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Biomedical subjects

R Rodriguez-Roisin

Publications and source records attributed to R Rodriguez-Roisin.

At least 163 records · Page 9Linked to original sources
PubMed1986

Effect of nifedipine on arterial hypoxaemia occurring after methacholine challenge in asthma.

To investigate whether the effects of nifedipine on methacholine induced broncho-constriction could impair pulmonary gas exchange in bronchial asthma a randomised, double blind, crossover study in 13 symptom free asthmatic subjects was designed. Each patient underwent a methacholine bronchial challenge test on two separate days one week apart, after having either oral nifedipine (20 mg thrice daily) or placebo for three days. Arterial blood gases were measured before and after methacholine challenge in nine subjects. Prechallenge values of forced expiratory volume in one second (FEV1) and arterial oxygen tension (Pao2) were similar after nifedipine and after placebo. After challenge, the cumulative doses of methacholine required to produce a 20% fall in FEV1 (PD20 FEV1) were significantly larger after nifedipine (280 (SD 347)) cumulative breath units (CBU) than after placebo (120 (183) CBU; p less than 0.01). After challenge the fall in Pao2 values (17.1 (1.6) mm Hg; (2.28 (0.21) kPa)) was significantly greater than after placebo (11.7 (2.4) mm Hg; (1.56 (0.32) kPa) p less than 0.03). Our data show that although oral nifedipine significantly reduces airway reactivity in patients with mild bronchial asthma, it also adversely affects pulmonary gas exchange, resulting in a lowered postchallenge Pao2, probably because of worsening ventilation-perfusion relationships.

Adult↗
PubMed1985

Fine structural changes in cryptogenic fibrosing alveolitis and asbestosis.

Lung biopsies from 17 patients with cryptogenic fibrosing alveolitis of a cellular rather than fibrotic pattern were examined by transmission electron microscopy in the hope that such cases would show features of pathogenetic significance. Further selection was made by choosing minimally affected areas. There was no ultrastructural evidence of immune complex deposition but alveolar epithelial and capillary damage was frequently found (17 and 14 of the 17 cases respectively). Alveolar epithelial injury consisted of patchy necrosis and regenerative hyperplasia. Alveolar capillary injury consisted of cytoplasmic swelling and basement membrane thickening and reduplication. Many of these features have not been emphasized in previous reports and their prominence in early stages of the disease suggest that they may have pathogenetic significance, possible mechanisms of which are discussed. Similar findings identified during the course of this study in 8 asbestos workers suggest that similar pathogenetic mechanisms may operate in asbestosis.

Asbestosis↗
PubMed1985

Subconjunctival haemorrhage: a feature of acute severe asthma.

Bilateral subconjunctival haemorrhage was observed on 5 separate occasions in 4 patients presenting a fulminant form of acute severe asthma. Four of these episodes required ventilatory support. All patients recovered from their asthma attack after treatment with bronchodilators, corticosteroids, and oxygen. The incidence of this previously unreported finding represents 5% of the total number of patients with acute severe asthma mechanically ventilated in our intensive care unit from 1976.

Adult↗
PubMed1985

Efficacy of high-frequency ventilation in presence of extensive ventilation-perfusion mismatch.

Ten anesthetized normal dogs were each given two methacholine inhalational challenges to produce large amounts of low ventilation-perfusion (VA/Q) regions but little shunt. After one challenge, high-frequency ventilation (HFV) was applied, whereas after the other conventional mechanical ventilation (MV) was used, the order being randomized. Levels of both ventilatory modes were selected prior to challenge so as to result in similar and normal mean airway pressures and arterial PCO2 levels during control conditions. Gas exchange was assessed by both respiratory and multiple inert-gas transfer. Comparing the effect of HFV and MV, no statistically significant differences were found for lung resistance, pulmonary hemodynamic indices, arterial and mixed venous PO2, expired-arterial PO2 differences, or inert-gas data expressed as retention-excretion differences. The only variables that were different were mean airway pressure (2 cm higher during HFV, P less than 0.04) and arterial PCO2 (10 Torr higher during HFV, P less than 0.002). These results suggest that in this canine model of lung disease characterized by large amounts of low VA/Q regions, HFV is no more effective in delivering fresh gas to such regions than is MV.

Animals↗
PubMed1984

The mechanisms of arterial hypoxemia during hemodialysis.

Hypoxemia during hemodialysis has variously been attributed to worsening ventilation-perfusion (VA/Q) relationships, alveolar hypoventilation combined with a reduced respiratory quotient, increased right-to-left shunting, and diffusion impairment. It is difficult to separate out these various effects, which explains lack of agreement in the literature. To more critically evaluate the causes of hypoxemia during hemodialysis, we used a multiple inert gas elimination technique to determine the distribution of ventilation-perfusion ratios during hemodialysis in 8 patients with chronic renal failure. Measurements were made before, during (at 60, 120, and 210 min), and after hemodialysis. Whereas arterial PO2 fell from 87 to 74 mmHg by 120 min, ventilation-perfusion relationships actually improved. Cardiac output fell from 5.3 to 4.0 L/min over the same time. Alveolar ventilation, respiratory quotient, and alveolar PO2 all fell, and the alveolar arterial PO2 difference remained essentially unchanged. These findings suggest that the hypoxemia observed during hemodialysis is primarily due to a decrease in alveolar ventilation and respiratory quotient associated with removal of metabolic CO2 in the dialyzer. Secondary factors affecting arterial PO2 were the slight improvement in ventilation-perfusion relationships tending to increase it, and the decrease in cardiac output tending to decrease it. There was no evidence for diffusion impairment because the measured VA/Q inequality accounted for the degree of hypoxemia.

Arteries↗
PubMed1984

Gas exchange responses to bronchodilators following methacholine challenge in dogs.

To determine how and why different bronchodilators affect ventilation-perfusion (V/Q) relationships differently in experimental asthma, 10 anesthetized dogs were exposed 3 times each (2-1/2 h apart) to aerosolized 1% methacholine over 3 to 5 min. Mechanical, hemodynamic, gas exchange, and catecholamine concentration measurements were made before challenge, and 10, 20, 30, and 135 min after challenge. Fifteen min after challenge the dogs were exposed to aerosolized epinephrine, isoproterenol, salbutamol, or isotonic saline in random order. The worsened V/Q inequality after isoproterenol paralleled increased cardiac output (QT) and decreased pulmonary vascular resistance (PVR). Because of increased QT, arterial PO2 (PaO2) did not fall in spite of the increased V/Q inequality. After administration of isoproterenol, improvement in air-flow obstruction was always associated with significantly less increase in mean PaO2 and more V/Q inequality than after saline. After epinephrine and salbutamol a similar significant decrease in airflow obstruction was associated with only slightly more V/Q mismatching than after saline. The effects of epinephrine on low V/Q ratio areas, shunt, PaO2, QT, heart rate, and PVR were less and of shorter duration than those of isoproterenol. Salbutamol resulted in changes similar to but more persistent than those induced by epinephrine. All variables approached prechallenge values within 2 h after bronchodilator administration, regardless of agent used. These studies show that in a repeatable canine asthma model, randomized administration of epinephrine, isoproterenol, and salbutamol produce different gas exchange responses in spite of similar improvements in air-flow obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Enhancement of hypoxic pulmonary vasoconstriction by almitrine in the dog.

In order to test the hypothesis of enhancement of hypoxic pulmonary vasoconstriction by Almitrine, 12 anesthetized and paralyzed dogs with normal lungs were studied under controlled ventilation. They were ventilated in random sequence with air, 12% O2, and 100% O2, and almitrine (0.1 mg/kg body weight) was infused over 30 min during each O2 mixture. The multiple inert gas elimination technique was used to detect alterations in ventilation-perfusion (VA/Q) mismatching before and during the interventions and to measure cardiac output (QT). Arterial, mixed venous and expired gases, inert gas concentrations, and hemodynamic measurements were made while the dogs were breathing the different O2 mixtures before infusing the drug, near the end of 30 min of infusion and 30 min after infusion had ended. There were no significant changes in pH, PaO2, PaCO2, QT, oxygen uptake, oxygen delivery index, systemic vascular resistance, mean systemic arterial pressure, heart rate, stroke volume index, or VA/Q distribution during the experiment. Significant increases in: (a) pulmonary artery pressure (PA), (b) the pressure difference between PA and pulmonary capillary wedge pressure (PCw), and (c) pulmonary vascular resistance (PVR) occurred when the drug was infused during 12% O2 and air, but not during 100% O2. The PVR increased 59.7% with almitrine infusion during 12% O2 and 38.4% during air breathing (p less than or equal to 0.01), but there was no significant change during 100% O2. Vascular responses were not dependent on the order in which the different O2 mixtures were administered. These data strongly suggest that almitrine enhances hypoxic vasoconstriction in the lung, and this effect may explain reported improvement in PaO2 in hypoxic patients given the drug.

Almitrine↗
PubMed1981

Pulmonary involvement in primary biliary cirrhosis.

The association of pulmonary fibrosis and primary biliary cirrhosis (PBC) remains controversial. To determine the frequency of pulmonary fibrosis in PBC, a carefully selected series of 14 PBC patients, seven patients with Sicca complex, and 14 control subjects have been studied. Seven of the 14 patients with PBC had Sjögren's syndrome, four of whom had some clinical evidence of pulmonary disease. Evaluation of ventilatory capacity, gas transfer factor, arterial blood gases, and lung mechanics were performed. Gas transfer was reduced in patients with PBC associated with Sjögen's syndrome and in patients with the Sicca complex. These results suggest that the respiratory, clinical, ad functional abnormalities found in PBC are related to the presence of an associated Sjögen's syndrome.

Adult↗
PubMed1980

Maximal expiratory flow volume curves in workers exposed to asbestos.

We have studied 40 workers with varying industrial exposure to asbestos, using routine spirometry and maximal expiratory flow volume curves (MEFVC). Abnormalities of MEFVC were common and seen in those with normal spirometry and total lung capacity. The high incidence of abnormal MEFVC suggests that air flow dysfunction in small airways may follow prolonged asbestos exposure. Our findings support, therefore, the idea that asbestos exposure may cause an obstruction to airflow arising particularly in small airways, and that one of the common functional abnormalities attributable to asbestos exposure is airways obstruction.

Adult↗
PubMed1976

Sleeping ventilatory patterns in patients with severe chronic airflow obstruction causing respiratory failure.

During sleep some patients with airways obstruction and hypoxaemia developed tachypnoea. This could not be explained by the severity of their abnormality of lung function, their CO2 responsiveness, the nature of their lung disease or their personality. This nocturnal tachypnoea correlated best with a raised resting arterial blood PCO2, and was not seen hypoxaemic patients with a normal PCO2 who showed the usual fall in respiratory rate when asleep. We suggest that in patients with both hypoxaemia and hypercapnia sleep removes a cortical inhibitory mechanism which slows breathing durigng waking hours, and is linked to the arterial blood PCO2.

Airway Obstruction↗