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Biomedical subjects

J P Herry

Publications and source records attributed to J P Herry.

11 recordsLinked to original sources
PubMed1995

[Cardiovascular effects of a calcium channel blocker in hypoxia caused by altitude].

OBJECTIVE: High altitude pulmonary oedema can be successfully treated and prevented by calcium channel blockers. Moreover, calcium entering in the cells could explain the congestive phenomena of acute mountain sickness (AMS). These findings led us to study the action of a calcium channel blocker, isradipine, in the prevention of non-complicated AMS. METHODS: In a double blind randomized study, 20 healthy volunteers received 5 mg of isradipine (n = 6) or placebo (n = 6) for 8 days. After 5 days of treatment in normoxia, the subjects were rapidly transported to an altitude of 4350 m. The efficiency of the treatment was then estimated by the AMS symptom score, haemodynamic parameters and renal function. RESULTS: The administration of isradipine did not significantly modify AMS symptom score nor most of other parameters measured in high altitude hypoxia. Heart rate was an average of 15 b/min lower in the isradipine group, probably because of a direct action of isradipine on the sinus node. Otherwise, the effects of hypoxia were similar in both groups and were in accordance with the literature. There was no clear explanation for the increase in cardiac output and stroke volume when the subjects moved from supine to standing position. Renal blood flow, measured by Doppler or para-aminohippuric acid clearance was not modified by hypoxia. Cerebral blood flow was elevated, due to the direct vasodilator effect of hypoxia. However this increase did not seem to be the main mechanism responsible for the congestive phenomena. On the other hand, the increase in capillary permeability (demonstrated by the increased transcapillary escape rate of albumin, and albuminuria) appeared to play a major role in the pathogenesis of AMS and high altitude cerebral oedema. Isradipine had no protective effect on these phenomena and its use should be restricted to the treatment of high altitude pulmonary oedema.

Adult↗
PubMed1993

Pressurization and acute mountain sickness.

Numerous cases of acute mountain sickness (AMS) during trekking were reported to have been successfully treated with portable pressure chambers. The effect of early pressurization during acute altitude exposure in the Alps had not been previously studied. In order to test the hypothesis that an early pressurization of unacclimatized subjects for 3 h could prevent or delay the appearance of symptoms of AMS, 51 previously healthy subjects climbed from 1,030 to 4,360 m within 12 h. Upon arrival at 4,360 m, AMS scores (Lake Louise Consensus Questionnaire '91), oxygen saturation (SaO2), and heart rate (HR) were determined at rest. The subjects were then randomly divided in two groups; one group was pressurized to 200 mBar for 3 h while the other rested. AMS score, HR, and SaO2 were similar in both groups before treatment. AMS score had decreased (from 2.44 +/- 0.41 (S.E.) to 0.89 +/- 0.26, p < 0.05) and SaO2 had increased (from 75.22 +/- 1.32% to 79.07 +/- 1.27%, p < 0.05) in the treatment group 15 min after leaving the pressure chamber whereas the control group had unchanged AMS score (2.50 +/- 0.40 vs. 2.40 +/- 0.40, N.S.) and SaO2 (77.83 +/- 1.41 vs. 76.67 +/- 1.24, N.S.). The next morning, however, AMS score, HR, and SaO2 were similar for both groups. It is concluded that during acute ascent in the Alps, an early 3-h pressurization of unacclimatized subjects does slightly delay the onset of AMS but does not prevent the illness nor does it attenuate its severity upon appearance.

Acute Disease↗
PubMed1992

Detection of high-risk subjects for high altitude diseases.

The variability in sensitivity to acute mountain sickness among individuals is a phenomenon well known to physicians and high altitude alpinists. The measurement of cardiac and respiratory responses to hypoxia (FIO2 = 0.115) at rest and during exercise (50% VO2max) allows the detection of those subjects who are more liable to suffer from high altitude diseases. In a retrospective study performed on 288 subjects evaluated with a hypoxic test during a Mountain medicine consultation, we found that the most clinically susceptible subjects had at least one abnormal response to the hypoxic tests, especially during exercise. The observation of one or several abnormal values in cardiac or respiratory responses to hypoxia leads us to advise a modification in the alpine or trekking objective, an increase in the acclimatization time and/or prevention by acetazolamide.

Altitude Sickness↗
PubMed1992

Myoelectrical and metabolic changes in muscle fatigue.

In isometric contraction-induced fatigue force loss has been related to mostly myoelectrical or intramuscular events. However, some factors potentially involved may interfere at more than one site in these events and it has proven difficult to distinguish between those influences. The study of the relationships between force generating capacity, the metabolic state of a muscle and its myoelectrical properties may therefore help broaden our understanding of the fatigue process. In order to investigate these relationships, we have evaluated changes in force-generating capacity, NMR-determined metabolic variables, and myoelectrical activity, as measured from surface EMG, simultaneously in brachial biceps muscle of healthy subjects, during different types of fatiguing isometric exercise and during recovery. Factors studied include intramuscular pH, inorganic phosphate and its diprotonated form concentrations, root-mean square and mean power frequency of the EMG power spectrum, and neuromuscular efficiency index. Results show that different mechanisms are likely to contribute to force loss in fatiguing muscle and during different phases of recovery from fatigue. Indeed, relationships between variables from the three groups differed according to exercise protocol as well as in fatiguing and recovering muscle.

Electromyography↗
PubMed1992

Use of a hypobaric chamber for pre-acclimatization before climbing Mount Everest.

Climbing Mount Everest needs an acclimatization period of 3 to 4 weeks between 3000 and 6000 m. In order to reduce this period of time spent in dangerous conditions, an experience of pre-acclimatization was performed with 5 elite alpinists (4 male, 1 female), aged 30 +/- 4 yrs (mean +/- SD), before their attempt to climb Mount Everest. Subjects first remained one week on Mont-Blanc (between 4350 and 4807 m), then spent a total of 38 hours in a hypobaric chamber (in 4 consecutive days) from 5000 to 8500 m standard altitude. Then, they flew to Kathmandu and reached 7800 m five days only after leaving the base camp. The pre-acclimatization period showed a 12% increase in hemoglobin concentration, and no change in ventilatory response to hypoxia. Arterial oxygen saturation at submaximal exercise in hypoxia (FIO2 = 0.115) increased from 75 +/- 4 to 82 +/- 3%, probably because of an efficient ventilatory acclimatization. On Mount Everest, the speed of ascent was very high (5600 m of altitude gain in 6 days), knowing that in conventional expeditions, 12 to 32 days are generally necessary to reach, safe, the same altitude. In conclusion, pre-acclimatization seems to have triggered efficient mechanisms which allowed climbers to save 1 to 3 weeks of time in mountain conditions.

Acclimatization↗
PubMed1992

Energy expenditure climbing Mt. Everest.

Weight loss is a well-known phenomenon at high altitude. It is not clear whether the negative energy balance is due to anorexia only or an increased energy expenditure as well. The objective of this study was to gain insight into this matter by measuring simultaneously energy intake, energy expenditure, and body composition during an expedition to Mt. Everest. Subjects were two women and three men between 31 and 42 yr of age. Two subjects were observed during preparation at high altitude, including a 4-day stay in the Alps (4,260 m), and subsequently during four daytime stays in a hypobaric chamber (5,600-7,000 m). Observations at high altitude on Mt. Everest covered a 7- to 10-day interval just before the summit was reached in three subjects and included the summit (8,872 m) in a fourth. Energy intake (EI) was measured with a dietary record, average daily metabolic rate (ADMR) with doubly labeled water, and resting metabolic rate (RMR) with respiratory gas analysis. Body composition was measured before and after the interval from body mass, skinfold thickness, and total body water. Subjects were in negative energy balance (-5.7 +/- 1.9 MJ/day) in both situations, during the preparation in the Alps and on Mt. Everest. The loss of fat mass over the observation intervals was 1.4 +/- 0.7 kg, on average two-thirds of the weight loss (2.2 +/- 1.5 kg), and was significantly correlated with the energy deficit (r = 0.84, P < 0.05). EI on Mt. Everest was 9-13% lower than during the preparation in the Alps.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Acute hypoxia decreases cardiac response to catecholamines in exercising humans.

Cardiac chronotropic response to adrenergic activity at rest and exercise has been studied in 8 sea-level natives on the first two days of exposure to high altitude hypoxia (3823 m, 473 mmHg). Maximal O2 uptake (VO2max) was determined at low altitude (day 0:D0) and high altitude (day 2:D2). Submaximal exercise tests were performed at low altitude (day 1:D1) and high altitude (days 3 and 4: D3, D4). Plasma venous norepinephrine (NE) and epinephrine (E) concentrations were determined at rest and at the end of submaximal exercise. From D0 to D2, maximal heart rate decreased by 7% (p less than 0.01), and VO2max decreased by 17% (p less than 0.01). During submaximal exercise, plasma NE did not vary significantly (D1: 1.36 +/- 0.57, D3: 1.48 +/- 0.51, D4: 1.31 +/- 0.54 ng.ml-1). In contrast, relative work load decreased at high altitude (% VO2max at D1, D3 and D4 were respectively: 90.2 +/- 6.1, 83.3 +/- 9.8, 76.9 +/- 8.2). Linear relationships were found, both at low and high altitudes, between NE and VO2, NE and % VO2max, and between the increases in NE and heart rate during exercise. Covariance analysis indicates that these relations shifted to the left at high altitude:for the same NE or increase in NE, VO2 or increase in heart rate was lower at high altitude. Variations in E were similar but not significant. We conclude that hypoxia induced a decrease in cardiac chronotropic response to adrenergic activation during submaximal exercise.

Adult↗