American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Aug 1995
Comparative StudyAcute and chronic effects of cigarette smoking on exhaled nitric oxide.
Cigarette smoking is associated with an increased risk of respiratory tract infections, chronic airway disease, and cardiovascular diseases, all of which may be modulated by endogenous nitric oxide (NO). We have investigated whether cigarette smoking reduces the production of endogenous NO. We compared exhalations of 41 current cigarette smokers with normal lung function and 73 age-matched non-smoking controls. ⋯ Inhalation of carbon monoxide and NO had no effect on exhaled NO in normal subjects. Cigarette smoking decreased exhaled NO, suggesting that it may inhibit the enzyme NO synthase. Since endogenous NO is important in defending the respiratory tract against infection, in counteracting bronchoconstriction and vasoconstriction, and in inhibiting platelet aggregation, this effect may contribute to the increased risks of chronic respiratory and cardiovascular disease in cigarette smokers.
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The aim of the study was to determine whether closing pressures or vascular distensibility can be used to describe liver venous hemodynamics when right atrial pressure is raised. The study was performed using a vascularly isolated pig liver preparation that allowed the independent control of portal vein and hepatic artery inflows and of outflow pressure (Pout). Pressure-flow (P-Q) relationships of both liver vessels were generated at multiple levels of Pout. ⋯ The behavior of the liver vein system is characterized by a zero flow pressure mimicking a classic vascular waterfall and by distensibility, once the waterfall is exceeded. Both factors act to minimize the reduction in venous return with an increased central venous pressure. Flow through the hepatic artery is affected by an increase in backpressure occurring upstream from the sinusoids, reducing arterial inflow for a constant perfusion pressure.
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Am. J. Respir. Crit. Care Med. · Aug 1995
Role of nitric oxide in endotoxin-induced metabolic and vascular dysregulation of the canine diaphragm.
We assessed the role of nitric oxide (NO) in the regulation of diaphragmatic O2 uptake (Vo2di) and phrenic vascular resistance during endotoxemia in anesthetized, mechanically ventilated dogs. Left diaphragmatic vasculature was isolated and briefly pump perfused with arterial blood at a normal flow rate, at a high rate (50% higher than normal), and at low rat (60 to 70% lower than normal). At each rate, Vo2di and phrenic perfusion pressure (Pphr) were measured. ⋯ Serum arterial and phrenic venous NO concentrations measured in separate groups of animals increased significantly after endotoxin infusion, whereas saline infusion had no effect on these parameters. These results indicate that enhanced NO release plays a significant role in endotoxin-induced phrenic and systemic vasodilation. However, the increase in Vo2di in the endotoxin group does not seem to be mediated by NO release.
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Am. J. Respir. Crit. Care Med. · Jul 1995
Variability of patient-ventilator interaction with pressure support ventilation in patients with chronic obstructive pulmonary disease.
In 12 patients with chronic obstructive pulmonary disease (COPD) receiving pressure support ventilation (PSV), we studied the variability of respiratory muscle unloading and defined its physiologic determinants using a modified pressure-time product (PTP). Inspiratory PTP/min decreased as PSV was increased (p < 0.001), but there was considerable interindividual variation: coefficients of variations of up to 96%. ⋯ At PSV of 20 cm H2O, expiratory effort, quantitated by an expiratory PTP, was clearly evident in five patients before the cessation of inspiratory flow, signifying that the patient was "fighting" the ventilator; of note, these five patients had a frequency of < or = 30 breaths/min. In conclusion, patient-ventilator interactions in patients with COPD are complex, and events in expiration need to be considered in addition to those of inspiration.
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Am. J. Respir. Crit. Care Med. · Jul 1995
A dual-binding antibody to E- and L-selectin attenuates sepsis-induced lung injury.
Many studies indicate a pivotal role for neutrophil adhesion in sepsis-associated lung injury. Neutrophil adhesion to endothelium depends on activation and expression of selectin and integrin adhesion receptors. We studied the effects of pretreatment with a dual-binding porcine anti-E- and anti-L-selectin monoclonal antibody (EL-246) on a porcine model of sepsis-induced lung injury. ⋯ There was no significant difference in pulmonary and systemic hemodynamics between Groups 2 and 3. Group 4 animals exhibited a transient neutropenia, but otherwise no other differences in measured parameters were found compared with Group 1 control animals. In conclusion, EL-246 significantly reduced neutrophil accumulation in lung and attenuated sepsis-induced lung injury, but failed to attenuate deranged pulmonary and systemic hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)