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Biomedical subjects

E Troncy

Publications and source records attributed to E Troncy.

17 recordsLinked to original sources
PubMed2001

Brown bear (Ursus arctos arctos) femoral head and neck excision.

A 30-yr-old untamed European female brown bear (Ursus arctos arctos) with a craniodorsal luxation of the right femoral head and bilateral degenerative joint disease of the coxofemoral joint had a femoral head and neck excision following unsatisfactory conservative medical therapy. The bear was injected with zolazepam-tiletamine, and anesthesia was induced with i.v. thiopental and maintained with isoflurane in oxygen via endotracheal tube. A lumbosacral epidural injection of medetomidine-bupivacaine provided additional analgesia. Slight initial cardiorespiratory depression was counteracted with fluid and inotropic drug administration and ventilatory assistance. The bear's gluteal muscle anatomy differs from that of the dog. Recovery was uneventful. The bear was confined indoors for 6 wk and was able to ambulate normally within 6 mo.

Anesthetics, Combined↗
PubMed1998

Inhaled nitric oxide: technical aspects of administration and monitoring.

OBJECTIVES: Clinical applications of inhaled nitric oxide (NO) therapy resulted in the development of delivery systems and monitoring devices applicable to routine clinical care. This article presents the various components necessary for an adequate clinical use of inhaled NO, and discusses the NO gas mixture cylinders, inhaled NO delivery techniques and specifications, monitoring devices, and ending with an exhaustive description of the scavengers of nitrogen oxides (NOx). DATA SOURCES: Computerized search (CURRENT CONTENTS, MEDLINE) of published original research and review articles (approximately 200), conference abstracts and compendiums up to May 1997 (approximately 50), personal files, and contact with expert informants. STUDY SELECTION: Technical, experimental, and clinical reports were selected from the recent English, French, German, and Spanish literature, if pertinent to the administration or monitoring of inhaled NO. DATA EXTRACTION: The authors extracted all applicable data. DATA SYNTHESIS: The production of NO gas mixture cylinders must be certified with respect to gas purity, stability, and concentration (limits between 100 and 1000 ppm), guaranteed calibration, and specific color. An ideal inhaled NO delivery device requires a synchronized delivery, a minimal production of nitrogen dioxide (NO2), and should be simple to use (verification, calibration, convenient flushing, cylinder change possible while in use and a simple alarm setting) with full information (high and low alarms and available precision monitoring of NO, NO2, and O2). Emergency and transport systems must be readily available. The choice of the monitoring device (chemiluminescence or electrochemistry) should be made based on the knowledge of their strength and weakness for a particular clinical application. Finally, scavengers of NOx should be used with caution until specific filters are proven safe and effective. CONCLUSIONS: The great expectancies generated by inhaled NO action have led researchers to design personal inhaled NO delivery systems, but only with mitigated results. At present, medical companies are finding a financial interest in designing a delivery system which will suit the needs of clinicians and this, along with official governmental approval, will only then permit the use of inhaled NO safely and on a larger scale.

Administration, Inhalation↗
PubMed1998

Inhaled nitric oxide in acute respiratory distress syndrome: a pilot randomized controlled study.

This pilot randomized controlled clinical trial of patients with ARDS was implemented to study the impact of inhaled nitric oxide (inhNO) on lung function, morbidity, and mortality. Thirty patients with ARDS were randomly allocated to usual care or usual care plus inhNO. The optimal dose of inhNO was determined to be between 0.5 and 40 parts-per-million daily. All therapeutic interventions were standardized. ARDS resulted mainly from sepsis (25 of the 30). During the first 24 h, the hypoxia score increased greatly in patients treated with inhNO +70.4 mm Hg (+59%) versus +14.2 mm Hg (+9.3%) for the control group (p = 0.02), venous admixture decreased from 25.7 to 15.2% in the inhNO group, and from only 19.4 to 14.9% in the control group (p = 0.05). After the first day of therapy no further beneficial effect of inhNO was detected. Forty percent of the patients treated with inhNO were alive and weaned from mechanical ventilation within 30 d after randomization compared with 33.3% in the control group (p = 0.83). The 30-d mortality rate was similar in the two groups; most deaths (11 of 17) were due to multiple organ dysfunction syndrome. This study shows that inhNO, in this population, may improve gas exchange but does not affect mortality.

Administration, Inhalation↗
PubMed1998

Molecular mechanisms underlying the role of nitric oxide in the cardiovascular system.

In the cardiovascular system, nitric oxide (NO) is involved in the short and long-term regulation of haemodynamics, and in a number of their pathological alterations. Investigation into the biochemistry of NO-synthase isoforms has confirmed that they also all produce superoxide anion (O(*)). The free radical NO can interact with many targets on which novel information has been recently obtained. The major results of these interactions are not only the well known activation of guanylyl cyclase, but also the formation of potentially cytotoxic peroxynitrite (ONOO(-)), and the formation of S-nitrosothiols and non-haem iron-dinitrosyl dithiolate complexes. Tissue O(2), O(*), low molecular weight thiols and transition metals (especially FeII) play a pivotal role in directing NO towards targets responsible for biological effects, or storage or release from these stores. In addition, circulating forms of NO have been proposed with S-nitrosation of blood proteins. All these mechanisms provide potential pharmacological targets for future therapeutic strategies.

Journal Article↗
PubMed1997

Inhaled nitric oxide: clinical applications, indications, and toxicology.

PURPOSE: Although the analogy of nitric oxide (NO) to Endothelium-derived Relaxing Factor remains controversial, medical use of exogenous NO gas by inhalation has grown exponentially. This review presents the mechanisms of action of inhaled NO in pulmonary hypertension, hypoxaemia, inflammation and oedema, as well as its therapeutic and diagnostic indications with emphasis on acute respiratory distress syndrome (ARDS) and toxicology. SOURCE: Two medical databases (Current Contents, Medline) were searched for citations containing the above-mentioned key words to December 1996. Moreover, many presentations in congresses such as 4th International Meeting of Biology of Nitric Oxide, 52nd and 53rd Annual Meeting of Canadian Anaesthetists' Society or 10th Annual Meeting of European Association of Cardiothoracic Anaesthesiologists were used. PRINCIPAL FINDINGS: Inhaled NO is now recognized as an invaluable tool in neonatal and paediatric critical care, and for heart/lung surgery. Other clinical applications in adults, such as chronic obstructive pulmonary disease and ARDS, require a cautious approach. The inhaled NO therapy is fairly inexpensive, but it would seem that it is not indicated for everybody with regards to the paradigm of its efficiency and potential toxicity. The recent discovery of its anti-inflammatory and extrapulmonary effects open new horizons for future applications. CONCLUSION: Clinical use of inhaled NO was mostly reported in case series, properly designed clinical trials must now be performed to establish its real therapeutic role. These trials would permit adequate selection of the cardiopulmonary disorders, and subsequently the patients that would maximally benefit from inhaled NO therapy.

Administration, Inhalation↗
PubMed1997

Extra-pulmonary effects of inhaled nitric oxide in swine with and without phenylephrine.

We have compared the effects of inhaled nitric oxide (iNO) and i.v. nitroglycerin (ivGTN) on the haemodynamic response to phenylephrine-induced hypertension (PEHT) in anaesthetized pigs. PEHT did not change either pulmonary vascular resistance or gas exchange throughout all experiments. Both treatments lowered pulmonary arterial pressure to the same extent (-12.4% iNO; -13.7% ivGTN) and passively via an effect on left atrial pressure (-26.3% iNO; -31.4% ivGTN). Both treatments failed to reverse the decrease in renal blood flow (RBFc) induced by PEHT, but both increased urinary flow (UF) (+128% iNO; +148% ivGTN). IvGTN significantly increased plasma concentrations of nitrite and nitrate during (+22.7% arterial blood; +26.2% venous blood) and beyond the period of infusion (iNO: +6.4% and +4.9%, respectively). In four control pigs (no PEHT), iNO markedly increased RBFc (+109%), glomerular filtration rate (+72.5%) and UF (+68.7%). We conclude that iNO may have direct cardiac and renal effects, probably via intervention of NO carrier forms such as S-nitroso compounds.

Administration, Inhalation↗
PubMed1997

Effects of reducing reagents and temperature on conversion of nitrite and nitrate to nitric oxide and detection of NO by chemiluminescence.

To measure the concentration of nitrites and nitrates by chemiluminescence, we examined the efficiency of five reducing agents [V(III), Mo(VI) + Fe(II), NaI, Ti(III), and Cr(III)] to reduce nitrite (NO2-) and (or) nitrate (NO3-) to nitric oxide (NO). The effect of each reducing agent on the conversion of different amounts of NO2- and (or) NO3- (100-500 pmol, representing concentrations of 0.4 to 2 mu molar) to NO was determined at 20 degrees C for NO2- and at 80 degrees C for NO3-. The effect of temperature from 20 to 90 degrees C on the conversion of a fixed amount of NO2- or NO3- (400 pmol or 1.6 mu molar) to NO was also determined. These five reducing agents are similarly efficient for the conversion of NO2- to NO at 20 degrees C. V(III) and Mo(VI) + Fe(II) can completely reduce NO3- to NO at 80 degrees C. NaI and Cr(III) were unable to convert NO3- to NO. Increased temperature facilitated the conversion of NO3- to NO, rather than that of NO2- to NO. We evaluated the recovery of NO2- and NO3- from plasmas of pig and of dog. Recovery from plasma of both animals was reproducible and near quantitative.

Animals↗
PubMed1996

Comparison of the effect of inhaled nitric oxide and intravenous nitroglycerine on hypoxia-induced pulmonary hypertension in pigs.

Pulmonary hypertension is usually treated with intravenous (i.v.) vasodilators, but their use is limited by systemic effects. In the current study, we compared the effects of inhaled nitric oxide and intravenous nitroglycerine on pulmonary and systemic haemodynamic responses as well as on gas exchange measurements in anaesthetized pigs whose pulmonary pressure was increased by hypoxia (FiO2 = 15%). Both treatments reduced pulmonary pressure to the control level. Inhaled nitric oxide did not affect systemic arterial pressure but intravenous nitroglycerine decreased it from 126.2 to 108.8 mmHg (P = 0.04). Unlike intravenous nitroglycerine, inhaled nitric oxide increased arterial PaO2 from 5.3 to 5.9 kPa (P = 0.02). Both treatments diminished central venous pressure and left atrial pressure, suggesting a possible cardiac effect. Inhaled nitric oxide was shown to be a potent pulmonary vasodilator which attenuated pulmonary hypertension and improved arterial oxygenation without important direct effects on systemic pressure in porcine hypoxia-induced pulmonary hypertension.

Administration, Inhalation↗
PubMed1996

Pharmacokinetics of epidural butorphanol in isoflurane-anaesthetized dogs.

Sixteen healthy male dogs were used at random in this protocol. The dogs were anaesthetized with isoflurane in oxygen. Eight of the dogs received 0.25 mg/kg of butorphanol (group B) and the others an equal volume of isotonic saline (group S) administered by a catheter inserted in the lumbosacral epidural space. Butorphanol concentrations in plasma and cerebrospinal fluid (CSF) were measured using high-performance liquid chromatography with electrochemical detection. Maximum concentration of butorphanol and time to obtain this concentration were 42.28 ng/mL at 13.88 min in blood, and 18.03 ng/mL at 30 min in CSF. Volume of distribution, clearance, mean distribution and elimination half-lives were respectively 4.39 L/kg, 2.02 L/h.kg, 16.5 min and 189.1 min. Mean isoflurane minimal alveolar concentration values for group B obtained following hind- or forelimb stimulation decreased by 31% after epidural butorphanol. Cutaneous analgesia (to pin-prick test) persisted for 3 h after the end of isoflurane anaesthesia in group B and was in correlation with the plasmatic analgesic dose of butorphanol (9 ng/mL). These results suggested that analgesia was predominantly obtained by action of butorphanol on the supraspinal structures following its vascular systemic absorption.

Analgesia, Epidural↗
PubMed1996

Evaluation of analgesia and cardiorespiratory effects of epidurally administered butorphanol in isoflurane-anesthetized dogs.

OBJECTIVE: To determine variations in minimal alveolar concentration (MAC) of isoflurane and analgesic and cardiorespiratory effects of lumbosacral epidural administration of 0.25 mg of butorphanol/kg of body weight in dogs. ANIMALS: 16 healthy male dogs. PROCEDURE: Dogs were anesthetized with isoflurane alone. Eight dogs received butorphanol (group B) and the others an equal volume of isotonic saline solution (group S) administered by a catheter inserted in the lumbosacral epidural space. Isoflurane MAC was determined before and 30 minutes after the epidural injection, along with noxious stimulation to the fore- and bind limbs. Cardiorespiratory variables were recorded prior to and until 120 minutes after epidural administration. At that time, isoflurane anesthesia was ended, and nociception (toe pinch and pin-prick responses) was evaluated for 7 hours. Dogs were observed for 3 days to determine presence of neurologic side effects. RESULTS: For group-B dogs, isoflurane MAC decreased by 31 +/- 8.6% after butorphanol was administered Cutaneous insensitivity (to pin-prick nociceptive test) persisted for 3 hours after the end of isoflurane anesthesia in group-B dogs. No response was observed to toe pinch stimulation for 80 minutes after anesthesia. CONCLUSIONS: Epidural administration of 0.25 mg of butorphanol/kg in dogs was safe; minimal cardiorespiratory and no neurologic side effects were observed, and analgesia and an isoflurane-sparing effect were apparent. CLINICAL RELEVANCE: The short duration of action of epidurally administered butorphanol limits its value for clinical practice.

Analgesia, Epidural↗
PubMed1995

Comparison of two administration techniques of inhaled nitric oxide on nitrogen dioxide production.

The purpose of this study was to verify whether, compared with the introduction of the NO-N2 mixture at the air inlet of the ventilator (classical method), a direct injection of NO-N2 into the inspiratory line of the ventilator circuit with a new injection device (new method), would reduce NO2 formation by reducing contact time between O2 and NO. The effect of two FIO2(0.21 and 0.90) and NO concentrations on NO2 production was determined. In the classical method, NO and O2 were mixed with an air/oxygen blender before the gas mixture entered the ventilator. In the new method, NO was injected directly into the respiratory line with the injection system. Nitric oxide and nitrogen dioxide gases were measured using a chemiluminescence analyzer. For a FI02 of 0.90 and 90 ppm of NO2, the amount of NO2 produced was decreased from 8.9 +/- 0.8 ppm (mean +/- SD) with the classical injection system to 4.4 +/- 0.2 ppm with the new injection system (P = 0.0039, Mann-Whitney test), and NO2 production was decreased from 4.5 +/-0.2 ppm to 2.1 +/- 0.4 ppm (P = 0.02) at 60 ppm of NO. However, at a FIO2, no difference was found in the amount of NO2 produced. We conclude that, compared with the classical method of NO administration, the new NO injection system reduces considerably the concentration of inhaled NO2 when a high FIO2 and a high concentration of NO are used.

Administration, Inhalation↗
PubMed1995

[Intravenous anesthesia in the horse: comparison of xylazine-ketamine and xylazine-tiletamine-zolazepam combinations].

Intravenous anesthesia in the horse: Comparison of xylazine-ketamine and xylaxine-tiletamine-zolazepam combinations. Six healthy adult horses were anesthetized twice at random with following intravenous combinations: 1.1 mg/kg of body weight (BW) of xylazine followed by 2.2 mg/kg BW of ketamine (X-K) and 1.1 mg/kg BW of xylazine followed by 1.65 mg/kg BW of tiletamine-zolazepam (X-TZ). The modifications of some cardiorespiratory parameters and the duration of anesthesia were evaluated and compared for the 2 protocols used. Few significant differences were observed between the 2 protocols in regard to the cardiorespiratory parameters measured. The respiratory rate was lower (7 breaths per minute) and the heart rate was higher (34 beats per minute) with the X-TZ combination. The duration of anesthesia with this technique was 33 +/- 3 minutes (X +/- Sx) and longer than with X-K (18 +/- minutes (X +/- Sx)). Superficial analgesia lasted 14,5 +/- 3 minutes with the X-K combination and 31,7 +/- 3,2 minutes for the X-TZ combination. The 2 protocols are associated with a reduction of PaO2.

Anesthesia, Intravenous↗