflammatory cytokines may be one of the most important cytoprotective mechanisms of PGE1.

Nicorandil (NCR), a KATP channel opener, has been reported to preserve microvascular integrity in patients with reperfused myocardial infarction. We tested the hypothesis that NCR suppresses myocardial ischemia and reperfusion injury via the attenuation of cytokine production. Forty patients who underwent coronary artery bypass graft surgery were studied. The patients were randomly divided into two groups, i.e., the patients with NCR (4-6 mg/h; N group, n = 20) or without NCR (C group, n = 20). Cardiac surgery was performed under anesthesia using fentanyl and propofol. Blood were sampled at the time of induction of anesthesia, pre-cardiopulmonary bypass, 60 min after aortic occlusion, and 60, 120, and 180 min after declamping the aorta. The activation of NF-kappaB, expression of adhesion molecules, and cytokine production were evaluated in blood samples from the control volunteers by flow cytometric analysis with or without lipopolysaccharide (LPS) stimulation in vitro. Serum IL-6 and IL-8 levels in both groups increased 60 min after declamping the aorta compared with the preoperative value (P < 0.001); the increases of these parameters in N group were lower than those in C group (P < 0.05). Serum creatine kinase with muscle and brain subunits and troponin-T levels increased 60 min after declamping the aorta in two groups (P < 0,001), but the increases of both parameters in N group were lower than those in C group (P < 0.05). NF-kappaB activation, CD11b/CD18 expression, and the production of TNF-alpha, IL-8, and IL-6 in monocytes and granulocytes were inhibited by NCR in vitro. NCR suppressed the increase of inflammatory cytokines such as IL-6 and IL-8 levels, and reduced myocardial reperfusion injury. The inhibition on NF-kappaB activation, adhesion molecule expression, and cytokine production may be one of the important mechanisms of myocardial protection of NCR.

Near-infrared spectroscopy (NIRS) may be a useful method for monitoring the regional oxygen saturation (rSO(2)) of the lower extremity during endovascular aortic repair. Eighteen patients with thoracic descending and/or abdominal aortic aneurysm were enrolled in this study. NIRS probes were placed bilaterally on the calves. Muscular rSO(2) (mrSO(2)) was monitored every 30 s throughout the operation. In the leg in which the femoral artery was clamped, mrSO(2) values were selected at 3 or 4 points-just before clamping (control value), 30 min after clamping, 10 min after the first declamping, and 10 min after the second declamping following repair of the femoral artery, if necessary. In all patients, mrSO(2) decreased significantly during clamping, from 64 ± 11 % (mean ± SD) of the control value to 32 ± 15 %. After declamping, mrSO(2) recovered to 69 ± 14 % of the control value in 16 patients. In the 2 other patients, however, mrSO(2) did not recover after the first declamping, because of femoral artery dissection. After additional repair, mrSO(2) recovered quickly to the control value. These data suggested NIRS may objectively and quantitatively reflect oxygenation of the lower extremities, and may indicate an ischemic event that needs additional repair during endovascular aortic repair.

The current study clarified the peak glucose concentration during aortic surgery. These data may contribute to the management of blood glucose levels during aortic surgery.