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Biomedical subjects

M M Puig

Publications and source records attributed to M M Puig.

At least 19 recordsLinked to original sources
PubMed2005

A procedure-specific systematic review and consensus recommendations for postoperative analgesia following laparoscopic cholecystectomy.

BACKGROUND: Laparoscopic cholecystectomy has advantages over the open procedure for postoperative pain. However, a systematic review of postoperative pain management in this procedure has not been conducted. METHODS: A systematic review was conducted according to the guidelines of the Cochrane Collaboration. Randomized studies examining the effect of medical or surgical interventions on linear pain scores in patients undergoing laparoscopic cholecystectomy were included. Qualitative and quantitative analyses were performed. Recommendations for patient care were derived from review of these data, evidence from other relevant procedures, and clinical practice observations collated by the Delphi method among the authors. RESULTS: Sixty-nine randomized trials were included and 77 reports were excluded. Recommendations are provided for preoperative analgesia, anesthetic and operative techniques, and intraoperative and postoperative analgesia. CONCLUSIONS: A step-up approach to the management of postoperative pain following laparoscopic cholecystectomy is recommended. This approach has been designed to provide adequate analgesia while minimizing exposure to adverse events.

Analgesia↗
PubMed2005

Low- vs high-dose almitrine combined with nitric oxide to prevent hypoxia during open-chest one-lung ventilation.

BACKGROUND: Almitrine combined with inhaled nitric oxide (NO) can prevent hypoxia during one-lung ventilation (OLV). The optimal dose of almitrine that would provide therapeutic advantage with few side-effects during open-chest OLV has not been established. METHODS: Forty-two patients undergoing thoracotomy were randomly allocated to three groups: placebo, almitrine 4 microg kg(-1) min(-1) and inhaled NO 10 p.p.m. (ALM4+NO), and almitrine 16 microg kg(-1) min(-1) and inhaled NO 10 p.p.m. (ALM16+NO). Gas exchange, haemodynamic and respiratory variables and plasma concentrations of almitrine and lactate were monitored. Measurements were obtained with the patient awake (baseline), after induction of anaesthesia with two-lung ventilation (control 2LV), 20 min after treatment (2LV+T), and then at 10, 20 and 30 min of OLV (OLV10', OLV20' and OLV30') with FI(O2)1. RESULTS: In the placebo group, OLV impaired Pa(O2) and increased pulmonary shunt [16 (SD 7) kPa and 42 (10)% respectively]. These improved with ALM4+NO [26 (10) kPa and 31 (7)%; P<0.001]. ALM16+NO further improved PaO2) to 36 (13) kPa (P<0.0001) but gave no improvement in the shunt. Mean pulmonary artery pressure was similar in the placebo and ALM4+NO groups [20 (4) vs 23 (5) mm Hg], whereas it was increased in the ALM16+NO group to 28 (8) mm Hg (P<0.01). Plasma concentrations of almitrine and lactate were unaltered by the treatments. CONCLUSIONS: Low-dose almitrine (4 microg kg(-1) min(-1)) together with inhaled NO significantly improves oxygenation during open-chest OLV, without modifying pulmonary haemodynamics. An increased dose of almitrine (16 microg kg(-1) min(-1)) with inhaled NO further improves arterial oxygenation, but also increases mean pulmonary artery pressure.

Adolescent↗
PubMed2004

Comparative assessment of the effects of alfentanil, esmolol or clonidine when used as adjuvants during induction of general anaesthesia.

BACKGROUND AND OBJECTIVE: This randomized, double-blinded, prospective study compared the effects of clonidine, esmolol or alfentanil on the level of hypnosis and haemodynamic responses to intravenous induction of anaesthesia and endotracheal intubation. METHODS: Forty-five patients scheduled for elective surgery were allotted to one of three groups. They were given either alfentanil 3 microg kg(-1) min(-1) (n = 15); esmolol 1 mg kg(-1) min(-1) (n = 16) or clonidine 3 microg kg(-1) (n = 14) as a 10 min infusion. The infusions of alfentanil and esmolol, but not of clonidine, were maintained during endotracheal intubation. Anaesthesia was induced with midazolam (2 mg) and thiopental as required to suppress the eyelash reflex. Atracurium (0.5 mg kg(-1)) was given to produce neuromuscular block. Mean arterial pressure, heart rate, and bispectral index were recorded on arrival (baseline), after study drug infusion, after injecting midazolam and thiopental, as well as after endotracheal intubation. ANOVA and chi2-test were used for analysis. RESULTS: Blood pressure, heart rate and the bispectral index were unaltered by the study drugs, but thiopental requirements were reduced by alfentanil and clonidine (P < 0.014). Mean arterial pressure values (mean +/- standard error of mean) in the alfentanil, esmolol and clonidine groups were: baseline: 107.8 +/- 3.8; 106.6 +/- 3.9; 103.4 +/- 3.7 mmHg; after thiopental: 74.0 +/- 4.2; 85.6 +/- 4.3; 94.2 +/- 4.1 mmHg and after endotracheal intubation: 91.7 +/- 5.3; 114.1 +/- 6.9; 123.6 +/- 5.6 mmHg, respectively (two-way ANOVA, P < 0.001). Mean arterial pressure changed significantly after intubation from baseline (P < 0.001) after alfentanil (-15%) and clonidine (+20%) but not after esmolol (+7%), while the changes between pre- and postintubation values were similar in all groups (24-33% increase). The bispectral index indicated that all patients had an adequate level of hypnosis, but the variability was higher in the esmolol group (P < 0.002). CONCLUSIONS: None of the study drugs blocked the increase in mean arterial pressure induced by endotracheal intubation, but esmolol provided better overall haemodynamic stability. All groups had an adequate level of hypnosis.

Adjuvants, Anesthesia↗
PubMed2003

Simple method to determine the size of the laryngeal mask airway in children.

BACKGROUND AND OBJECTIVE: The size of the laryngeal mask airway in children is determined by the patient's weight. However, in some instances an alternative method may be wanted. The aim was to search for a new method that would be easy to perform at the bedside. METHODS: The size of the laryngeal mask airway was determined in 183 children by choosing the laryngeal mask that best matched the combined widths of the patient's index, middle and ring fingers. The results were compared with the standard method recommended by the manufacturer's weight-related guidelines. The patients were classified in different groups depending on the laryngeal mask airway sizes determined by both methods. A kappa coefficient evaluated the agreement between both techniques. RESULTS: The kappa coefficient was 0.81, showing an 'excellent agreement' between both methods. The size was the same for both methods in 142 children (78%). The disagreement between both techniques was only of one size in the remaining 41 patients (22%). In such patients, the weight was a borderline value that would indicate a change in the size of the laryngeal mask airway using the classic method. CONCLUSIONS: This new approach is of valid and practical use in children, particularly as an alternative in those situations where the patient's weight is unknown, such as in emergency situations or in those borderline instances where an alternative measurement would be useful.

Adolescent↗
PubMed2001

Antisense oligodeoxynucleotides to mu- and delta-opioid receptor mRNA block the enhanced effects of opioids during intestinal inflammation.

Intestinal inflammation enhances the inhibitory effects of mu- and delta-opioids in the gut, possibly related to an increased receptor expression. We evaluated the effects of opioids after intraperitoneal administration of antisense oligodeoxynucleotides to mu- and/or delta-opioid receptor mRNA. Inflammation was induced in mice by intragastric administration of croton oil; gastrointestinal transit was assessed with charcoal and permeability with [51Cr]etylenediaminetetraacetate ([51Cr]EDTA). Baseline values were unaltered after antisense oligodeoxynucleotides. In controls, antisense oligodeoxynucleotides to mu-opioid receptor mRNA decreased the antitransit effects of morphine (27%) and [N-MePhe3D-Pro4]morphiceptin (PL017) (26%), and the reduction was significantly greater during inflammation (50% and 47%). A similar effect was observed on permeability (control: 41-21% decrease; inflamed: 66-45%). In both assays, antisense oligodeoxynucleotides to delta-opioid receptor mRNA also reduced the effects of [D-Pen2,5]enkephalin (DPDPE) in a higher percentage during inflammation (43-32% controls, 60-49% inflamed). We show that antisense oligodeoxynucleotides to mu- and/or delta-opioid receptor mRNA are efficiently blocking the intestinal effects of opioids during inflammation, suggesting that an increased transcription of these receptors in the gut mediates the enhanced effects of opioids during inflammation.

Animals↗
PubMed2001

Management of postoperative pain in Spain.

BACKGROUND: The management of postoperative pain is suboptimal world-wide. This survey was carried out to determine current management in Spanish hospitals. METHODS: Spanish hospitals were divided into two groups: <200 beds (n=346) and >200 beds (n=186). A structured questionnaire was mailed to the heads of the anaesthesiology services of a random sample of 150 of hospitals of <200 beds, and all larger hospitals. RESULTS: Only 19% of hospitals with <200 beds responded and further analysis of this group was not possible; 53% of hospitals with >200 beds responded. In this sample (>200 beds), 45% of patients receive information on postoperative pain, given by the anaesthesiologist in 78% of cases. Over 70% of the hospitals do not have an acute pain unit and responsibility for postoperative pain lies with the anaesthesiology team in 71%, with the surgical team in 40% and with nursing in 33%, with an overlap of pain caretakers. Pain is measured on the surgical wards in 36% and recorded with the vital signs in 34%. On post-anaesthetic recovery wards, analgesia is most frequently given by intravenous (83%), epidural (78%) and continuous intravenous (66%) administration. On surgical wards, the most frequent routes that are available are epidural (72%), intravenous (69%) and intramuscular (58%). Only 28% of the anaesthesiology services are satisfied with the pain treatment carried out in their hospitals. No significant differences on postoperative pain management were observed between teaching and non-teaching institutions. CONCLUSION: The survey shows that the management of postoperative pain in hospitals with >200 beds in Spain is suboptimal and this is associated with dissatisfaction among many anaesthesiologists.

Data Collection↗
PubMed2001

Inflammation enhances mu-opioid receptor transcription and expression in mice intestine.

Opioid receptors (ORs) and their mRNA are present in the central and peripheral nervous systems of mammals and in different peripheral tissues, including the gut. Using a model of croton oil-induced (CO) intestinal inflammation in mice, we have shown a 6-fold increase in the potency of the antitransit and antisecretory effects of mu-OR agonists, mediated by peripheral ORs. We postulate that the enhanced effects are mediated by an increase in the expression of intestinal OR. We used jejunum (stripped of the mucosal layer) from mice with CO-induced intestinal inflammation and, as control subjects, saline-treated animals (SS). We evaluated the quantity of mu-OR mRNA determined by a competitive reverse-transcriptase polymerase chain reaction; the levels of mu-OR protein by Western blot immunoassay, and the localization and number of cells expressing mu-OR using immunohistochemistry. The results show a significant increase of mu-OR mRNA (7.7-fold) and receptor protein (3-fold) during intestinal inflammation. Inflammation also induced a 64.3% increase in the number of neurons expressing mu-OR immunoreactivity in the myenteric plexus but not in the submucosal plexus. Our results show that intestinal inflammation enhances the transcription and translation of mu-OR mRNA, thus explaining the increased potency of mu-opioids during inflammation.

Animals↗
PubMed2001

Intestinal inflammation enhances the inhibitory effects of opioids on intestinal permeability in mice.

The inhibitory effects of central and peripherally acting opioid agonists on intestinal permeability (PER) were evaluated during acute and chronic intestinal inflammation in mice. Inflammation was induced by the intragastric (p.o.) administration of one (acute) or two (chronic) doses of croton oil (CO), whereas controls received saline (SS). Intestinal PER was assessed by the blood-to-lumen transfer of 51Cr-ethylenediaminetetraacetate (51Cr-EDTA). CO significantly increased PER during acute (2.5 times) and chronic (3.2 times) inflammation. The potency of s.c. morphine-inhibiting PER was enhanced 3.8 and 8.7 times in acute and chronic CO, whereas that of s.c. fentanyl was increased 2.0 and 4.3 times, respectively, compared with SS. Similarly, s.c. [D-Pen(2,5)]-enkephalin was 4.7 and 11.1 times more potent during acute and chronic CO, and the E(max) values of the dose-response curves increased 35% during inflammation. The potency of s.c. U50,488H was 5.6 (acute) and 6.7 times (chronic) greater compared with SS. All effects were reversed by specific antagonists. The i.p. administration of beta-funaltrexamine differentially blocked morphine effects during acute and chronic CO, suggesting that the effects are mediated by different populations of functional mu-opioid receptors (OR). The increase in potencies of s.c. PL017 and ICI-204,448 during CO were comparable to those observed with fentanyl and U50,488H and their effects were antagonized by s.c. naloxone methiodide. Moreover, the potency of the agonists during inflammation was unaltered when administered i.c.v. The results show that intestinal inflammation enhances the effects of delta- > mu- > kappa-opioid agonists on PER by activation of peripheral OR.

Analgesics, Opioid↗
PubMed2000

Effects of mu-opioid receptor agonists on intestinal secretion and permeability during acute intestinal inflammation in mice.

We evaluated and compared the effects of mu-opioid receptor agonists on mucosal fluid transport and permeability, during acute intestinal inflammation. We hypothesized that inflammation would sensitize mu-opioid receptors in the submucosal plexus and/or enterocytes enhancing the effects of mu-opioid receptor agonists. Inflammation was induced by intragastric administration of croton oil, whereas controls received saline. Fluid transport was assessed by enteropooling, and intestinal permeability by blood-to-lumen passage of [51Cr] etylenediaminetetraacetate ([51Cr] EDTA). Intestinal inflammation induced a significant increase in enteropooling (1.9 times) and permeability (2.5 times). In saline- and croton oil-treated animals, mu-opioid receptor agonists produced dose-related inhibitions of enteropooling and intestinal permeability. During inflammation, the potency of morphine increased 4.8 and 3.7 times, inhibiting enteropooling and intestinal permeability, respectively; the potencies of fentanyl and PL017 similarly increased by approximately three (enteropooling) and two times (permeability) in croton oil animals. All effects were reversed by naloxone and naloxone methiodide. The results show that inflammation increases the inhibitory potency of mu-opioid receptor agonists on secretion and permeability, suggesting a sensitization of peripheral mu-opioid receptors.

Acute Disease↗
PubMed2000

Use of intravenous patient-controlled analgesia for the documentation of synergy between tramadol and metamizol.

The quantification of the synergistic interactions (beneficial and adverse) of analgesic drug combinations in humans has been elusive. We propose a new procedure based on analgesic requirements (i.v.-PCA) and pain intensity (VAS-PI). One hundred and one post-hysterectomy patients received at the time of analgesia request (TAR) tramadol (100 mg, group I) or metamizol (1.2 g, group II) alone, or combined in 1:1 (III), 1:0.3 (IV) or 1:3 ratio (V). After 15 min, they received the same treatment by PCA. VAS-PI, analgesic consumption and adverse effects were assessed at TAR, and periodically for 24 h. Data were analysed using interaction indexes and isobolograms. All treatments produced equivalent VAS-PI, per cent efficacy and adverse effects. When drugs were combined in a 1:1 ratio, synergy was present for the analgesic and adverse effects; all other treatments were additive.

Adult↗
PubMed2000

Intestinal inflammation and morphine tolerance alter the interaction between morphine and clonidine on gastrointestinal transit in mice.

BACKGROUND: Morphine and clonidine show synergy or antagonism inhibiting gastrointestinal transit depending on their proportion and level of effect. Their interaction during morphine tolerance and intestinal inflammation were assessed. METHODS: Gastrointestinal transit in mice was evaluated with charcoal and antitransit effects expressed as percent mean values +/- SEM. Tolerance was induced with a morphine pellet (75 mg) implanted for 72 h, and inflammation with intragastric croton oil. Dose-response curves for morphine and clonidine alone and combined at a 1:1 potency ratio were obtained, and doses producing a 50% and 60% inhibition were calculated (ED50, ED60). Interaction was established by isobolograms, interaction indexes, and analysis of variance. RESULTS: In naive and tolerant mice, the combination induced linear dose-response curves up to the ED60 and then reached a plateau. In naive mice, ED50 values were as follows: morphine 1.52 +/- 0.15 mg/kg, clonidine 0.09 +/- 0.008 mg/kg, and combined 0.506 +/- 0.084 mg/kg (0.478 +/- 0.08 mg/kg morphine plus 0.028 +/- 0.004 mg/kg clonidine). During tolerance, ED50 values were as follows: morphine 9.73 +/- 0.8 mg/kg, clonidine 0.09 +/- 0.007 mg/kg, combination 0.131 +/- 0.09 mg/kg (morphine 0. 13 +/- 0.09 mg/kg plus clonidine 0.0013 +/- 0.0005 mg/kg). In both groups, the interaction was synergistic up to the ED60 and antagonistic thereafter; synergy was enhanced during tolerance. During inflammation, ED50 values were as follows: morphine 0.17 +/- 0.04 mg/kg, clonidine 0.015 +/- 0.006 mg/kg, combined 0.62 +/- 0.04 mg/kg (morphine 0.568 +/- 0.04 mg/kg plus clonidine 0.052 +/- 0.004 mg/kg); thus, potencies of morphine and clonidine increased 9.3 and 7.1 times, while the combination remained unaltered. Moreover, inflammation transformed synergy into antagonism. CONCLUSIONS: The interaction between morphine and clonidine was significantly altered during tolerance and inflammation. During tolerance, synergy was present up to 60% effect and then became antagonistic. Inflammation converted synergy to antagonism. A common pathway in signal transduction could partially explain the results.

Analgesics↗
PubMed2000

Antinociceptive/anti-edema effects of liposomal morphine during acute inflammation of the rat paw.

We evaluated the anti-edema/antinociceptive effects of subcutaneous free and liposomal morphine in rats with carrageenan-induced inflammation of the paw. We assessed antinociception by the paw pressure test and edema by plethysmography. Unilamellar liposomes (150-200 nm) with 0.3% morphine hydrochloride were used; encapsulation significantly reduced the rate for release of morphine in vitro. During inflammation, the antinociceptive potency of free, but not liposomal morphine increased 2.5 times; moreover, duration of the effects was prolonged by encapsulation (p < 0.001). The anti-edema effects of liposomal morphine were more pronounced (p < 0. 001) and of longer duration (p < 0.05). All the effects were reversed by naloxone. The results show that morphine encapsulation enhances the anti-edema effects and prolongs antinociception.

Analgesics, Opioid↗
PubMed1999

Antibodies and antisense oligodeoxynucleotides to mu-opioid receptors, selectively block the effects of mu-opioid agonists on intestinal transit and permeability in mice.

1. We have studied the effects of mu and delta opioids on intestinal function (permeability, PER; gastrointestinal transit, GIT), and their antagonism after the intracerebroventricular (i.c.v.) administration of specific antibodies (ABs) or antisense oligodeoxynucleotides (ODN) to mu-receptors (OR). Central versus peripheral site/s of action of subcutaneous (s.c.) mu-opioids, were also assessed. 2. Male Swiss CD-1 mice were used. GIT was measured with charcoal and PER by the passage of 51Cr-EDTA from blood to lumen. 3. Morphine and fentanyl (i.c.v. and s.c.) inhibited GIT and PER in a dose-related manner; they were more potent by i.c.v. route, both on GIT and PER (70 and 17 times for morphine and fentanyl). They also had a greater effect on GIT than PER (4.3 and 1.6 times). DPDPE had a lower potency than mu-agonists in all experiments, and no dose-response could be obtained after s.c. administration on GIT. 4. Pretreatment with i.c.v. ABs (24 h) or antisense ODN (5 days), decreased the effects (GIT and PER) of i.c.v. morphine and fentanyl, while those of DPDPE remained unchanged. The ABs did not alter the peripheral effects of mu-opioids. 5. The results show that (i.c.v. or s.c.) mu opioids produce dose-related inhibitions of PER and GIT, being more potent by the i.c.v. route. Delta-opioids had a greater effect on PER than GIT, while the opposite occurred for mu-agonists. Pretreatment with ABs or ODN to mu-OR, blocked the central effects of mu (but not delta) agonists on GIT and PER.

Animals↗
PubMed1998

Pharmacy savings generated by preoperative administration of clonidine.

STUDY OBJECTIVE: To evaluate the effects of the preoperative administration of clonidine by the oral, intramuscular (i.m.), or epidural routes, on isoflurane expense during total abdominal hysterectomy. DESIGN: Randomized, double-blind, placebo-controlled study. SETTING: University hospital. PATIENTS: 80 ASA physical status I and II patients scheduled for total abdominal hysterectomy. INTERVENTIONS: Patients were distributed into four groups of treatment: oral, i.m., epidural, and control. Each group received 300 microg clonidine according to the treatment group, plus placebo by the other routes. The control group received placebo by all three routes. Depth of anesthesia was evaluated by changes in blood pressure and heart rate over baseline values. Cost evaluation was based on three components: expense of isoflurane, cost of 300 microg of clonidine (tablets or ampoules), and the disposable material required to dispense clonidine to each group. MEASUREMENTS AND MAIN RESULTS: Groups were comparable regarding demographic data, duration of surgery, and time to discharge from recovery room. Postoperatively, none of the patients had recall of intraoperative events. Clonidine reduced isoflurane pharmacy cost by approximately 45%, regardless of the route of administration. However, when cost of clonidine and the disposable equipment used for its administration were taken into account, the cost of the epidural kit surmounted the savings in isoflurane expense. CONCLUSION: In the patient population studied, premedication with 300 microg oral, i.m., or epidural clonidine, similarly and significantly reduced the expense of isoflurane during general anesthesia of an approximate duration of two hours. However, the cost of the epidural kit offsets the savings in isoflurane.

Administration, Oral↗