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Biomedical subjects

A F Junod

Publications and source records attributed to A F Junod.

At least 109 records · Page 6Linked to original sources
PubMed1980

[Physiopathology of chronic respiratory insufficiency].

The use by West et al. of gases with different solubilities and of appropriate models has indicated that impairment of gas exchange in patients with chronic obstructive pulmonary disease and respiratory failure resulted essentially from altered ventilation/perfusion ratios. To understand why some patients do not appear to be capable of compensating this impairment and become hypercapnic, it is necessary to examine the other components of the respiratory system (control of ventilation, respiratory muscles) and their interactions. The measurement of occlusion pressure and of average inspiratory flow, and analysis of the timing of the respiratory cycle provides interesting information on the output of the control system and the efficiency of respiratory muscles. Electromyography of respiratory muscles also affords useful information on the degree of fatigue of these muscles. The use of this data should help to clarify the problem that has remained unanswered for many years: is the patient with hypercapnia someone who does not want to, or cannot, increase his ventilation? Other studies in the same group of patients during sleep have supplied evidence for the presence of numerous episodes of arterial oxygen desaturation with marked effects on the cardiovascular system. Pathophysiology should also consider this aspect of respiratory failure which occurs in the third of our lifetime devoted to sleep.

Carbon Dioxide↗
PubMed1980

Time course of lung function changes in atypical pneumonia.

We measured pulmonary function in each of 21 patients suffering from "atypical", non-bacterial pneumonia during the acute illness and during convalescence (two to 18 months) to study the course and the nature of functional impairment at different stages of the disease. In six patients, no aetiological agent was found. An aetiological agent was identified in 15 of the patients: Mycoplasma pneumoniae (seven patients), influenza A (three patients), parainfluenza 3 (one patient), varicella (two patients), Q fever (one patient), coxsackie B3 (one patient). At the time of admission we observed a restrictive pattern in 52%, an obstructive pattern (decreased FEV1/FVC ratio) in 52% abnormalities in distribution of ventilation (abnormal slope of phase 3) in 63%, and abnormalities in gas exchange (increased AaDO2) in 75% of the patients. The frequency of abnormalities in these pulmonary function tests decreased dramatically after two to four weeks and nearly disappeared in most patients during convalescence. The only major residual abnormality was a decreased FEV1/FVC ratio in five subjects, four of whom were smokers. However, when MMEF and V75 were measured at this stage, their average value for all the groups of patients with the exclusion of the Mycoplasma pneumoniae group, was markedly reduced. These data suggest that small airways involvement can be demonstrated during the convalescence of patients recovering from various types of atypical pneumonia other than those caused by Mycoplasma pneumoniae.

Adult↗
PubMed1980

[Measurement of pulmonary endothelial function; its potential clinical value].

For almost 10 years, numerous studies have shown that the pulmonary endothelium is endowed with a certain number of metabolic properties related to the uptake and hydrolysis of circulating vasoactive substances. Noradrenaline, serotonin, adenosine and possible certain prostaglandins are transported in the endothelial cells, according to processes which have now been clearly defined, and are there metabolised. Other compounds, including peptides (bradykinin, angiotensin I), or nucleotides (ATP, ADP, AMP) are hydrolysed in contact with the plasma membrane of the endothelium, without penetrating within the cell. For certain substrates (serotonin, angiotensin I), the properties of the pulmonary endothelial cell may be extended to systemic endothelial cells. For other substances, there would appear to be a specificity of endothelial function according to the site. It would appear that the lung, by virtue of its richness in endothelial cells, is capable of influencing concentrations of the circulating substances and, as a result, vascular tone. The existence of delicate processes of the uptake of substances has also been used to test the integrity of the cellular function of the pulmonary endothelium under experimental pathological condition, such as hyperoxia. However, before such a technique, based upon measurement os extraction of amines or other substances from various parts of the pulmonary circulation could be applied clinically, a critical consideration must be undertaken of the multiple factors involved in these processes. The major problem lies in the difficulty of distinguishing between dysfunction of the endothelial cells or a decrease in their number.

Endothelium↗
PubMed1979

PGA1 and PGF2 alpha metabolism by pig pulmonary endothelium, smooth muscle, and fibroblasts.

To determine the cellular site for uptake and degradation of circulating prostaglandins (PGs) by the lung, the metabolism of PGA1 and PGF2 alpha was studied in pig lung slices, smooth muscle preparations, and pulmonary valves, as well as in isolated and cultured endothelial cells and cultured fibroblasts. Formation of 15-keto metabolites of both PGA1 and PGF2 alpha by lung slices was confirmed. No evidence of PGF2 alpha degradation could be found in any of the remaining preparations. For PGA1, however, 15-hydroxyprostaglandin dehydrogenase activity was detected in the three smooth muscle preparations studied (trachea, aorta, pulmonary artery) and found to be similar to that measured in lung slices. But the inhibitory effect of diphloretin phosphate and bromcresol green was much more marked in smooth muscle tissues than in lung slices, which suggested that PGA1 metabolism by the lung was not due to smooth muscle cells. Endothelial cells, freshly isolated and cultured, originating from the pulmonary artery and from the aorta, formed a PGA1-glutathione adduct, poorly extractable in ethyl acetate. This reaction, also present in cultured fibroblasts, was inhibited by ethacrynic acid. The cellular site responsible for the pulmonary degradation of circulating PGs remains undetermined.

Animals↗
PubMed1978

[Hemoptysis].

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Bronchoscopy↗
PubMed1978

[Endogenous factors in the development of emphysema].

The relationship between the development of pulmonary emphysema and the presence of proteolytic enzymes with elastolytic properties released by polymorphonuclear leukocytes or by alveolar macrophages is briefly reviewed. The possible role of various antiproteolytic substances present in the lung is also described. The pathogenesis of pulmonary emphysema is discussed in the light of hypotheses recently put forward implicating an excess of proteolytic factors and/or a relative or absolute lack of protection substances.

Chymotrypsin↗
PubMed1977

Amine uptake and metabolism by endothelium of pig pulmonary artery and aorta.

The uptake and metabolism of 5-hydroxytryptamine (5HT) and l-norepinephrine (NE) were measured in endothelial cells of pig pulmonary artery and aorta, as well as in lung slices. Evidence for oxidative deamination and for a saturable uptake mechanism, sensitive to cold, imipramine, and NA+-free medium was obtained for 5HT in lung slices and in the pulmonary as well as in the aortic endothelium, separated from the lumen by absorption to Millipore filters or by exposure to collagenase. For NE, however, a similar type of uptake could be deomonstrated in lung slices only. In the aortic and pulmonary endothelium, NE was metabolized, but its uptake was not influenced by imipramine, Na+-free medium, and high substrate concentration. The aortic and pulmonary endothelium have, therefore, similar properties and exhibit for 5HT, but not for NE, a type of uptake similar to that existing in lung capillaries.

Animals↗
PubMed1977

Converting enzyme activity in endothelial cells isolated from pig pulmonary artery and aorta.

Converting enzyme activity was studied in endothelial cells, isolated from pig pulmonary arteries and aorta by exposure to collagenase. The measure was based on the release of His-Leu from Z-Phe-His-Leu was related to the DNA content of the cellular suspension. The same activity was found in the two types of endothelium: 1 nmol His-Leu/mug DNA per 30 min. Subendothelial cells showed a very low activity, amounting to 10% of the value found for the endothelium. The enzyme activity was 2inhibited by the nonapeptide SQ 20881, EDTA, and the lack of Cl- in the same fashion for the two types of endothelium. The presence of another enzyme hydrolyzing His-Leu was detected in both endothelial populations. Isolated fragments of plasma membrane, however, exhibited only converting enzyme activity. It can be concluded that endothelial cells isolated from large vessels of the pulmonary and the systemic circulations have similar properties when dipeptidyl carboxypeptidase activity is measured.

Angiotensin II↗
PubMed1976

Concentration of (+/-)-propranolol in isolated, perfused lungs of rat.

1 The metabolism and the accumulation of (+/-)-propranolol have been studied in isolated lungs of the rat, perfused with an artificial medium. 2 Little or no metabolism took place during the perfusion periods (up to 10 minutes). 3 Accumulation was observed with high tissue/medium ratios for substrate concentrations of 0.2 muM to 1 mM; there was evidence for saturability, but no real plateau could be seen. The presence of two binding sites with different affinities was established. 4 Cold greatly inhibited the accumulation process at low substrate concentrations, but had no effect at 1 mM propranolol. 5 Inhibition of accumulation was measured in the presence of imipramine, desmethylimipramine, nortryptiline, chlorpromazine and of Na+-free medium. Cocaine, 5-hydroxytryptamine and noradrenaline had no effect. Lidocaine enhanced the accumulation process. Release of previously bound propranolol was accelerated in the presence of propranolol and imipramine, unaffected by a Na+-free medium and decreased by cold and by lidocaine. 6 Experiments on lung tissue slices yielded qualitatively similar results to those obtained with perfused lungs. Ouabain and KCN had no or little effect on propranolol accumulation.

Animals↗
PubMed1975

[The lung and the metabolism of vasoactive substances].

The lung is the site of a number of reactions affecting vasoactive substances: hydrolysis of angiotensin I, bradykinin and ATP, occurring at the surface of endothelial cell; uptake and intracellular metabolism of 5-hydroxytryptamine and norepinephrine; and intracellular oxidation of prostaglandins. Mediators, including prostaglandins, histamine and SRS-A (slow reacting substance of anaphylaxis), can also be released from the lung. The possible implications of these recent findings are analysed.

Adenosine Triphosphate↗