[A case of bronchial hyperreactivity induced by a single inhalation of a large quantity of phthalic anhydride].
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Biomedical subjects
Publications and source records attributed to A Frans.
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In a previous paper, published in this journal, we showed that the data obtained in patients with severe ketoacidosis suggest that inorganic phosphates (K2HPO4) can increase their P50 and therefore enhance tissue oxygenation without concomitant alteration of the 2,3 diphosphoglycerate (DPG). In order to test the hypothesis that K2HPO4 could influence the oxyhemoglobin dissociation curve (ODC) by a mecanism which was not DPG mediated we have measured the total ODC on whole blood with and without addition of 13-80 mmol/l of inorganic phosphates. On average, the level of DPG remained unchanged when the P50 with K2HPO4 was significantly higher (p greater than 0.001) (P50 = 29.9 +/- 3.7 mmHg) than when phosphates were not administered (P50 = 25.5 +/- 2.8 mmHg). The relationship between P50 (mmHg) and K2HPO4 (= X mmol/l) was delta P50 = -2.97 10(-3)(X)2 +0.26(X)-0.42 (r = 0.78). Seeing that phosphates have an immediate action on the ODC, we calculated in our ketoacidosis patients, the relationship between the P50, the inorganic phosphates (P(i) in mg%) and the DPG in mumol/gHb. Both factors exert a highly significant effect (p less than 0.001) on the P50, according to the following equation: P50 = 0.35 DPG +0.26 P(i) + 18.92 (r = 0.73). Our data are important in two points. First it is useful to add inorganic phosphates to the treatment of patients with severe ketoacidosis in order to enhance their tissue oxygenation. Second they recall that the ODC is not only determined by the classical effects of temperature, pH and DPG but also by inorganic anions, like phosphates as described by Benesh and Benesh in their pioneering work.
Inhalation of the platelet activating factor (PAF) produces symptoms of bronchial asthma, a disease in which PAF plays an important role. This lipid mediator released by many kinds of cells exerts its effects on blood cells and on cells of the bronchial wall both directly and indirectly. The crucial role played by PAF in the inflammatory cascades explains the current interest in specific PAF antagonists. These antagonists have both bronchodilator and anti-inflammatory properties and act simultaneously as beta-adrenoceptor agonists and corticosteroids. The first clinical trials of PAF antagonists in the treatment of resistant asthma have given results that are interesting but not superior to those obtained with the conventional anti-asthmatic drugs. The indications for PAF antagonists combined with other specific antagonists will soon be determined.
The aim of this study is to establish whether or not the inhalation of a puff of salbutamol (Ventoline, 100 micrograms) could induce hypoxemia. Twenty-five chronic obstructive pulmonary disease (COPD) patients were investigated. In a first group of 20 patients arterial blood gases and related indices were measured before and 5, 10, 30, 60 and 90 minutes after inhalation of salbutamol. The oxyhemoglobin dissociation curve was traced before and 90 minutes after the drug intake. Except in two subjects in whom salbutamol dramatically improves arterial blood gases, the drug had no effect on the investigated parameters. It is concluded that salbutamol does not affect the blood gases in COPD patients. In this respect the behaviour of COPD patients differs from that of asthmatics in whom salbutamol generally induced hypoxemia.
Over an 18-month period 31 patients (27 female and 4 male) were referred to the ENT department of our clinic for a 1-month to 14-year history of isolated non-productive cough. As ENT examination, including posterior rhinoscopy, was normal, these patients were sent to the pneumology department. Physical examination and X-ray films of the chest were negative, and the patients did not take an angiotensin converting enzyme inhibitor that could have induced this cough. Inhalation of acetylcholine lowered vital capacity by 32 +/- 14% and forced expiratory volume by 34 +/- 16%, a test which is the hallmark of bronchial hyperreactivity. Three patients were atopic. We believe that this cough can be the only manifestation of bronchial asthma. In these patients, cough was suppressed or strongly attenuated by the inhalation, 5 times a day, of salbutamol 200 mg puffs and beclomethasone dipropionate 250 mcg. In addition, the atopic patients were prescribed 10 puffs of sodium cromoglycate per day. Complaints of isolated non-productive cough must always suggest that possibility of bronchial asthma, and a bronchial provocation test must be performed to confirm this diagnosis.
The effect of oral molsidomine (M) on the pulmonary artery hypertension of patients with chronic obstructive pulmonary disease (COPD) was investigated during an acute study (4 mg once) and after a 3 week-treatment (3 times 4 mg a day), on a double-blind basis in 16 patients, 8 receiving a placebo, and 8 molsidomine. Ventilatory and cardiocirculatory indices were obtained at rest and during exercise. When acutely given, molsidomine reduces the mean pulmonary arterial pressure (PAP), the pulmonary vascular resistance (PVR) and the arterial O2 partial pressure (PaO2), increasing heart rate (HR) as well as the alveo-arterial O2 partial pressure difference (P(A-a)O2). During exercise, pulmonary arterial pressure and pulmonary vascular resistance decrease while heart rate increases without modification of arterial blood gases. After a 3-week treatment, molsidomine no more improves any index but significantly reduces cardiac output during exercise and consequently the O2 delivery to the tissues. The same feature has already been observed for other nitrates. It thus seems inappropriate to prescribe nitrates or nitrate-like drugs to chronic obstructive pulmonary disease patients with a view to lower their pulmonary hypertension.
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It is widely known that there might occur three different responses to the administration of ASA or NSAID to patients with bronchial asthma-bronchoconstriction, bronchodilatation or lack of bronchopulmonary action. Nevertheless, the beneficial effect of SAID has been confirmed in patients who are both nonallergic and cortico-dependent asthmatics. Our hypothesis is that in these specific cases the arachidonic acid metabolism is diverted towards cyclo-oxygenase products and that this metabolic diversion leads to an increased production of bronchoconstriction prostaglandins. The administration of NSAID inhibits the cyclo-oxygenase suppressing the enhanced basal production of these bronchoconstrictors and relieving the bronchospasm. The suspected abnormality in arachidonic acid metabolism would be restricted to the respiratory system.
In more than a thousand chronic obstructive lung disease (COLD) patients we have observed in six cases, that exercise-induced hypercapnia was accompanied by a concomitant improvement in arterial oxygen tension (PaO2) and a decrease in the alveolo-arterial O2. This behaviour was not due to technical errors. We explained the increase in PaO2 during exercise by three nonmutually exclusive mechanisms: 1) an increase in the respiratory quotient; 2) the exercise induced increase in alveolar ventilation, although inadequate to match the increase in CO2 production, would be redistributed to previously poorly ventilated regions of the lung, these regions therefore receiving enough oxygen to arterialize the blood flowing through the alveolar capillaries; 3) alternatively, perfusion would be redistributed in a more efficient way during exercise, so that even in the presence of hypoventilation, oxygenation would be improved.
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The effects of intravenous phosphate administration on the hemoglobin-oxygen affinity, the 2,3 diphosphoglycerate level and blood gases were investigated in twenty severe diabetic patients with ketoacidosis in the intensive care unit. Ten received phosphate (mean total amount for each patient = 300 mEq) and the others did not. The only significant difference noted in all indices measured during the recovery period of eight days was seen to occur after 48 h; the P50 in vivo (Torr) was slightly higher in the group who received phosphate (22.5 +/- 1.6 vs 20.5 +/- 2.2) and for the Hill coefficient (2.4 +/- 0.2 vs 2.2 +/- 0.1). This drop in the oxygen affinity of hemoglobin may be useful in subjects at risk of hypoxia, for example those with cardiac or respiratory failure and justifies the use of phosphate in the first 48 h of treatment of patients with diabetic ketoacidosis.
The inotropic agents, dopamine (DP) and dobutamine (DB), both decrease PaO2, probably by a redistribution of the VA/Q ratio. The aim of this study was to assess the effect of both drugs on the VA/Q ratio, using the multiple inert gas elimination method. Ten artificially ventilated patients (eight males), aged 45-74 years were investigated. Blood gases, cardiac output and concentrations of inert gases were measured before and 30 min after infusion of DB or DP. DP and DB were administered alternatively at a rate of 5 micrograms.k-1 min-1. The decrease in PaO2 was significantly greater with DP (12 +/- 9 torr) than with DB (7 +/- 9 torr) (P less than 0.01). Both drugs similarly increased cardiac output: +2.61.min-1 +/- 1.4 for DP and 2.21.min-1 +/- 1.5 for DB. Both DP and DB significantly (P less than 0.01) increased the perfusion of alveoli with VA/Q = 0 (+4 +/- 7% for DP and +3 +/- 7% for DB) and 0 less than VA/Q less than 0.1 (+11 +/- 8.5% for DP and +5.5 +/- 10.5% for DB) (no significant difference between the drugs). When shunt and "shunt-like" effect are considered together, there was a significantly greater increase in the amount of blood going to alveoli with a low VA/Q ratio with DP compared to DB. Both drugs decreased the perfusion of alveoli with 0.1 less than VA/Q less than 10, but the decrease was significantly less for DB than for DP (-15 +/- 6.5% for DP and -8.5 +/- 7% for DB, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
The authors report 18 patients who presented to the ENT department with isolated cough, which had begun one month to 14 years previously. As the ENT examination was negative, the patients were referred to the Department of General Medicine where a bronchial reactivity test with acetylcholine was found to be positive, leading to a diagnosis of airway hyperreactivity. The group was predominantly female (15/18) and atopy was rare; indeed, only one patient, who had a history of allergic rhinitis, was found to be atopic. Bronchodilators and inhaled steroids cured or helped the cough in 16/18 patients. When a patient presents with chronic cough without other respiratory symptoms it is important to consider a diagnosis of airway hyperreactivity and to confirm this with a challenge test of bronchoconstriction.
There is some discordance in the literature on the evolution of the alveolo-arterial oxygen tension difference (A-a)DO2 from rest (R) to graded exercise (E) in healthy subjects. For some authors and not for others (A-a)DO2 increased during exercise. In order to solve this problem we have examined 9 healthy, non-smoking sedentary students (5 males). In every subject PaO2 increased from rest to the highest level of exercise. (A-a)DO2 significantly increased from R and E1 to E2 and from E3 to E4. (A-a)DO2 at rest was 7.5 +/- 4.1 torr; at E1: 7.0 +/- 4.3 torr; at E2: 11.5 +/- 4.2 torr; at E3: 12.5 +/- 3.9 torr; and at E4: 16.5 +/- 4.3 torr. The oxyhemoglobin dissociation curve (ODC) was significantly shifted to the right from 53 to 92% saturation. This shift favours the liberation of O2 from hemoglobin to the tissues but cannot explain the evolution of (A-a)DO2. We believe that the increase in (A-a)DO2 is due to an increased maldistribution of the ventilation-perfusion ratio.
Chronic obstructive lung diseases (COLD) are very often complicated by pulmonary arterial hypertension and right heart failure. Several drugs including nitrates have been used to counteract this type of hypertension. Molsidomine (M) is a recent nitrates-like drug acting for a longer time than the classical nitrates. Our aim was to investigate whether M could significantly lower pulmonary arterial hypertension of patients suffering from COLD. Ten male patients were investigated before and after intake of 4.0 mg M given sublingually. Ventilatory and cardiocirculatory indices were measured at rest and during a 30 and a 50 watts exercise. During exercise, M significantly lowers pulmonary arterial pressure and pulmonary vascular resistance without detrimental effect on arterial blood gases. M seems to be a promising drug to counteract the pulmonary hypertension of patients with COLD.
Some particular cases of bronchial asthma are improved by acetylsalicylic acid. The clinical characteristics of these patients are very similar to those of asthmatic ASA-sensitive cases: a cortico-dependent asthma occurring in later life, in nonatopic patients with chronic rhinitis, sinusitis and/or nasal polyposis. The patient notices that taking an occasional aspirin tablet for some other problem reduces his respiratory symptoms. The bronchodilator effect of aspirin and other Non Steroidal Anti-Inflammatory Drugs in such patients has been clearly demonstrated, although all drugs don't have the same effectiveness. It is important to diagnose these aspirin-relieved asthma cases, using an oral aspirin test, because the treatment with aspirin allows us then to reduce the needed corticosteroid dose. We hypothesize that a diversion of the arachidonic acid metabolism towards cyclo-oxygenase products causes this syndrome.