A method for the evalutation of the frequencies of incidental events related to the ships traffic inside a port using a statistical approach

Aim of this paper is to present a semi-probabilistic, semi-deterministic methodology to evaluate the risk of dangerous spills, and related public and environmental hazard, associated to the navigation in a narrow channel-port. The model is based on a Monte Carlo method with variance reduction technique and can simulate different kinds of ship (tonnage, carried substance) and different kinds of routes to reach or to leave the jetties and the port. The basic event probability (operating error) can evolve in collision with: other flowing or moored ships, sand banks, free jetties, dangerous structures. The possible consequences can be spills of hazardous materials, In addition, the probabilistic model evaluates the frequencies of the events at jetty, as onboard fire and/or explosion, load or unload and berth or unberth accidents. The simulation of the system in study can be performed automatically by a package of two programs: the first (input module) accepts the topological and traffic information about the port; the second (simulation module) simulates the port and the traffic using the inputs created by the first. The simulation program can handle sensitivity analysis. Finally, the methodology has been applied to an idealised but realistic situation of channel-por

Computer methods for reliability data processing

SIGLEITItal

Evaluation of two different oxygen inspiratory fractions on the hemodynamic effects of N-omega-nitro-L-arginine methyl ester in anesthetized dogs

The effect of two different oxygen inspiratory fractions (FiO(2)=21% and 100%) on the hemodynamic responses induced by N(o)mega-nitro-L-arginine methyl ester (L-NAME) was investigated in anesthetized dogs. L-NAME (0.01-10.0mg/kg), but not D-NAME: induced dose-dependent changes in the hemodynamic parameters of the animals. At the highest dose, L-NAME increased mean arterial blood pressure in both room air (from 86.2-/+3.2 to 125.1-/+7.8 mmHg) and pure oxygen (from 100.0-/+7.5 to 139.0-/+3.2 mmHg) ventilated animals. L-NAME also increased systemic and pulmonary vascular resistances. These effects were accompanied by a decrease in cardiac output and bradycardia (37% and 31% decreases far pure oxygen and room air, respectively). However, there were no significant differences in the responses to L-NAME between the dogs ventilated with FiO(2)=21% and those ventilated with FiO(2)= 100%. L-NAME did not modify blood gas analyses, despite the expected difference in pO(2) levels between the two experimental groups of animals (3 times higher in the animals ventilated with pure oxygen). These results indicate that nitric oxide release accounts for the maintenance of hemodynamic function in the anesthetized dog, and that L-NAME-induced effects are not affected by hyperoxemiaAssociação Brasileira de Divulgação Científica2913339BrasilBrazilian journal of medical and biological researchBrazilian J. med. biol. res.São Paulo, S

Evaluation of two different oxygen inspiratory fractions on the hemodynamic effects of N omega-nitro-l-arginine methyl ester in anesthetized dogs

The effect of two different oxygen inspiratory fractions (FiO2 = 21% and 100%) on the hemodynamic responses induced by N omega-nitro-L-arginine methyl ester (L-NAME) was investigated in anesthetized dogs. L-NAME (0.01-10.0 mg/kg), but not D-NAME, induced dose-dependent changes in the hemodynamic parameters of the animals. At the highest dose, L-NAME increased mean arterial blood pressure in both room air (from 86.2 +/- 3.2 to 125.1 +/- 7.8 mmHg) and pure oxygen (from 100.0 +/- 7.5 to 139.0 +/- 3.2 mmHg) ventilated animals. L-NAME also increased systemic and pulmonary vascular resistances. These effects were accompanied by a decrease in cardiac output and bradycardia (37% and 31% decreases for pure oxygen and room air, respectively). However, there were no significant differences in the responses to L-NAME between the dogs ventilated with FiO2 = 21% and those ventilated with FiO2 = 100%. L-NAME did not modify blood gas analyses, despite the expected difference in pO2 levels between the two experimental groups of animals (3 times higher in the animals ventilated with pure oxygen). These results indicate that nitric oxide release accounts for the maintenance of hemodynamic function in the anesthetized dog, and that L-NAME-induced effects are not affected by hyperoxemia.The effect of two different oxygen inspiratory fractions (FiO2 = 21% and 100%) on the hemodynamic responses induced by N omega-nitro-L-arginine methyl ester (L-NAME) was investigated in anesthetized dogs. L-NAME (0.01-10.0 mg/kg), but not D-NAME, induced dose-dependent changes in the hemodynamic parameters of the animals. At the highest dose, L-NAME increased mean arterial blood pressure in both room air (from 86.2 +/- 3.2 to 125.1 +/- 7.8 mmHg) and pure oxygen (from 100.0 +/- 7.5 to 139.0 +/- 3.2 mmHg) ventilated animals. L-NAME also increased systemic and pulmonary vascular resistances. These effects were accompanied by a decrease in cardiac output and bradycardia (37% and 31% decreases for pure oxygen and room air, respectively). However, there were no significant differences in the responses to L-NAME between the dogs ventilated with FiO2 = 21% and those ventilated with FiO2 = 100%. L-NAME did not modify blood gas analyses, despite the expected difference in pO2 levels between the two experimental groups of animals (3 times higher in the animals ventilated with pure oxygen). These results indicate that nitric oxide release accounts for the maintenance of hemodynamic function in the anesthetized dog, and that L-NAME-induced effects are not affected by hyperoxemia291333

Small-dose Inhaled Nitric Oxide Attenuates Hemodynamic Changes After Pulmonary Air Embolism In Dogs.

Inhaled nitric oxide (NO) has been used to treat pulmonary hypertension. Experimental studies have suggested therapeutic effects of NO after pulmonary microembolism. We evaluated the protective effects of NO in dogs during a pulmonary air embolism (PAE). NO (3 ppm) was administered to six anesthetized mongrel dogs (NO group) but not to the seven dogs in the control group. After 20 min, each dog received a venous air injection of 2.5 mL/kg. Hemodynamic evaluation was performed, and blood samples were drawn for blood gas analysis before and after NO inhalation and 5-60 min after the PAE. Both arterial blood pressure and cardiac output were decreased in the control group for >15 min after PAE, whereas NO-treated animals showed only transient hypotension. NO attenuated the pulmonary hypertension after PAE, as demonstrated by small (P < 0.05) increases in pulmonary artery pressure and pulmonary vascular resistance index in NO-treated animals (90% and 135%, respectively) compared with the controls (196% and 282%, respectively). These hemodynamic effects of NO were associated with higher mixed venous O2 tensions and saturations in the NO group compared with the controls. We conclude that small-dose NO (3 ppm) attenuated the hemodynamic changes induced by PAE in dogs. This protective effect of NO on hemodynamics is not accompanied by improvement in pulmonary oxygenation in this setting. In this study, we evaluated the protective effects of inhaled nitric oxide in a pulmonary air embolism setting. Nitric oxide attenuated the hemodynamic changes induced by pulmonary air embolism without improving pulmonary oxygenation.881025-