Combined angiotensin and endothelin receptor blockade attenuates adverse cardiac remodeling post-myocardial infarction in the rat: possible role of transforming growth factor beta(1)

A. Tzanidis, S. Lim, R. D. Hannan, F. See, A. M. Ugoni and H. Krum. Combined Angiotensin and Endothelin Receptor Blockade Attenuates Adverse Cardiac Remodeling Post-Myocardial Infarction in the Rat: Possible Role of Transforming Growth Factor beta(1). Journal of Molecular and Cellular Cardiology (2001) 33, 969-981. Myocardial infarction (MI) is associated with activation of the vasoconstrictor peptides, angiotensin II (AngII) and endothelin-1 (ET-1), which are thought to contribute to adverse cardiac remodeling and dysfunction. The present study sought to determine whether combined AngII and ET receptor blockade improves cardiac remodeling over individual treatments in an experimental model of left ventricular myocardial infarction (LVMI) in the rat. Groups of eight female Sprague-Dawley rats were randomized at 24 h post-LVMI to 1 week treatment with either vehicle, an ET(A/B)receptor antagonist (bosentan), an AT(1)receptor antagonist (valsartan), or combined treatment. Vehicle-treated animals developed LV dysfunction with extensive accumulation of collagen type I and increased alpha(1)(I) procollagen mRNA compared to sham controls. Whilst individual receptor blockade with either bosentan or valsartan reduced LVEDP towards sham control levels, there were no significant changes to myocardial collagen deposition in comparison to vehicle. In contrast, improved ventricular function by combined treatment was associated with reduced type I collagen deposition within left ventricular non-infarct regions, as well as reduced peptide distribution and cardiac gene expression of the profibrogenic peptide, transforming growth factor beta(1)(TGF beta(1)). These data demonstrate that combined AngII and ET receptor blockade has beneficial effects on myocardial fibrogenesis over individual treatments during adverse cardiac remodeling early post-MI

Detection tasks in nuclear power plant operation: Vigilance decrement and physiological workload monitoring

Nuclear power plant (NPP) operators perform a variety of tasks that differ in mental workload. These include detection tasks that may be vulnerable to vigilance decrement. The present study used a simulation of NPP operation to investigate possible loss of vigilance during detection. Metrics used to assess operator functioning included subjective measures of workload and stress, physiological indices of workload, and objective performance. Detection, checking and response implementation tasks were compared, in the context of a simulated Emergency Operating Procedure (EOP). Study findings suggested three conclusions. First, detection imposed higher subjective workload and distress than other tasks, but physiological data suggested more complex differences between tasks. Second, vigilance decrements in detection performance were observed within 5-min task \u27steps\u27. However, analyses of physiological metrics suggested that multiple temporal processes may operate. Third, there were consistent individual differences in task-induced workload responses. Implications of the findings for evaluating NPP interface designs and monitoring operators are discussed