Biomedical subjects

X Combes

Publications and source records attributed to X Combes.

3 recordsLinked to original sources

PubMed2000

The effects of residual pain on oxygenation and breathing pattern during morphine analgesia.

UNLABELLED: To determine the influence of pain on opioid-induced respiratory depression, we studied oxygenation and breathing patterns in 40 patients scheduled for knee surgery during postoperative patient-controlled analgesia (PCA). After 1 h of morphine PCA, patients were randomized to receive either 20 mL of placebo or bupivacaine 0.25% through a crural nerve catheter and allowed to use PCA for one more hour. Abnormal breathing events were identified and characterized by using the Edentrace II device (Nellcor, Jouy-en-Josas, France). The Spo2 below which the patient spent 25% and 50% of a studied period was calculated (Spo2(25), Spo2(50)). Pain relief with regional analgesia increased the incidence of abnormal respiratory events associated with oxygen desaturation: during the second period, the pain score was lower in the bupivacaine group (0.7+/-1 vs 4.1+/-1.2), morphine consumption was larger in the placebo group (4.2+/-1.3 vs 0.7+/-1.4 mg), and there were more abnormal obstructive breathing events in the bupivacaine group (11+/-16 vs 3.7+/-4.3). Spo2(25) and Spo2(50) were lower in the bupivacaine than in placebo group (91.5%+/-2.8% vs 93.1%+/-2.1%, 92.9%+/-2.4% vs 94.2%+/-1.8%). IMPLICATIONS: Pain relief with regional analgesia in patients previously treated with opioids increases the incidence of abnormal respiratory events associated with oxygen desaturation.

Analgesia, Patient-Controlled↗

PubMed1999

Postoperative obstructive apnea.

UNLABELLED: We studied electromyography (EMG) of the geniohyoid muscle (Gh) and diaphragm (Di) in 12 postoperative, premedicated (flunitrazepam 2 mg PO), asymptomatic patients who snored after recovering from general anesthesia, the induction of which was partly achieved by i.v. midazolam. After extubation of the trachea, integrated EMG activity of Gh (E-Gh(MTA)) and Di (E-Di(MTA)) were measured. For Gh, tonic and phasic activity were distinguished. Patients were studied during obstructive apnea, at the end of apnea, while breathing through an artificial Guedel airway, and during quiet breathing 5 min after flumazemil. All patients experienced episodes of postoperative upper airway obstruction and nine became apneic. Flumazenil restored consciousness and predominant tonic E-GhMTA associated with upper airway patency in all patients. Reduced tonic E-GhMTA characterized postoperative obstructive apnea. Resolution of apnea required a burst of both tonic and phasic E-GhMTA associated with intense E-Di(MTA). Breathing through the Guedal airway resulted in patent airway in 8 of 10 patients and was associated with low tonic and phasic E-GhMTA and reduced E-Di(MTA). In this study, we demonstrated that the tonic pharyngeal muscular support modulates airway patency in the postoperative period. Because it is reversed by flumazemil, benzodiazepines are certainly the main cause of airway obstruction in these patients. IMPLICATIONS: Upper airway obstruction during recovery from general anesthesia induced by i.v. midazolam is associated with low tonic pharyngeal muscular support, which modulates upper airway patency in the postoperative period.

Adult↗

PubMed1997

Effect of 48 hours of nitric oxide inhalation on pulmonary vasoreactivity in rats.

Nitric oxide (NO) has been shown to down regulate its own synthesis in vitro. We tested the hypothesis that NO inhalation (30 ppm under normoxic conditions) could decrease the release of endogenous endothelial NO, and thus alter pulmonary vasoreactivity. Pulmonary vasoreactivity was assessed in isolated perfused rat lungs immediately or 6 h after a 48 h NO inhalation period, and compared with a control group. NO inhalation resulted in an increase in pulmonary vasoconstrictor reactivity to angiotensine II and U-46619, a reduction in the potentiation by the eNOS inhibitor L-NAME of the angiotensine II response, a decrease in endothelium-dependent vasodilation to arginine vasopressin, whereas non-endothelium-dependent vasodilation to sodium nitroprusside remained unaltered. These alterations returned to control values in the group studied 6 h after the end of NO inhalation, and were not prevented by inhibition of the prostanoid synthesis, or by pretreatment with the endothelin receptors antagonist Bosentan. These results indicate that NO inhalation over 2 d induces a reversible alteration of pulmonary vasoreactivity in relationship with a decrease in endogenous NO release. Inhibition of eNOS could be involved.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗