Conservation of whole body nitric oxide metabolism in human alcoholic liver disease: implications for nitric oxide production.

Objective: Patients with advanced liver diseases tend to develop a hyperdynamic circulation which complicates cirrhosis. Impairment of nitric oxide (NO) metabolism has been implicated in the pathogenesis of portal hypertension. The aim of this study was to determine nitric oxide synthase (NOS)-dependent whole body NO production in patients with decompensated liver cirrhosis and portal hypertension.

Decreased whole body endogenous nitric oxide production in patients with primary pulmonary hypertension.

Impaired pulmonary release of nitric oxide (NO) is one of the characteristic phenotypic changes of vascular cells in pulmonary hypertension. The aim of this study was to determine nitric oxide synthase (NOS)-dependent whole body NO production in patients with primary pulmonary hypertension. NOS-dependent whole body NO production was assessed by giving an intravenous infusion of L-[(15)N](2)-arginine (50 micromol/min for 30 min) and measuring isotopic urinary enrichment of (15)N-nitrite and (15)N-nitrate.

Determination of trace concentrations of dissolved nitric oxide in a biological buffer.

A new real-time method for measuring a trace concentration of nitric oxide (NO) in a complex matrix routinely used in pharmacological studies of its bioactivity is described. NO was quantified as a gas by chemiluminescence after extraction from a continuous liquid sample flow with a limit of detection of 0.042 nmol dm(-3) at a signal to noise ratio of 3.

Flavohemoglobin Hmp protects Salmonella enterica serovar typhimurium from nitric oxide-related killing by human macrophages.

Survival of macrophage microbicidal activity is a prerequisite for invasive disease caused by the enteric pathogen Salmonella enterica serovar Typhimurium. Flavohemoglobins, such as those of Escherichia coli, Salmonella, and yeast, play vital roles in protection of these microorganisms in vitro from nitric oxide (NO) and nitrosative stress. A Salmonella hmp mutant defective in flavohemoglobin (Hmp) synthesis exhibits growth that is hypersensitive to nitrosating agents.

Nitric oxide gas decreases endothelin-1 mRNA in cultured pulmonary artery endothelial cells.

Inhaled nitric oxide gas (iNO) vasodilates the pulmonary circulation. The effective "dose" of iNO for chronic treatment of pulmonary hypertension is unknown. Increased abundance of pulmonary mRNA for preproendothelin-1 (ppET-1) with its associated increase in endothelin-1 (ET-1) could contribute to the development of both clinical and experimental pulmonary hypertension.

Circulating nitrite anions are a directly acting vasodilator and are donors for nitric oxide.

Inhaled nitric oxide (NO) is a pulmonary vasodilator, but also acts systemically, causing negative cardiac inotropic effects and a fall in systemic vascular resistance. Circulating metabolites of NO are presumed to be responsible. We questioned the role of nitrite anions and the manner in which they might contribute to these effects.

The direct and indirect action of inhaled agents on the lung and its circulation: lessons for clinical science.

Inhalation of particles, gases, and vapors from environmental pollution results in a number of localized and general responses by the lungs. In this article we report investigations performed in humans that have enabled the identification of these specific processes in response to inhaled materials. We also offer insights that could help generalize environmental inhaled pollutants and potential means of studying them in humans.

Exhaled nitric oxide is reduced in infants with cystic fibrosis.

Background: Exhaled nitric oxide levels are low in patients with cystic fibrosis (CF), despite the chronic inflammation present in the airways. This study aimed to determine whether levels of exhaled nitric oxide were reduced prior to the onset of respiratory symptoms in infants with CF.

Methods: The levels of exhaled nitric oxide were measured using a chemiluminescence analyser in five infants with CF and 11 healthy control subjects, both groups having a mean age of 48.

Minimizing the inhaled dose of NO with breath-by-breath delivery of spikes of concentrated gas.

Background: Pulmonary vasodilatation with a 100 ppm concentration of NO given as a short burst of a few milliliters at the beginning of each breath (NOmin) was compared with conventionally inhaled NO, in which a full breath of 40 ppm of NO was inhaled (NOCD).

Methods And Results: NOmin was studied in 16 patients with severe pulmonary hypertension and in 16 isolated porcine lungs with experimentally induced pulmonary hypertension. We compared volumes of 8 to 38 mL of 100 ppm NO in N2 injected at the beginning of each breath with conventional inhalation of 40 ppm NO in air.

Lack of effect of nitric oxide inhibition on bronchial tone and methacholine-induced bronchoconstriction in man.

The role of nitric oxide (NO) as a bronchodilator has been studied in humans with controversial results. The aim of the present study was to investigate the role of endogenous NO on bronchial tone by studying whether nitric oxide synthase (NOS) inhibition with NGnitro-L-arginine-methyl-ester (L-NAME) influences basal bronchial tone, or potentiates methacholine-induced bronchoconstriction. In a preliminary experiment in five subjects, a significant reduction in exhaled NO was found after delivering L-NAME (15 mg in saline) (from 3.

Nitric oxide and exercise in the horse.

1. The effects of exercise on the production rate of nitric oxide (NO) in exhaled air (VNO) and the effects of inhaled NO (80 p.p.

Elevated exhaled nitric oxide in patients with hepatopulmonary syndrome.

The hypoxaemia of hepatopulmonary syndrome, seen in severe chronic liver dysfunction, occurs as a result of precapillary pulmonary arterial dilatation and arteriovenous communications. These abnormalities contribute to the mismatch between ventilation and perfusion, and the right to left blood flow shunting. Nitric oxide (NO) is a powerful vasodilator concerned with the regulation of pulmonary vascular tone in man.