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Biomedical subjects

S Molliex

Publications and source records attributed to S Molliex.

8 recordsLinked to original sources
PubMed1995

[Effects of midazolam on respiratory drive in healthy volunteers].

OBJECTIVE: To compare the effects of a sedative dose of midazolam on mean inspiratory flow (VT/TI = index of central respiratory activity), known as being decreased by midazolam and the intercostal muscle activity, known as being increased by this agent. STUDY DESIGN: Laboratory study. PATIENTS: Seven healthy volunteers. METHODS: After assessment of baseline values of ventilatory variables and intercostal electromyographic activity (in arbitrary units), midazolam 0.1 mg.kg-1 was administered by iv route. The measurements were repeated after 5 and 10 min, and finally 2 min after the i.v. injection of flumazenil 1 mg. RESULTS: Midazolam decreased VE and VT. Similarly VT/TI ratio decreased from 0.44 +/- 0.04 (baseline value) to 0.26 +/- 0.03 (5 min) and 0.3 +/- 0.03 L.s-1 (10 min later) respectively (P < 0.05). Conversely, midazolam increased the intercostal electromyographic activity from 4.0 +/- 0.7 (baseline value) to 26.5 +/- 16.6 (5 min) and 28.4 +/- 16.6 U (10 min later) respectively (P < 0.05). Within 2 min after flumazenil administration all variables returned to baseline values. CONCLUSIONS: The decrease of VT/TI ratio is probably linked to increased resistances in the upper airways. This ratio cannot act as an indicator of respiratory drive during sedation or anaesthesia. The assessment of the ventilatory effects of benzodiazepines must be based simultaneously of the various other indicators of the ventilatory drive, as these agents act on the different stages of the ventilatory cycle and therefore cannot be characterized by a unique variable.

Adjuvants, Anesthesia↗
PubMed1994

Effects of halothane on surfactant biosynthesis by rat alveolar type II cells in primary culture.

BACKGROUND: Pulmonary surfactant, which is synthesized by alveolar type II cells (ATII cells) almost exclusively, plays a major role in maintaining alveolar homeostasis by reducing surface tension at the fluid-gas interface. Phosphatidylcholine (PC), the main surfactant lipid component, is largely responsible for this surface activity. The effects of halothane on the phospholipid metabolism of the pulmonary surfactant by ATII cells are unknown, even though these cells are exposed directly to volatile anesthetics during anesthesia and even though any alteration in surfactant biosynthesis by anesthetics may have deleterious effects on lung function and thereby facilitate postoperative pulmonary complications. In the current study, the effects of halothane exposure on surfactant synthesis by rat ATII cells in primary culture were investigated. METHODS: ATII cells were isolated from adult rat lungs and used for the experiments after 24 h in primary culture. The ability of ATII cells to synthesize surfactant was assessed by the incorporation of radioactive precursors in PC. Cytotoxicity was measured by the rate of lactate dehydrogenase release into the culture medium, and the lactate metabolism was taken as an index of glycolytic metabolism. All metabolic measurements were made after 24 h in primary culture. Effects of various halothane concentrations (1, 2, 4, and 8%) exposure for 4 h were studied, as were the effects of 2% halothane for various durations of exposure (2, 4, 8, and 12 h). The reversibility of halothane effects on PC synthesis was assessed after a 2% halothane exposure for 4 h. PC secretion and adenosine triphosphate cellular content were also measured for 4 h exposure at the various halothane concentrations. RESULTS: During a 4-h exposure, PC synthesis was reduced by 10, 24, 29 and 36% for 1, 2, 4, and 8% halothane respectively when compared with control values. At 2% halothane concentration, the observed decreases in PC synthesis were 12, 24, 31 and 34% for 2, 4, 8, and 12 h exposure, respectively. The inhibitory effect of halothane was completely reversed 2 h after the end of exposure. PC secretion was unaffected by increasing halothane concentrations during a 4-h exposure. Halothane did not produce cell damage except for the longest exposure durations (8 and 12 h) at 2% vapor concentration. Whatever the exposure conditions, lactate production by ATII cells exposed to halothane was greater than production by unexposed cells. CONCLUSIONS: These results indicate that halothane decreases the biosynthesis of pulmonary surfactant by ATII cells in primary culture and alters the high energy phosphate metabolism of these cells.

Adenosine Triphosphate↗
PubMed1994

Effects of intravenous midazolam on the work of breathing.

Midazolam at sedative doses induces an increase in upper airway resistance, but its effects on the work of breathing have not been established. The flow-resistive work of breathing and pulmonary resistance (RL) of eight healthy volunteers were measured, with either midazolam 0.1 mg/kg or placebo in a random order. Esophageal pressures were measured using a balloon-tipped catheter, airflow using a pneumotachograph. Total resistive work expressed per minute (WTOT) and per liter of ventilation (WTOT/VE), and their inspiratory (WI) and expiratory (WE) components were determined. No change was observed after placebo injection. Five minutes after midazolam injection, an increase was observed in WTOT (from 3 +/- 0.4 J/min [mean +/- SEM] at control to 6.3 +/- 1.1 J/min; P < 0.01) and in WTOT/VE (from 360 +/- 30 mJ/L at control to 1250 +/- 120 mJ/L; P < 0.01), involving both WI and WE components. An increased inspiratory RL was observed from 13.7 +/- 2.6 cm H2O.L-1.s-1 at control to 32.8 +/- 3.9 cm H2O.L-1.s-1 after midazolam. Changes in inspiratory RL were correlated to changes in WI and WI/VE (r = 0.574, P < 0.001; and r = 0.762, P < 0.001, respectively). Our results suggest that airway obstruction plays a major role in the increased work of breathing observed during sedation with midazolam.

Adult↗
PubMed1993

[Neurotoxic role of glycocolle and derivatives in transurethral resection of the prostate].

72-year-old patient underwent an elective transurethral resection of the prostate (TURP) performed with a spinal anaesthesia. The irrigation solution contained glycine at a concentration of 15 g.l-1. The patient's level of consciousness deteriorated over the next 4 hours. He went in an areflexic coma with pupillary areflexia and left mydriasis. The diagnosis of TUR syndrome was substantiated by a sodium blood concentration of 98 mmol.l-1, an osmotic gap of 48 mosmol.kg-1 and blood ammonia at 415 mumol.l-1. To investigate the pathophysiological role of glycine and its metabolites, their concentrations were measured by chromatography and spectrometry in plasma and CSF 8, 24 and 48 hours postoperatively. Glycine and its metabolites (serine, alanine, glyoxylic acid and glycolic acid) accumulated during the postoperative period in both blood and CSF. The central nervous system is in direct contact with these neurotropic compounds. Glycine is an inhibitory neurotransmitter, whereas glyoxylic acid and glycolic acid are considered as to be neurotoxic.

Aged↗
PubMed1993

Effects of midazolam on respiratory muscles in humans.

Midazolam at sedative doses alters the breathing pattern; however, its effects on respiratory load and respiratory muscle activity have not been established completely. Therefore, the effects of midazolam (0.1 mg/kg) on total pulmonary resistances and on diaphragmatic, intercostal, and abdominal muscle patterns were studied in nine volunteers. Measurements were performed during control, 5 and 10 min after midazolam, and then 2 min after 1.0 mg of intravenous flumazenil. After midazolam, total pulmonary resistance increased from 6.3 +/- 0.65 to 36.6 +/- 8.1 cm H2O-L-1 x s-1 (P < 0.01), a pattern associated with an increased intercostal electromyographic activity (peak and slope; P < 0.05). By contrast, the ratio of gastric pressure on esophageal pressure changes decreased from 65.5% +/- 6.2% to 16.3% +/- 3.9% (P < 0.01), indicating reduced diaphragmatic activity. In 7/9 subjects, there was expiratory abdominal muscle activity. Flumazenil reversed all these effects. We conclude that midazolam 0.1 mg/kg increases total pulmonary resistance and elicits a compensatory load response characterized by an increase in inspiratory intercostal and expiratory abdominal muscle activities whereas diaphragmatic contribution is reduced.

Abdominal Muscles↗