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Biomedical subjects

M M Puig

Publications and source records attributed to M M Puig.

At least 91 records · Page 5Linked to original sources
PubMed1988

Effects of acute and chronic hyperglycemia on morphine-induced inhibition of gastrointestinal transit in mice.

Using the charcoal meal test, the effects of morphine (3, 5 and 7 mg/kg) on gastrointestinal transit was assessed in normoglycemic as well as in acute and chronic hyperglycemic mice. Acute hyperglycemia was induced by intraperitoneal injection of glucose (5.04 g/kg), while chronic hyperglycemia was induced by streptozotocin injection (200 mg/kg i.p., 7-8 days before). Acute hyperglycemia augmented the inhibitory effect of morphine on gut transit, however, chronic hyperglycemia failed to modify the effects of morphine. The results indicate that hyperglycemia per se may not be the primary mechanism for the altered sensitivity to morphine in experimental models of diabetes.

Acute Disease↗
PubMed1987

Naloxone elicits an excitatory response in the morphine-tolerant mouse vas deferens.

The effects of naloxone on the electrically stimulated vas deferens from mice implanted with morphine (tolerant) or placebo (naive) pellets were studied. In tolerant vas deferens, naloxone produced an 86.6% increase of the twitch contractions when the preparations were stimulated with 15 V, while only a 12% increase was observed with supramaximal voltage (40 V). Naloxone had no effect at either voltage in preparations from naive animals. The effect of morphine in naive vas deferens stimulated with 15 V, was reversed by naloxone without further increase over baseline contractions. The results suggest that opioid receptors other than those located in the neuronal soma and/or coupled to adenylate cyclase may be involved in the development of dependence.

Animals↗
PubMed1987

Effects of temperature on the interaction of morphine with opioid receptors.

The electrically stimulated guinea pig ileum preparation was used to determine the effects of temperature on the affinity of morphine for opioid receptors. The potency of morphine (expressed as the concentration which produces 50% inhibition--IC50) was significantly decreased at 30 degrees C (IC50 41.0 x 10(-8) mol litre-1) and increased at 40 degrees C (IC50 5.1 x 10(-8) mol litre-1) when compared with its potency at 37 degrees C (IC50 8.8 x 10(-8) mol litre-1). Experiments carried out in the presence of naloxone (a competitive opioid antagonist) indicated that the affinity of opioid receptors for this antagonist was not affected by temperature. Further studies using B-funaltrexamine (a mu-specific, non-reversible opioid antagonist) revealed an increase in morphine receptor affinity when temperature was increased from 30 to 37 degrees C. The data demonstrated that the potency of morphine increased with temperature; the affinity of naloxone for opioid receptors was unaltered by temperature; and the affinity of morphine for mu-receptors reached an optimal value within the range 30-37 degrees C.

Animals↗
PubMed1987

Postoperative analgesia induced by subarachnoid lidocaine plus calcitonin.

A randomized double-blind study tested the analgesic effects of subarachnoid administration of salmon calcitonin (sCT) in acute postoperative pain. Sixty patients were grouped according to type of surgery (intraabdominal, extraabdominal, and lower extremities), subdivided into those given subarachnoid lidocaine 1 mg/kg plus sCT (100 IU) or lidocaine plus saline. Pain was evaluated by a descriptive scale 3, 6, 12, 24, 48, and 72 hr after surgery, as well as by the frequency of the patients' requests for postoperative analgesics. In all instances, the sCT-treated patients had significantly less postoperative pain. Similarly, the requests for analgesics was significantly lower or absent in the sCT-treated group. Minor side effects such as nausea and vomiting, abdominal pain, and "nervousness" were observed in a small number of sCT-treated patients. In our series of 30 patients, subarachnoid administration of sCT was an effective analgesic with minimal side effects. Its safety remains to be proved by further studies.

Acute Disease↗
PubMed1986

Naloxone prevents hyperthermia induced convulsions in the immature rat.

There is increasing evidence suggesting that endogenous opioid peptides play a role both in temperature regulation and in the etiopathology of seizures. We have studied the effects of the opioid antagonist naloxone on hyperthermia-induced seizures in unrestrained 15 day old rat pups. Saline injected control animals exposed to an ambient temperature of 40 degrees C for one hr showed a gradual increase in body temperature reaching a maximum of 42 degrees C at 50 min of exposure; at this time, all animals had convulsions and 86% died. Animals pre-treated with 10 mg/kg naloxone reached a maximum core temperature of 41 degrees C after 60 min at 40 degrees C and no convulsions or deaths were observed. When animals were exposed for 60 min to a 27 degrees C environment, saline controls maintained their normal body temperature throughout the experiment, while 5 mg/kg naloxone produced a marked hyperthermic effect. These experiments suggest that endogenous opioids may play a role in both temperature adaptation and hyperthermia-induced seizures in the rat pup.

Adaptation, Physiological↗
PubMed1985

Cerebrospinal fluid leucine-enkephalin-like levels in febrile convulsions.

Enkephalin levels were measured in the cerebrospinal fluid (CSF) of 17 patients with febrile convulsions and 11 control patients without a history of pain or convulsive disorders. Enkephalins were extracted from CSF by adsorption with synthetic resin XAD-2 eluted with methanol, and assayed using the radioreceptor assay (RRA). Results were expressed as Leucine-Enkephalin (Leu-E) equivalents. Enkephalin levels in CSF were 2.27 +/- 0.42 pmol/ml (mean +/- SE) in the convulsion group and the 4.8 +/- 0.8 pmol/ml (mean +/- SE) in the control group. Statistical comparison in both groups shows significant differences (p less than 0.001). These results suggest a correlation between convulsions and enkephalin levels in CSF.

Adolescent↗
PubMed1984

Haloperidol treatment increases the biosynthesis and release of endorphins in guinea-pig ileum.

Guinea-pigs treated acutely (5 mg kg-1 i.p.) and chronically (2 or 5 mg kg-1 day-1 for 4 days) with haloperidol, show an increase of the inhibitory response produced by electrical stimulation at 10 Hz of the ileum myenteric plexus-longitudinal muscle (MPLM) preparation. The response can be reversed by the specific narcotic antagonist naloxone (5 X 10(-7) M), which suggests that the increase in the response produced by haloperidol is mediated by release of endorphins. When haloperidol-treated guinea-pigs received cycloheximide (24 and 12 h before death), there was a substantial decrease in the response indicating that the biosynthesis and release of endorphins are increased by haloperidol.

Animals↗
PubMed1982

Endorphin levels in cerebrospinal fluid of patients with postoperative and chronic pain.

The authors measured endorphin levels in the cerebrospinal fluid (CSF) of 12 patients with chronic pain due to lumbar disc syndrome and eight patients with acute postoperative pain. These were compared with CSF endorphin levels in 20 control patients with no history of pain. Endorphins were extracted by adsorption to a synthetic resin (Amberlite XAD-2), eluted with methanol, and assayed using the electrically stimulated mouse vas deferens. Results were expressed as methionine-enkephalin (Met-E) equivalents, which was the standard in the bioassay. The CSF endorphin level was 0.42 +/- 0.07 pmol/ml (mean +/- SE) in the postoperative group, 1.44 +/- 0.2 pmol/ml in the chronic pain group, and 4.36 +/- 0.89 pmol/ml in the control group. CSF endorphin levels in the two pain groups differed significantly from both the control group and each other. These results suggest a correlation between pain levels and endorphin concentration in the CSF; however, in the acute postoperative pain group the influence of other factors such as anesthesia or surgical stress cannot be evaluated.

Abdomen↗
PubMed1982

[Measurement of endorphins in human cerebrospinal fluid. Comparative study of various groups of patients].

Endorphin levels in human cerebrospinal fluid (CSF) have been determined by using the electrically stimulated mouse vas deferens bioassay. Endorphins were extracted by adsorption to a synthetic resin of Amberlite XAD-2 eluted with methanol, and dried under a nitrogen atmosphere. Three different groups of patients have been studied: a) control subjects without a history of pain (n = 25), b) patients with acute postoperative pain after high abdominal and thoracic surgery (n = 8) and c) patients with chronic pain due to discal hernia (n = 14). The endorphin levels (expressed as equivalents of Met-E) obtained from the control group were 4.36 +/- 0.7 pmol/ml. In the postoperative group an endorphin decrease of 0.42 +/- 0.07 pmol/ml, was found while in the chronic pain group the levels obtained were 1.39 +/- 0.2 pml/ml. Thus a significantly low level of CSF endorphins was observed in both the postoperative and the chronic pain group as compared with the controls (p less than 0.01). These results suggest a correlation between pain levels and endorphin concentration in CSF. However in the acute postoperative pain group other factors such as depletion of endorphins by drugs used for anesthesia or due to surgical stress cannot be excluded.

Adult↗