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M Potiron

Publications and source records attributed to M Potiron.

8 recordsLinked to original sources
PubMed2004

Brain magnetic resonance imaging, aerobic power, and metabolic parameters among 30 asymptomatic scuba divers.

The aim of the study was to evaluate the presence of cerebral lesions in asymptomatic scuba divers and explain the causes of them: potential risk factors associating cardiovascular risk factors, low aerobic capacity, or characteristics of diving (maximum depth, ascent rate). Experienced scuba divers, over 40 years of age, without any decompression sickness (DCS) history were included. We studied 30 scuba divers (instructors) without any clinical symptoms. For all of them, we carried out a clinical examination with fatty body mass determination and we questioned them about their diving habits. A brain Magnetic Resonance imaging (MRI), an assessment of maximal oxygen uptake, glycemia, triglyceridemia, and cholesterolemia were systematically carried out. Cerebral spots of high intensity were found at 33 % in the scuba diving group and 30 % in the control group. In the diving group, abnormalities were related to unsafe scuba-diving or metabolic abnormalities. In our study, we did not find a significant relationship between the lesions of the central nervous system, and the age, depth of the dives, number of dives, and ergometric performances (maximal oxygen uptake, V.O (2max), serum level of blood lactate). Nevertheless, we found a significant relationship between the lesions of the central nervous system and ascent rate faster than 10 meters per minute (r = 0.57; p = 0.003) or presence of high level of cholesterolemia (r = 0.6; p = 0.001). We found concordant results using the Cochran's Test: meaningful link between the number of brain lesions and the speed of decompression (Uexp = 14 < Utable = 43; alpha = 0.05, p < 0.01). We concluded that hyperintensities can be explained by preformed nitrogen gas microbubbles and particularly in presence of cholesterol, when the ascent rate is up to 10 meters per minute. So, it was remarkable to note that asymptomatic patients practicing scuba diving either professionally or recreationally, presented lesions of the central nervous system. This survey permitted us to highlight in a population of professional divers, neurological and also cardiovascular abnormalities (ventricular arrhythmias); although none of them present any symptoms today. It seems therefore important to us to propose in the future, for a better prevention of neurological injuries, a systematic follow-up by maximal oxygen consumption measure, brain MRI, and cholesterolemia. In the same way, our results suggest a modification of the diving tables with a maximal decompression rate at 9 m . mn (-1).

Brain↗
PubMed1999

[Asthma and diving with a cylinder].

Undersea diving is an activity that is practised more and more in holiday clubs. There is no precise legislation on the causes of unfitness of the amateur, in contrast to the professional diver, where the medical criteria are strict and controlled. When diving with a cylinder, on descent, the ventilatory load increases with increase of the ambient pressure and dynamic resistance in the airways increases. "As with an insufficient respiration on the surface, a healthy subject when diving has a ventilatory ability that is drastically reduced". Moreover with cylinder ventilation, the diver has available a reserve of gas under pressure from which he inspires with the aid of a breathing apparatus (regulator): he breathes dry gas that is dried before compression in the reservoirs, chilled by the relief valve on leaving the reservoir. This inhalation of cold, dry air associated with a hyperventilation during the descent produces ideal conditions to trigger exercise induced asthma. All subjects who present a bronchial hyperreactivity have the risk when diving with a cylinder of triggering a bronchospasm that is identical with that of a sporting asthmatic. During surfacing: the re-surfacing diver runs the risk of an accident of pulmonary suppression if he does not expire sufficiently during his return to the surface: the mass of intrapulmonary air of the resurfacer dilates and the excess of volume is exhaled by the diver: a volume of air of 5 l at 10 m depth corresponds to a volume of 10 l on the surface. Therefore the airways must remain free: an obstruction of the peripheral airways associated with an urgent re-surfacing produces a very rapid thoracic dilation which is responsible for pulmonary barotrauma (pulmonary barotrauma is frequently lethal with 30% of accidental deaths).

Asthma↗
PubMed1994

[Hypertrophic cardiomyopathy caused by cytochrome-oxidase deficiency].

Mitochondrial cytopathies are due to genetic anomalies in the oxidative phosphorylation enzymes (excepting Krebs cycle, pyruvate and certain other mitochondrial enzymes). Recently discovered, these diseases have a characteristic heterogeneous clinical expression because of the ubiquitous nature of this intracellular organelle. We observed a case in a 16-year-old girl who had cytochrome C oxidase deficiency. The child was born to non-consanguinous parents and had a healthy brother. The first manifestation of the disease was a systolic murmur heard at the age of 4 years. Progressively, exertion dyspnoea, lipothymia with cyanose led to the first echocardiography at 8 years revealing non-obstructive cardiomyopathy. Functional inadaptation of cardiac performance worsened requiring various symptomatic treatments. At the age of 16, the symptomatology included lower limb fatigue and the diagnosis of a metabolic disease was entertained. Phosphorylase A and B activity and phosphokinase activity were normal. High lactic acid levels after exertion suggested a mitochondrial enzyme deficiency. The diagnosis of cytochrome C oxidase deficiency was confirmed by spectrophotometric and polarographic assay of mitochondria from a peripheral muscle biopsy. Treatment with riboflavin, ascorbic acid, factor P, menadione, carnitine and iron sulfate has currently provided some symptomatic improvement. In patients with unexplained cardiomyopathy, the diagnosis of mitochondrial cytopathy should be entertained if oxidoreduction potentials (lactate/pyruvate ratio) are perturbed. The diagnosis is confirmed by enzyme studies of fresh muscle mitochondria. Currently therapeutic prospects are at best very poor. Genetic counselling may be advisable.

Adolescent↗
PubMed1993

Effect of a protein-sparing diet on responses to exercise in obese subjects.

We have studied muscular work efficiency and VO2 peak in seven obese individuals (body mass index: 38.9 +/- 5.8 kg.m-2) before and after twelve days of a low-caloric diet (protein-sparing modified fast) providing about 2460 kJ/day. Respiratory gas exchanges were measured at rest and during an exercise protocol through a rubber mask connected to a pneumotachograph and a mass spectrometer. A significant reduction in body mass was observed with the diet therapy (109 +/- 12 vs 105 +/- 14 kg; p < 0.02). No significant differences were observed in VO2 peak (1.78 +/- 0.32 vs 1.88 +/- 0.43 l/min, p > 0.05) and work efficiency (26 +/- 5 vs 24 +/- 4%, p > 0.05), after the diet protocol. It is concluded that the low-caloric diet used had no effect on muscular work efficiency.

Adolescent↗
PubMed1992

[Prognostic value after 1 year of post-infarction exercise test with measurement of oxygen consumption].

A symptoms-limited exercise stress test with measurement of myocardial oxygen consumption (VO2) was carried out in 56 patients on the 44th +/- 16 days after infarction and in 48 patients on the 119th +/- 31 days. Analysis of the expired gases was performed by mass spectrography, cycle by cycle. The second test was coupled with an exercise gamma-angiography in 40 cases. The parameters on exercise were analysed in two groups at one year: group 1 asymptomatic and group 2 symptomatic (subgroup 2a with angina but no dyspnoea, subgroup 2b with dyspnoea). At the second test, the peak VO2 was lower in group 2 (19.46 +/- 5.78 ml/mn/kg) than in group 1 (24.2 +/- 6.5 ml/mn/kg) (p less than 0.008) irrespective of the symptom (angina and/or dyspnoea). The oxygen pulse was lower in group 2a with angina at one year (42.4% +/- 14.3%) compared with asymptomatic group 1 patient (58.5 +/- 12.4%) (p = 0.03). The 3 parameters: VO2, blood pressure and ejection fraction on exercise were independent. The lack of physical fitness may partially explain the absence of variation of the peak VO2 at the first test. These preliminary results should be confirmed by a multivariate analysis in a larger patient group.

Aged↗
PubMed1987

[Medical treatment of hypertrophic myocardiopathy. Comparison of propranolol and verapamil].

It remains difficult to make a reasoned choice between betablockers and calcium antagonists in the medical treatment of hypertrophic cardiomyopathy. In order to help in making this choice, we compared the effects of 320 mg of propranolol and 480 mg of verapamil, prescribed in a random order for an average period of 2.5 months in 24 patients. In 15 patients the two therapeutic sequences were preceded and followed by a clinical examination and an exercise stress test after withdrawal of all treatment. The overall functional status correlated to oxygen consumption was unchanged by the two drugs, but patients felt better more often with verapamil. These was no significant change in maximal power developed during exercise testing although verapamil increased it by 9 p. 100 throughout with a corresponding increase in oxygen consumption. Two parameters were significantly changed by both drugs: the maximal heart rate fell from 161 +/- 22 to 122 +/- 18 with propranolol, and to 145 +/- 28 with verapamil; the oxygen pulse (equivalent to the systolic index) increased from 10.9 +/- 2.2 to 14.8 +/- 3.9 with propranolol, and to 13.7 +/- 2.4 with verapamil. There were no changes in the blood pressure profiles during exercise. Side effects were observed with both drugs; muscular weakness was the biggest problem with propranolol and sinus node dysfunction with verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1980

[Exercise testing in probable primary hypokinetic cardiomyopathies].

50 patients with primary congestive cardiomyopathy underwent one or several exercise tests at yearly intervals in order to evaluate exercise capacity and to assess the prognosis. Three parameters were studied: the workload, the elevation of the systolic blood pressure (SBP) on exercise and the appearance of premature ventricular beats (PVB) on exercise or during the recovery phase. The results show that when the work loads > 120 watts, an elevation of SBP greater than or equal to 50 mmHg and the appearance of less than 3 PVB per minute were compatible with a moderate degree of physical exertion. On the other hand these same poor prognostic factors were associated with a higher mortality rate after 20 months follow-up.

Adult↗