Biomedical subjects

Lionel Bourdon

Publications and source records attributed to Lionel Bourdon.

11 recordsLinked to original sources

PubMed2006

Haemodynamic changes induced by submaximal exercise before a dive and its consequences on bubble formation.

OBJECTIVES: To evaluate the effects of a submaximal exercise performed 2 h before a simulated dive on bubble formation and to observe the haemodynamic changes and their influence on bubble formation. PARTICIPANTS AND METHODS: 16 trained divers were compressed in a hyperbaric chamber to 400 kPa for 30 min and decompressed at a rate of 100 kPa/min with a 9 min stop at 130 kPa (French Navy MN90 procedure). Each diver performed two dives 3 days apart, one without exercise and one with exercise before the dive. All participants performed a 40 min constant-load submaximal and calibrated exercise, which consisted of outdoor running 2 h before the dive. Circulating bubbles were detected with a precordial Doppler at 30, 60 and 90 min after surfacing. Haemodynamic changes were evaluated with Doppler echocardiography. RESULTS: A single bout of strenuous exercise 2 h before a simulated dive significantly reduced circulating bubbles. Post-exercise hypotension (PEH) was observed after exercise with reductions in diastolic and mean blood pressure (DBP and MBP), but total peripheral resistance was unchanged. Stroke volume was reduced, whereas cardiac output was unchanged. Simulated diving caused a similar reduction in cardiac output independent of pre-dive exercise, suggesting that pre-dive exercise only changed DBP and MBP caused by reduced stroke volume. CONCLUSION: A single bout of strenuous exercise 2 h before a dive significantly reduced the number of bubbles in the right heart of divers and protected them from decompression sickness. Declining stroke volume and moderate dehydration induced by a pre-dive exercise might influence inert gas load and bubble formation.

Adult↗

PubMed2006

Cosignaling of adenosine and adenosine triphosphate in hypobaric hypoxia-induced hypothermia.

Purines, that is, adenosine and ATP, are not only products of metabolism but are also neurotransmitters. Indeed, purinergic neurotransmission is involved in thermoregulatory processes that occur during normoxia. Exposure to severe hypoxia elicits a sharp decrease in body core temperature (T(CO)), and adenosinergic mechanisms have been suspected to be responsible for this hypothermia. Because ATP per se and its metabolite adenosine could have complex interactions in some neural networks, we hypothesize that both adenosine and ATP are involved in the central mechanism of hypoxia-induced hypothermia. Their role in the thermoregulatory process was therefore investigated in a 24-h hypobaric hypoxia (Fi(O2) = 10%), using CGS-15943, a nonselective antagonist of adenosine receptors, and suramin, an ATP receptor antagonist. T(CO) and spontaneous activity (A(S)) were monitored by telemetry in conscious rats, receiving CGS-15943 (10 mg/kg ip), suramin (7 nmol icv), or both. The same treatments were done in normoxia to evaluate the specificity of their thermoregulatory action observed in hypoxia. Suramin/CGS-15943 treatment blunted the profound hypothermia observed in control rats throughout the hypoxia exposure, whereas CGS-15943 treatment blunted hypothermia during only 3 h, and suramin treatment had no effect. These results suggest that suramin potentiates the CGS-15943 effects and consequently that adenosine and ATP signaling act in synergy. In normoxia, suramin/CGS-15943 induced an increase in T(CO) but to a far lesser extent than observed in hypoxia. Thus it might be suggested that the suramin/CGS-15943 blunting of hypoxia-induced hypothermia would be specific to hypoxia-induced mechanisms.

Adenosine↗

PubMed2005

Clinical assessment of the entry into neurological state in rat experimental African trypanosomiasis.

Human African trypanosomiasis, caused by Trypanosoma brucei (T.b.) gambiense or rhodesiense, evolves in two stages: haemolymphatic stage and meningo-encephalitic stages, the latter featuring numerous neurological disorders. In experimental models infected with diverse T.b. sub-species, body weight (BW) loss, drop in food intake (FI), and hypo-activity after an asymptomatic period suggest the occurrence of a similar two-stage organization. In addition to daily measurement of BW and FI, body core temperature (T(co)) and spontaneous activity (SA) were recorded by telemetry in T.b. brucei-infected rats. After a 10--12-day symptom-free period, a complex clinical syndrome occurred suddenly. If the animal survived the access, the syndrome re-occurred at approximately 5-day intervals until death. The syndrome was made of a drop in FI and BW, a sharp decrease in T(co) and a loss of SA, suggesting a brisk alteration of the central nervous system functioning. Such events confirm the existence of a two-stage disease development in experimental trypanosomiasis. The entry into the second stage is marked by the occurrence of the first access, BW follow-up being essential and often sufficient its determination.

Animals↗

PubMed2005

Disruptions of ultradian and circadian organization of core temperature in a rat model of African trypanosomiasis using periodogram techniques on detrended data.

Periodogram techniques on detrended data were used to determine the incidence of Trypanosoma brucei brucei infection on the distribution of the core temperature of rats and the expression of temperature rhythms. In such an animal model, sudden episodic hypothermic bouts were described. These episodes of hypothermia are used here as temporal marks for the purpose of performing punctual comparisons on temperature organization. The experiment was conducted on 10 infected and 3 control Sprague-Dawley rats reared under a 24 h light-dark cycle. Core temperature was recorded continuously throughout the experiment, until the animals' death. Temperature distributions, analyzed longitudinally across the full duration of the experiment, exhibited a progressive shift from a bimodal to unimodal pattern, suggesting a weakening of the day/night core temperature differences. After hypothermic events, the robustness of the circadian rhythm substantially weakened, also affecting the ultradian components. The ultradian periods were reduced, suggesting fragmentation of temperature generation. Moreover, differences between daytime and nighttime ultradian patterns decreased during illness, confirming the weakening of the circadian component. The results of the experiments show that both core temperature distribution and temperature rhythm were disrupted during the infection. These disruptions worsened after each episode of hypothermia, suggesting an alteration of the temperature regulatory system.

Animals↗

PubMed2004

Effects of a tryptic hydrolysate from bovine milk alphaS1-casein on hemodynamic responses in healthy human volunteers facing successive mental and physical stress situations.

BACKGROUND: Preclinical results in rats have demonstrated anxiolytic-like effects of a tryptic bovine alphaS1-casein hydrolysate. AIM OF THE STUDY: We investigated the putative effects of this tryptic hydrolysate on systolic (SBP), diastolic (DBP) blood pressures, heart rate (HR) values and plasma cortisol concentrations (CC) in human healthy volunteers facing successive stress situations. METHODS: The subjects were (double blind) randomly allocated to ingest three times, 12 hours apart, two capsules containing either 200 mg of alphaS1-casein hydrolysate (TS) or bovine skimmed milk powder as a placebo (CS). On the morning of the test day, a first blood sample for baseline measurement of CC was taken before the subjects were submitted to the Stroop test (ST) and, after a 30-min rest, to a Cold Pressor test (CPT). SBP, DBP, and HR were continuously recorded for 5 min before the ST and during each stress situation. A second blood sample was taken 15 min after the end of the CPT condition. RESULTS: ST and ST + CPT combined test situations increased SBP, DBP and HR. The significant "Treatment x SBP" and "Treatment x DBP" interactions indicated the lower percentage changes in SBP and DBP of the TS. In addition, the results showed a significant decrease of the CC in the TS but not in the CS throughout the ST + CPT combined stress tests. HR remained stable in TS between the initial rest period and the CPT unlike what happened in CS. CONCLUSION: On the basis of blood pressure and cortisol changes, these results suggest an antistress profile of this alphaS1-casein hydrolysate in human subjects.

Analysis of Variance↗

PubMed2004

[Disorders caused by prolonged exposure to heat].

France has suffered last summer an unprecedented heat wave that led to an exceptional short-term surge of mortality. Cumulative deaths between August 1st to 14th are estimated at 14,800. Epidemiological studies carried out by the Institute de Veille Sanitaire will show the circumstances and risk factors leading to heat-related pathologies. A literature review already shows the principles of prevention, the circumstances of occurrences during similar past heat waves, the risk factors and the principles of treatment. Prolonged exposure to heat can be the initial cause of death, mainly in the elderly. The subject thus dies of an overload of his natural defenses, unable to preserve his thermal homeostasis. This is then a heat shock that reaches the central nervous system. Heat shocks could kill every second patient and leads to severe neurological sequel. During a heat wave, high temperatures can also trigger or worsen other illnesses or be responsible for other so called heat-related syndromes. It is crucially important to identify subjects at risk, situations of risk, and preventive measures, knowing that heat shock leads 25% of patients to develop multi-organ failure, even when appropriately treated.

Age Factors↗

PubMed2004

Twenty-four-hour disruption of the sleep-wake cycle and sleep-onset REM-like episodes in a rat model of African trypanosomiasis.

STUDY OBJECTIVES: Patients with human African trypanosomiasis (sleeping sickness) due to the inoculation of Trypanosoma brucei gambiense or rhodesiense show a major disruption of the 24-hour sleep-wake distribution, accompanied by the occurrence of sleep-onset rapid-eye-movement (REM) sleep episodes, proportional to the severity of the illness. Although animal models of human African trypanosomiasis have been developed to understand the pathogenic mechanisms leading to immune alterations, the development of an animal model featuring the alterations of endogenous biologic rhythms remains a necessity. ANIMALS: Sprague-Dawley rats (N = 10) entrained to a 12:12-hour dark-light regimen. INTERVENTIONS: Rats were infected with Trypanosoma brucei brucei AnTat 1.1E and instrumented with electrocorticographic and electromyographic electrodes. Polysomnography was recorded continuously from 2 days before infection until the animal's death. MEASUREMENTS AND RESULTS: The analysis of the spontaneous sleep-wake architecture revealed an increased proportion of slow-wave sleep (SWS) and a decreased amount of wakefulness 2 days before death. Considerable sleep fragmentation was observed in the infected rats, with numerous changes in sleep-wake stages and an increased number of episodes of wakefulness and SWS. Infected rats presented a fragmented pattern of SWS and a marked reduction in the mean paradoxical-sleep (PS) latency, resulting in a considerable disruption of the PS-SWS sequences. Abnormal transitions, particularly the appearance of sleep-onset REM episodes, marked the disruption of the internal sleep structure. The electrocorticogram traces were modified during SWS, with the occurrence of abnormal hypersynchronic slow waves and a disappearance of spindles. CONCLUSION: The Trypanosoma brucei brucei-infected rat is a good model of the syndrome seen in human African trypanosomiasis, ie, the 24-hour disruption of the sleep-wake cycle and the occurrence of sleep-onset REM-like sleep episodes.

Animals↗

PubMed2004

Megazol combined with suramin improves a new diagnosis index of the early meningo-encephalitic phase of experimental African trypanosomiasis.

In human African trypanosomiasis (HAT), the parasites invade the central nervous system (CNS), leading to the development of meningo-encephalitis and an irreversible demyelinating process, which kills the patient unless specific treatment is undertaken. Among the experimental trypanocides, the nitroimidazole derivative megazol alone at optimal doses does not cure late-stage disease tested in mouse models, however the combination of suramin and megazol is able to cure infected mice without CNS involvement. We recently developed an experimental model of HAT with a sharp decrease in both the food intake and the body weight which may constitute an effective index of the early meningo-encephalitic phase. Using this model, we tested this hypothesis by the exclusive effectiveness of a megazol and suramin combination treatment to eliminate CNS trypanosomes. Sprague-Dawley rats were infected with Trypanosoma brucei brucei AnTat 1.1E. Food intake and body weight were measured daily from the day of infection to death. Haematocrit was measured twice a week. Treatment consisted of 20 mg suramin per kg body weight administered intraperitoneally (i.p.) alone, or three daily doses (80 mg/kg) of megazol given per os, or suramin (20 mg/kg, i.p.) followed 24 h later by three daily doses (80 mg/kg) of megazol given per os. Treatment was followed by an increase in daily body weight and food intake similar to those of the control animals, 2 weeks after treatment. The anaemia developed after infection is also cleared as shown by the haematocrit measurements. The rats treated with megazol alone died about 29 days after treatment and those treated with suramin, after about 26 days. Seven months later, no signs of relapse were seen in 10 of 12 rats treated with the therapeutic combination, indicating that this chemotherapy regimen was curative. The results support our previous finding, i.e. the decrease in body weight may constitute a diagnosis index of the early meningo-encephalitic phase.

Anemia↗

PubMed2003

Behavioural changes after an acute stress: stressor and test types influences.

Behavioural consequences of different acute stressors (30 min of restraint, 20 min of forced swim stress, 15 min of inescapable footshocks) applied at the beginning of the active period were assessed in using two behavioural tests: a 20 min light extinction test 24 h after the stressor exposure in order to explore the psychomotor ability and a 10 min open field session within the dark period 48 h after the stressor exposure to estimate the emotional status and the locomotor activity of the rat. Different behavioural responses were observed depending on the nature of the applied stressor. In the light extinction test, the footshock-stressed rats developed a very low activity independent on light conditions whereas the rats submitted to forced swim and restraint exhibited an activity level depending on the strain. Moreover, restrained rats had a higher transient activity than forced swim rats under light condition. In the open field test, none of the stressed rats did develop differences in behaviour. The efficacy of a 24 h recovery period on the behavioural response to an acute stressor exposure depends on the intensity of the applied stressor and the behavioural demands.

Adaptation, Psychological↗

PubMed2003

Distinctive effects of modafinil and d-amphetamine on the homeostatic and circadian modulation of the human waking EEG.

RATIONALE: Modafinil is a wake-promoting agent that affects hypothalamic structures involved in the homeostatic and circadian regulation of vigilance. Administered during sleep deprivation, it reduces the need for prolonged recovery sleep and decreases the rebound in EEG slow-wave activity. These diachronic effects suggest an action of modafinil on a homeostatic sleep regulatory process. OBJECTIVES: The aim of this study was to determine whether modafinil, in comparison to the d-amphetamine reference psychostimulant and to placebo, interferes with the vigilance regulatory processes reflected in the EEG during waking. METHODS: Thirty-three healthy subjects were investigated during 60 h of sustained wakefulness in a double-blind placebo-controlled parallel-design study. A 4-min maintenance-of-wakefulness test administered hourly allowed the concomitant assessment of alertness and waking EEG activity. The effects of equipotent psychostimulant dosages (modafinil 300 mg and d-amphetamine 20 mg) were evaluated at the beginning of the first sleep deprivation night, at the end of the second sleep deprivation night and in the afternoon preceding the first recovery night. RESULTS: One hour following ingestion, both psychostimulants increased alertness during 10-12 h, independently of the time of administration. At the level of the waking EEG, d-amphetamine attenuated the natural circadian rhythm of the different frequency bands and suppressed the sleep deprivation-related increase in low frequency (0.5-7 Hz) powers. In contrast, modafinil, which exhibited a transient amphetamine-like effect, had slight effect on circadian rhythms. Its selective action was characterized by maintenance of the alpha(1) (8.5-11.5 Hz) EEG power, which under placebo exhibited a homeostatic decrease paralleling that of alertness with a circadian trough at night. CONCLUSIONS: These findings demonstrate that the alertness-promoting effects of modafinil and d-amphetamine involve distinct EEG activities and do not reside on the same vigilance regulatory processes. While d-amphetamine inhibits the expression of a sleep-related process, probably through a direct cortical activation masking EEG circadian rhythms, modafinil, through a synchronic effect, preferentially disrupts the homeostatic down-regulation of a waking drive.

Adolescent↗

PubMed2002

MK801 impairs thermoregulation in the heat.

The effects of MK801 (dizocilpine), a glutamate NMDA receptor antagonist, on thermoregulation in the heat were studied in awake rats exposed to 40 degrees C ambient temperature until their body core temperature reached 43 degrees C. Under these conditions, MK801-treated rats exhibited enhanced locomotor activity and a steady rise in body core temperature, which reduced the heat exposure duration required to reach 43 degrees C. Since MK801-treated rats also showed increased striatal dopaminergic metabolism at thermoneutrality, the role of dopamine in the MK801-induced impairment of thermoregulation in the heat was determined using co-treatment with SCH23390, a dopamine D1 receptor antagonist. SCH23390 normalized the locomotor activity in the heat without any effect on the heat exposure duration. These results suggest that the MK801-induced impairment of thermoregulation in the heat is related to neither a dopamine metabolism alteration nor a locomotor activity enhancement.

Animals↗