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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
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↗
PubMed1998

Peripheral effects of opioids in a model of chronic intestinal inflammation in mice.

The study describes a model of chronic intestinal inflammation in mice. Inflammation was induced by the administration of one dose of croton oil (CO) (acute CO) or two doses (chronic CO) of intragastric CO, whereas controls received saline (SS); GI transit was measured with charcoal. Chronic CO induced intestinal inflammation substantiated by optical microscopy, weight loss (20%) and a 25% increase in GI transit. The ED50 values in SS animals were 1.67 +/- 0.13 mg/kg for morphine and 0.038 +/- 0.006 mg/kg for fentanyl; chronic CO significantly decreased the ED50 values to 0.16 +/- 0.03 mg/kg (morphine) and 0.006 +/- 0.0005 mg/kg (fentanyl). Thus the potency of morphine increased 10.4 times and that of fentanyl 6.3 times. The effects of enkephalin, but not those of U-50488H, were also significantly enhanced during chronic CO. The antitransit effects of p.o. loperamide increased 11.7 times during chronic CO. All effects were reversed by specific antagonists. The fraction of the active opioid receptor that mediates the antitransit effects of morphine was evaluated using beta-funaltrexamine. In chronic CO, the doses of beta-funaltrexamine needed to antagonize 1 mg/kg of morphine were significantly higher than in SS and acute CO, and the ED50/KA ratio was 20 times lower. These results suggest an increase in the active concentration of mu-opioid receptors during chronic inflammation.

Animals↗
PubMed1997

Ondansetron facilitates neuromuscular transmission in the guinea-pig ileum.

The effects of ondansetron on the neuromuscular function of the guinea-pig ileum were investigated in vitro. Ondansetron, but not tropisetron or MDL 72222 (1alpha-H-3alpha-5alpha-H-tropan-3-yl-3,5-dichlo robenzoate), enhanced submaximal electrically induced contractions (EC50) = 1.3 x 10(-5) M). Desensitization with 5-hydroxytryptamine (1 x 10(-5) M) or 2-methyl-5-HT (1 x 10(-5) M) abolished this facilitatory response, which remained unaltered after desensitization with 5-methoxytryptamine (1 x 10(-5) M) or addition of tropisetron, MDL 72222, N-acetyl-5-hydroxytryptophyl-5-hydroxytryptophan, SB203186 (1-piperidinylethyl-1H-indole-3 carboxylate hydrochloride), pirenzepine or hexamethonium. At higher concentrations, ondansetron decreased the electrically induced contractions (EC50 = 1 x 10(-4) M); the inhibitory response was unaffected by (-)-naloxone (1 x 10(-6) M) or idazoxan (1 x 10(-6) M). We conclude that, in the guinea-pig ileum, ondansetron elicits a biphasic response: facilitation of neuromuscular transmission mediated by a serotonergic receptor distinct from the 5-HT3, 5-HT4 or putative 5-HT1P receptors, and an inhibitory response that does not involve opiate or alpha2-adrenoceptors.

5-Methoxytryptamine↗
PubMed1997

Reversal of tolerance to the antitransit effects of morphine during acute intestinal inflammation in mice.

1. The aim of investigation was to establish and compare the reversibility of tolerance to the antitransit effects of morphine by three different procedures: (a) acute inflammation of the gut, (b) lorglumide a cholecystokininA (CCKA) receptor antagonist, or (c) MK-801, an N-methyl-D-aspartate (NMDA) receptor ion channel blocker. The type of interaction between morphine and lorglumide or MK-801 on the inhibition of gastrointestinal transit (GIT) in naive animals was also evaluated. 2. Male Swiss CD-1 mice were implanted with 75 mg of morphine base or placebo pellets. Gastrointestinal transit was assessed with a charcoal meal and results expressed as % inhibition of GIT. Inflammation was induced by the intragastric (p.o.) administration of croton oil (CO), while controls received castor oil (CA) or saline (SS). Morphine was administered by subcutaneous (s.c.) or intracerebroventricular (i.c.v.) injection, to naive and tolerant animals treated with CO, CA or SS. Dose-response curves for s.c. morphine were also performed in naive and tolerant mice receiving 5.2 or 7.4 nmol (s.c.) lorglumide or MK-801, respectively. 3. The ED50 values for inhibition of GIT by s.c. morphine were: 45.9 +/- 2.7 and 250.1 +/- 3.1 nmol in naive and tolerant animals, respectively, demonstrating a five fold decrease in the potency of morphine. In naive animals, inflammation (CO) decreased the ED50 of morphine three times (14.4 +/- 2.2 nmol). However, no tolerance to s.c. morphine (ED50 16.4 +/- 2.6 nmol) was manifested during intestinal inflammation. After i.c.v. administration, a similar degree of tolerance to morphine was observed (4.8 fold decrease in potency). Intestinal inflammation had no effect on the ED50 values of i.c.v. morphine in naive and tolerant animals, showing that reversal of tolerance is related to local mechanism/s. Mean values for intestinal pH were 6.9 +/- 0.04 and 6.2 +/- 0.04 in SS and CO treated mice, respectively. In addition, morphine was 74 times more potent by the i.c.v. than by the s.c. route (naive-SS). 4. Morphine and lorglumide interacted synergistically in naive animals; in addition, the administration of lorglumide reversed tolerance to s.c. morphine. No interaction (additivity) was observed in naive animals when morphine and MK-801 were administered in combination. However, the drug completely reversed tolerance to the antitransit effects of morphine. 5. The present investigation shows that acute inflammation of the gut reverses tolerance to the antitransit effects of s.c. morphine by a peripheral mechanism. Qualitatively similar results were obtained after the administration of lorglumide or MK-801. Our results suggest that a local decrease in pH could play an important role during inflammation, while antagonism of endogenous compensatory systems would explain the reversal of tolerance induced by lorglumide or MK-801.

Acute Disease↗
PubMed1996

Comparative assessment of the anaesthetic and analgesic effects of intramuscular and epidural clonidine in humans.

PURPOSE: The aim of the study was to assess and compare in analogous controlled experimental conditions, the anaesthetic sparing and analgesic effects of the same dose of clonidine administered by the intramuscular (im) and epidural (ep) routes. METHODS: We used a randomized, double blind and placebo controlled protocol. Sixty patients undergoing abdominal hysterectomy were distributed into three groups who, 30 min before surgical incision, received: 300 micrograms ep clonidine plus im saline; ep saline plus 300 micrograms im clonidine; or ep and im saline (ss). General anaesthesia was maintained with 60% N2O in O2, and isoflurane administered at concentrations to maintain mean arterial pressure (MAP) and heart rate (HR) within 20% of basal values. Isoflurane requirements (mass spectrometry), cardiovascular variables (MAP, HR), and plasma concentrations of glucose, cortisol and prolactin were evaluated at critical time points. In the recovery room (RR), sedation (Ramsay) and pain intensity (VAS) were estimated at the time of analgesia request (TAR). RESULTS: Intramuscular and ep clonidine decreased isoflurane requirements similarly by about 85% (P < 0.001). Patients in the ep group had lower MAP (P < 0.03) and HR (P < 0.001) than in the im group, but im and ep clonidine similarly blunted the plasma prolactin increase induced by intubation. In RR, ep but not im clonidine (P < 0.01) induced postoperative analgesia demonstrated by a prolonged TAR 80.8 +/- 7.3 (ep) 35.9 +/- 3.2 (im) and 44.5 +/- 5.1 (ss) min and a lower VAS (P < 0.05). CONCLUSIONS: Epidural and intramuscular clonidine decreased isoflurane requirements similarly, but only the epidural route provided postoperative analgesia, suggesting a spinal site for the analgesic action.

Adult↗