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C Rathat

Publications and source records attributed to C Rathat.

At least 19 recordsLinked to original sources
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↗
PubMed1991

Plasma prostaglandins, leukotrienes and thromboxane in acute high altitude hypoxia.

To explore the hypothesis that acute exposure to altitude hypoxia and acute mountain sickness (AMS) are associated with the release of vasoactive eicosanoids, 10 adult subjects were studied at sea-level and after 1-8 days (H1-H8) of exposure to an altitude of 4350 m (Observatoire Vallot). Plasma concentrations of 6 eicosanoids were determined in peripheral venous blood samples by radioimmunoassay after extraction with cooled ethanol and chromatographic separation by HPLC. All subjects experienced symptoms of AMS. Maximal clinical scores were observed at H1 or H2. Symptoms were no longer noted at H8. Hypoxia induced a very large increase in plasma concentration of most eicosanoids; thromboxane B2 (TxB2) and leukotriene B4 (LTB4) were maximum at H1 and H2 (about 5 times the normoxic value); prostaglandins PGE2, 6-keto-PGF1 alpha and PGF2 alpha were maximum at H3 or H4 (about 2.5-5 times of normoxic value). All eicosanoids returned almost to normoxic values by H8. Vasoconstricting mediators were released mostly at the initial phase (H1, H2), vasodilating mediators becoming predominant thereafter (H3, H4). The time pattern of appearance in blood of mediators acting on vascular permeability was strikingly parallel to the clinical score of AMS. In conclusion, exposure to acute hypoxia induced a large increase in plasma concentration of eicosanoids, the variation with time of which is compatible with a hydrostatic-permeability hypothesis of AMS pathophysiology.

Adult↗
PubMed1991

Optimal dose of lignocaine for preventing pain on injection of propofol.

The purpose of this study was to define the optimum dose of lignocaine required to reduce pain on injection of propofol. We conducted a prospective, randomized, double-blind trial on 310 patients undergoing anaesthesia. Patients were allocated to four groups according to the lignocaine dosage: group A (control), no lignocaine; group B, lignocaine 0.1 mg kg-1; group C, lignocaine 0.2 mg kg-1; group D, lignocaine 0.4 mg kg-1. Our results showed that a dose of lignocaine 0.1 mg kg-1 significantly reduced the incidence of pain and that there was no improvement when the dose was increased.

Adolescent↗
PubMed1990

MIBG scintigraphic assessment of cardiac adrenergic activity in response to altitude hypoxia.

High altitude hypoxia induces a decrease in the cardiac chronotropic function at maximal exercise or in response to isoproterenol infusion, suggesting an alteration in the cardiac sympathetic activation. Iodine-123 metaiodobenzylguanidine [( 123I]MIBG) was used to map scintigraphically the cardiac sympathetic neuronal function in six male subjects (aged 32 +/- 7 yr) after an exposure to high altitude that created hypoxic conditions. Results obtained just after return to sea level (RSL) were compared with the normal values obtained after 2 or 3 mo of normoxia (N). A static image was created as the sum of the 16-EKG gated images recorded for 10 min in the anterior view of the chest at 20, 60, 120, and 240 min after injection. Regions of interest were located over the heart (H), lungs (L), and mediastinum (M) regions. There was a significant decrease in the H/M and the L/M ratios in RSL compared to N condition. Plasma norepinephrine concentration was elevated during the stay at altitude but not significantly different in RSL compared to N. In conclusion, cardiac [123I]MIBG uptake is reduced after an exposure to altitude hypoxia, supporting the hypothesis of an hypoxia-induced reduction of adrenergic neurotransmitter reserve in the myocardium. Furthermore, the observed significant decrease in pulmonary MIBG uptake suggests an alteration of endothelial cell function after exposure to chronic hypoxia.

3-Iodobenzylguanidine↗
PubMed1989

Reversal of hypoxia-induced decrease in human cardiac response to isoproterenol infusion.

A decrease in heart rate response to isoproterenol (IP) infusion has been previously described in humans exposed to acute (2-3 days) or chronic (21 days) exposure to altitude hypoxia (J. Appl. Physiol. 65: 1957-1961, 1988). To evaluate this cardiac response in subacute (8 days) hypoxia and to explore its reversal with restoration of normoxia, six subjects received an IP infusion under normoxia (condition N), after 8 days in altitude (4,350 m, condition H8), on the same day in altitude after inhalation of O2 restoring normoxic arterial O2 saturation (SaO2, condition HO), and 6-11 h (condition RN) and 4-5 mo (condition ND) after the return to sea level. Cardiac chronotropic response to IP, evaluated by the mean increase in heart rate from base value (delta HR, min-1), was lower in condition H8 [mean 30 +/- 13 (SD)] than in condition N (50 +/- 14, P less than 0.03); it was slightly higher in condition HO (38 +/- 14) or condition RN (42 +/- 15) than condition H8 but still significantly different from condition N (P less than 0.03), despite normal values of SaO2. delta HR in condition ND (55 +/- 10) returned to base N value. These findings confirm the hypothesis of a hypoxia-induced decrease in cardiac chronotropic function. Two possible mechanisms are suggested: an O2-dependent one, rapidly reversible with recent restoration of normoxia, and a more slowly reversible mechanism, probably a downregulation of the cardiac beta-receptors.

Adult↗
PubMed1989

[Cardiac response to hypoxia and susceptibility to mountain sickness].

Exercising in high altitude is impeded during the first days of exposure to altitude hypoxia by the symptoms of Acute Mountain Sickness (AMS). Susceptibility to AMS is independent of endurance training and determined by the sensitivity of carotid chemoreceptors to hypoxemia and induced hyperventilation and tachycardia. Cardiac response to hypoxia is not as well known as ventilatory response, especially at exercise. A group of 138 male alpinists has been explored before their departure to a high altitude expedition using an hypoxic gas mixture (equivalent altitude = 4.800 m), at rest and at exercise (5 minutes at 50 p. 100 maximal O2 consumption). Cardiac response to hypoxia was assessed by the ratio DFc/DSaO2: variation in heart rate (hypoxia - normoxia)/variation in arterial O2 saturation, at rest (r) and during exercise (e). After the expedition, subjects were classified in AMS+ or AMS- group if they suffered or not from severe AMS, and also following their climbing skill. Cardiac response to hypoxia at rest is lower in AMS+ subjects (DFc/DSaO2 = - 0.86 +/- 0.40 nn - 1.% - 1) than in AMS- subjects (-1.12 +/- 0.69, p less than 0.05), but is not linked to the climbing skill. Similar differences were observed at exercise: DFc/DSaO2e = - 0.88 +/- 0.32 (AMS+) and - 1.05 +/- 0.50 (AMS-) (p less than 0.05). Associated with the respiratory response to hypoxia, the cardiac response allows the detection of AMS high-risk subjects and may be used in an much less than aptitude to altitude much greater than test.

Adolescent↗
PubMed1989

Diurnal variations of acute mountain sickness, colour vision, and plasma cortisol and ACTH at high altitude.

Time dependence of colour vision in the green/red axis, signs of acute mountain sickness (AMS), and plasma cortisol and ACTH concentrations were studied in eight sea-level male natives exposed 79 h to altitude hypoxia at 4,350 m. Colour vision (CV) was explored every 2 h from 08:00 to 20:00 hours by means of two portable anomaloscopes, one derived from Essilor CHROMOTEST and the other from the OSCAR. Significant diurnal variations in CV were found using both anomaloscopes, major alterations in green relative to red sensitivity being seen in the early morning. AMS scores also showed remarkable diurnal variations, parallel to those of plasma cortisol and CV, with maximum values observed at 08:00 hours. Cortisol diurnal rhythm was maintained in hypoxia, with mean concentrations higher than in normoxia. ACTH followed the same trend, but variations were not significant. Significant correlations were found between instant values of CV, cortisol, and AMS score, but no causal relationship between these variables can be ascertained.

Adrenocorticotropic Hormone↗
PubMed1988

Changes in plasma lipids and lipoprotein cholesterol during a high altitude mountaineering expedition (4800 m).

Effects of high altitude exposure on plasma lipids and lipoprotein cholesterol were studied in 8 mountaineers who spent 3 weeks at the Annapurna IV base camp (4800 m) after a 12 day trek. In spite of the moderate physical exertion at the camp, the loss of body weight was more pronounced during the stay at high altitude than during the trekking period. Compared with baseline values observed at sea level, marked reductions in plasma cholesterol (-27%) and phospholipids (-19%) were found 3 days after arrival at the camp and persisted during the next 17 days. A less marked fall in plasma triglycerides occurred, weakly significant at the end of the stay. Because there were no relevant changes in very low density lipoproteins or in high density lipoprotein (HDL)-cholesterol, the low plasma cholesterol levels at the high altitude resulted mainly from the reduction in low density lipoprotein (LDL)-cholesterol: the mean HDL/LDL cholesterol ratio changed from 0.39 at sea level to 0.63 at the end of the stay at 4800 m. Fluctuations in LDL-cholesterol were not concomitant with those in body weight and were independent of the exercise training during the expedition. This study shows moreover that the early drop in LDL-cholesterol was associated with an opposite change in plasma levels of catecholamines and thyroid hormones. Taking into account that such hormonal responses are classically observed at high altitude, the concomitant decrease in LDL-cholesterol might be interpreted as being a relevant adaptative response to hypoxic conditions at high altitude.

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↗
PubMed1988

Decreased cardiac response to isoproterenol infusion in acute and chronic hypoxia.

The hypothesis of a blunted chronotropic response of cardiac beta-adrenergic receptors in altitude hypoxia was tested in nine subjects at sea level (SL) by infusion of isoproterenol. Observations were made at SL, in acute hypoxia (2 days at 4,350 m, condition H1), in more prolonged hypoxia [13 days between 850 and 4,800 m, condition H2] and in chronic hypoxia [21 days at 4,800 m, condition H3]. Resting heart rate was higher in all hypoxic conditions. Resting norepinephrine concentrations were found to be significantly higher in conditions H2 (1.64 +/- 0.59) and H3 (1.74 +/- 0.76) than at SL (0.77 +/- 0.18 ng/ml). Isoproterenol, diluted in saline, was infused at increasing doses of 0.0, 0.02, 0.04, and 0.06 micrograms.kg-1.min-1. For the highest dose, there was a significantly smaller increase in heart rate in conditions H1 (35 +/- 9), H2 (33 +/- 11), and H3 (31 +/- 11) than at SL (45 +/- 8 min-1). The increase in pulse (systolic/diastolic) pressure, considered as the vascular response to isoproterenol infusion, was smaller in condition H3 (29 +/- 16) than at SL (51 +/- 24 mmHg). There was a significant increase in the dose of isoproterenol required to increase heart rate by 25 min-1 and decrease in slope of heart rate increase vs. log(dose) relationship in conditions H2 and H3. Thus an hypoxia-related attenuated response of beta-adrenergic receptors to exogenous stimulation was found in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1985

[Computerized report of anesthesia in real time].

The computerized report of anesthesia (C.R.A.) is an equivalent of the document filled out by the anesthesiologist, linked to a multicriteria research program giving the opportunity to study connections between different performances of anesthesia. To obtain these results, the authors are introducing a microcomputerized system in real time, including a microcomputer (capacity 64 kO), a visual display monitor (80 column format), two floppy disks controllers and a printer. Through a "menu", there is an access to the following functions: identity, patient story, drug prescriptions, anesthetics used, chronology of administration, monitoring of parameters, incidents/accidents, multicriteria research, editing of the C.R.A. The operational realisation shows that this computerized system offers storage capacity and allows a retrospective analysis of anesthesia. As it is inexpensive and easy to use, it may become a very important device in every-day practice.

Anesthesia, General↗