CPAP at 10 cm H(2)O during cardiopulmonary bypass does not improve postoperative gas exchange

Objective: To compare postoperative (PO) pulmonary gas exchange indexes in patients submitted to myocardial revascularization (MR) with or without the application of continuous positive airway pressure (CPAP) during cardiopulmonary bypass (CPB). Methods: Thirty adult patients submitted to MR with CPB between March and September 2005 were randomly allocated to two groups: CPAP (n=15), patients that received CPAP at 10 cmH(2)O during CPB, and control (n=15), patients that didn't receive CPAP. PaO(2)/FiO(2) and P(A-a)O(2) were analyzed at four moments: Pre dust before CPB, with FiO(2)=1.0); Post (30min post-CPB, with FiO(2)=1.0); immediate PO period (12h post-surgery, with FiO(2)=6.4 by using a Venturi (R) facial mask) and first PO day (24h post-surgery, with FiO(2)=0.5 by a facial mask). Results: PaO(2)/FiO(2) and P(A-a)O(2) tend to get significantly worst as time elapsed during the postoperative period in both groups, but no differences were observed between them at any moment. When PaO(2)/FiO(2) was subdivided into three categories, a greater prevalence of patients with values between 200 mmHg and 300mmHg were observed in CPAP group only at moment Post (30min post-CPB; p = 0.02). Conclusion: CPAP at 10cmH2O administered during CPB, although had lightly improved PaO(2)/FiO(2) at 30 minutes post-CPB, had no significant sustained effect on postoperative pulmonary gas exchange. We concluded that in patients submitted to MR, application of 10 cmH(2)O CPAP does not improve postoperative pulmonary gas exchange.23220921

A review of Brazilian scientific output on crack - contributions to the political agenda

Object: scientific literature about crack abuse published in Brazilian journals indexed in SCIELO.Objective: systematic review of literature treating findings as a framework for agenda-setting orienting policy decision makers.Methodology: SCIELO online journals research since 02/06/2013 on tag crack as "key word searched" and in indexes as "research amplitude". An amount of 199 references were identified and their abstracts were analyzed getting to a final group of 59 articles specifically studying crack issues in Brazil. Analysis: institutional criteria (journal, subject area, and publishing time) and analytical categories created by the authors: "Social Risk", "Treatment", "Use/Abuse", "Profile", "Social Relations", and "Study".Results: crack use impact Brazilian journals since 2011; health field is prominent; articles about "Associated Risk" and "Treatment" prevail; SUS cannot face demand;investment improvement in CAP and harm reduction; therapeutic communities need to match with SUS standards; youngers, black people and poor express users profile; rave style use; repressive policies were not well succeeded; and multidisciplinary approach are necessary

Trypanosoma cruzi induces edematogenic responses in mice and invades cardiomyocytes and endothelial cells in vitro by activating distinct kinin receptor subtypes (B-1/B-2)

Trypanosoma cruzi, the protozoan that causes Chagas' heart disease, invades endothelial cells in vitro by activating the B-2 kinin receptor (B2R). Here, we demonstrate that mice infected with trypomastigotes develop potent edema after treatment with the angiotensin-converting enzyme (ACE) (or kininase II) inhibitor captopril. Experiments performed with specific kinin receptor (B2R/B1R) antagonists and knockout mice revealed that the early-phase (3-h) edema is mediated by the constitutive B2R, whereas the late-phase (24-h) response depends on stimulation of the up-regulated B1R. Given previous evidence that parasite invasion of cells expressing B2R is potentiated by captopril, we investigated the prerequisites for in vitro infection of Chinese hamster ovary cells overexpressing either B1R or B2R, human umbilical vein endothelial cells activated by lipopolysaccharide, and neonatal rat cardiomyocytes. Our results indicate that captopril potentiates parasite invasion regardless of the kinin (B-2/B-1) activation pathways, whereas DL-2-mercaptomethyl-3-guanidino-ethylthiopropanoic acid (MGTA), an inhibitor of kininase I (carboxypeptidase M/N), selectively decreases parasite infectivity for B1R-expressing cells. These data suggest that formation of the B1R agonist, i.e., [des-Arg] kinins, critically depends on the processing action of kininase I, here proposed as a potential pathogenesis cofactor. Collectively, our data suggest that fluctuations in the levels of kininases may modulate parasite infectivity and pathological outcome in Chagas' disease.Univ Brasil, CCS, Inst Biofis Carlos Chagas Filho, BR-21944900 Rio de Janeiro, BrazilUniversidade Federal de São Paulo, Dept Biofis, Escola Paulista Med, São Paulo, BrazilMax Delbruck Ctr Mol Med, Berlin, GermanyUniv Colorado, Sch Med, Dept Biochem & Mol Genet, Denver, CO 80262 USAUniv Frankfurt, Sch Med, Inst Biochem 2, D-6000 Frankfurt, GermanyUniv Rio de Janeiro, Dept Biol Celular & Genet, Rio de Janeiro, BrazilFundacao Oswaldo Cruz, Inst Oswaldo Cruz, Rio de Janeiro, BrazilUniversidade Federal de São Paulo, Dept Biofis, Escola Paulista Med, São Paulo, BrazilWeb of Scienc