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Objective: To investigate the concordance between novel and conventional surveillance paradigms for ventilator-associated pneumonia (VAP)., Methods: This study was conducted at a regional teaching hospital in southern Taiwan with 5 acute intensive care units. To assess the validity of novel ventilator-associated event (VAE) surveillance, we retrospectively applied the VAE algorithm to analyze all VAP cases that were identified using conventional definitions between April 2010 and February 2014. Patient outcomes, including ventilator days, hospital stay lengths, and in-hospital mortality were recorded., Results: Among 165 episodes of conventional VAP, 55 (33.3%), 40 (24.2%), 20 (12.1%), and 2 (1.2%) episodes were classified as a ventilator-associated condition, an infection-related ventilator-associated complication, possible VAP, and probable VAP, respectively, according to the new VAE algorithm. Changes in positive end-expiratory pressure and inspired oxygen fraction levels during the development of VAP were significant higher among each VAE category than for conventional VAP (all P < .001). In-hospital mortality was significantly higher among patients with ventilator-associated condition than for patients with conventional VAP (P = .0185)., Conclusions: In our study population, novel VAE surveillance only detected one-third of conventional VAP cases. Thus, more studies are needed to further validate VAE surveillance compared with conventional VAP by using strong microbiologic criteria, particularly bronchoalveolar lavage with a protected specimen brush for diagnosing VAP., (Copyright © 2015 Association for Professionals in Infection Control and Epidemiology, Inc. Published by Elsevier Inc. All rights reserved.)

Background and Purpose: Data on the role of nitric oxide (NO) in monocrotaline (MC)-induced pulmonary hypertension of rats have all been derived from in vitro measurements. In vivo pulmonary hemodynamics and microvascular responses to NO blockade in MC-treated rats have not been reported. The current study evaluated the role of NO in live MC-treated rats., Methods: Male Sprague-Dawley rats (n = 29) were divided into saline control and MC-treated groups. Three to 4 weeks after either saline or MC injection, pulmonary hemodynamics were measured using pulmonary arterial catheter and thermodilution techniques. Pulmonary microvascular diameter changes were assessed using an intravital microscope., Results: Three to 4 weeks after subcutaneous injection of MC (50 mg/kg), MC-treated rats showed elevated pulmonary arterial pressure compared to control rats (23.6 +/- 2.9 mm Hg vs 14.5 +/- 0.8 mm Hg). N(omega)-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg, intravenously), an NO synthase inhibitor, produced significant increases in pulmonary arterial pressure and total pulmonary vascular resistance compared to control rats (12.3 +/- 2.5 mm Hg vs 1.0 +/- 0.9 mm Hg; 0.21 +/- 0.04 mm Hg/mL/min vs 0.05 +/- 0.02 mm Hg/mL/min, p < 0.05). Intravital microscopic observation of the subpleural vessels showed significant vasoconstriction in medium-sized (> 40 microm) pulmonary arterioles of MC-treated rats following L-NAME administration (58.4 +/- 3.6 microm vs 47.1 +/- 3.4 microm, p < 0.05) while no significant diameter changes were found in either the small-sized (< 40 microm) pulmonary arterioles or pulmonary venules. Diameters of pulmonary arterioles and venules in control rats were not affected by L-NAME administration., Conclusion: Pulmonary arterial pressure and pulmonary vascular resistance increased after NO blockade in live MC-treated rats. The site of vasoconstriction after NO blockade included medium-sized pulmonary arterioles but not small-sized pulmonary arterioles. This study has provided both macro- and microhemodynamic evidence of a modulatory role of NO in live MC-treated rats.