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Biomedical subjects

H L Fields

Publications and source records attributed to H L Fields.

At least 109 records · Page 6Linked to original sources
PubMed1982

Lumbar intrathecal naloxone blocks analgesia produced by microstimulation of the ventromedial medulla in the rat.

In lightly barbiturate-anesthetized rats. low threshold (less than 10 micro A) electrical stimulation within the rostral ventromedial medulla inhibited the tail-flick response to noxious heat. Naloxone applied intrathecally at the lumbar level reversed this inhibition, but the same dose of naloxone applied to the cervical intrathecal space had no effect. Doses of naloxone 1- to 4-fold greater than the intrathecal dose did not antagonize tail-flick suppression when given systemically. Because neither systemic nor intrathecal naloxone had any effect on base-line tail-flick latencies, we conclude that the inhibition of the tail-flick response resulting from microstimulation in the ventromedial medulla is mediated by a spinal opioid synapse.

Animals↗
PubMed1982

Post-operative pain: effect of extent of injury and attention.

The relationship to pain level of extent of injury (as measured by number of teeth extracted) and attention paid to the injury (as measured by frequency of pain ratings) was studied in patients with dental postoperative pain. Patients had either 2 or 4 impacted wisdom teeth removed and rated their pain either 2 or 5 times during the experiment. A positive correlation was found between extent of injury and reported pain level as well as between frequency of pain rating and pain level. The correlation between frequency of pain rating and pain level was found only in patients with 4 teeth extracted. To our knowledge, this is the first study which quantitatively evaluates the relationship between amount of injury and level of pain. This study also suggests that the degree to which manipulations of psychological variables alter an individual's pain perception may depend on the extent of injury.

Adolescent↗
PubMed1981

Naloxone-reversible analgesia produced by microstimulation in the rat medulla.

Using microstimulation of the rostral medulla in the barbiturate-anesthetized rat, a map was constructed of loci for inhibition of the tail-flick response to noxious heat. Low threshold sites (less than or equal to 10 microA) were found in both the nucleus raphe magnus and the nucleus reticularis paragigantocellularis. Chronaxie determinations indicate that analgesia was not produced by activation of large myelinated axons of passage. Systemic naloxone only antagonized the inhibition generated from stimulation at low threshold sites. Inhibition from higher threshold sites, for example from the nucleus reticularis gigantocellularis, was not naloxone reversible. Depending on the area stimulated, either an opioid-or a non-opioid-mediated inhibition results from microstimulation within the rat medulla.

Afferent Pathways↗
PubMed1981

ACTH1-24 blocks opiate - induced analgesia in the rat.

Samples of 1 microliter containing 15 microgram of morphine sulfate with or without 1 microgram of synthetic ACTH were injected into the fourth ventricle of rats. The inclusion of ACTH eliminated the analgesic effect of morphine as evaluated by the tail-flick test, both in restrained and in unrestrained, lightly sedated animals. The same result was obtained when beta-endorphin was used to bring about analgesia. Since the effect of the peptides was shown to be mediated by central actions alone, the results are discussed in light of the brain ACTH/beta-endorphin system.

Adrenocorticotropic Hormone↗
PubMed1981

Pain II: new approaches to management.

There is an intrinsic analgesia system in the brain with both endogenous opioid and biogenic amine links. This system provides a basis for understanding how different therapeutic approaches relieve pain. The present review critically evaluates the analgesic efficacy of the following therapies: placebo administration, transcutaneous electrical nerve stimulation, acupuncture, intrathecal and epidural opiate injection, electrical stimulation of the brain, and psychotropic drugs.

Acupuncture Therapy↗
PubMed1980

A study of the quantal (all-or-none) change in reflex latency produced by opiate analgesics.

The properties of opiate-induced changes of tail-flick latency were studied in the rat. (1) Morphine and pentazocine produced a stepwise increase in latency which rose from near baseline to cut-off (usually greater than 20 sec) in less than 30 sec. Abrupt return to pre-treatment latencies was observed either spontaneously or when the rat was back-titrated with the narcotic antagonist naloxone. (2) The proportion of rats showing this stepwise change increased with increasing dose; however, the step itself was independent of dose. The same step was produced by a slow, constant infusion of morphine but was not produced by ice-water stress or barbiturate administration. (3) Increasing heat intensity to the tail shortened the baseline latency and raised the mean dose of morphine required to produce a step latency increase. (4) A step increase in latency was also observed when paw withdrawal instead of tail-flick was measured. We hypothesize that the analgesic behavior described partly defines the operating characteristics of an intrinsic endorphin-mediated analgesia system which mediates narcotic suppression of withdrawal reflexes.

Animals↗
PubMed1980

Dissociation of supraspinal and spinal actions of morphine: a quantitative evaluation.

Opiate suppression of spinal withdrawal reflexes was tested in rats with lesions of several spinal funiculi to determine the relative contribution of supraspinal descending systems. The latency of tail-flick to noxious heat was used to assess "analgesia". The effect of lesions of dorsolateral funiculus (DLF), dorsal columns (DC) and ventral quadrant (VQ) were compared to that of sham operations. None of the lesions produced a change in baseline latency. Each animal was tested with varying doses of morphine sulfate over several weeks. Only DLF lesions consistently antagonized tail-flick suppression by morphine across the dose range studied (5-15 mg/kg i.p.), although VQ lesions were somewhat effective. The reduction of morphine's action was proportionally greater for lower doses. The results indicate that both spinal and supraspinal sites contribute significantly to the analgesia produced by systemic administration of opiates.

Animals↗
PubMed1979

The origin of descending pathways in the dorsolateral funiculus of the spinal cord of the cat and rat: further studies on the anatomy of pain modulation.

There is considerable evidence that the dorsolateral funiculus (DLF) of the spinal cord contains descending pathways critical for both opiate and brainstem stimulation-produced analgesia. To obtain a comprehensive map of brainstem neurons projecting to the spinal cord via the DLF, large injections of horseradish peroxidase (HRP) were made into the lumbosacral spinal cord of cat and rat. These injections were made caudal to midthoracic lesions which spared only a single DLF or ventral quadrant (VQ); thus only those neurons whose axons descended in the spared funiculus would be labelled. Cells with descending axons in the VQ were concentrated in the medullary nucleus raphe pallidus and obscurus, nucleus retroambiguus and in various subregions of the reticular formation including the nucleus reticularis ventralis, gigantocellularis, magnocellularis, pontis caudalis and pontis oralis. Significant numbers of neurons were also found in medial and lateral vestibular nuclei and in several presumed catecholamine-containing neurons of the dorsolateral pons. In the rat, but not in the cat, considerable numbers of cells are present in the mesencephalic reticular formation just lateral to the periaqueductal gray. In both species, some cells were found in the paraventricular nucleus of the hypothalamus. Brainstem cells projecting in the DLF were concentrated in the nucleus raphe magnus and in the adjacent nucleus reticularis magnocellularis, ipsilateral to the spared funiculus. Significant numbers of cells were found in the dorsolateral pons, differing somewhat in their distribution from those projecting in the VQ. DLF-projecting cells were also present in the ipsilateral Edinger-Westphal nucleus and periaqueductal grey contralateral red nucleus of the midbrain and in the ipsilateral hypothalamus. Smaller projections from other sites are described. These results are discussed in terms of the differential contribution of several brainstem neuronal groups, including the serotonergic nucleus, raphe magnus, the ventromedial reticular formation of the medulla, and various catecholamine-containing neurons of the dorsolateral pontine tegmentum to the analgesia produced by opiates and electrical brain stimulation.

Animals↗
PubMed1979

Evidence that an excitatory connection between the periaqueductal gray and nucleus raphe magnus mediates stimulation produced analgesia.

Both electrical stimulation and injection of morphine into the midbrain periaqueductal gray (PAG) produce analgesia in the rat. There is evidence that this analgesic effect is mediated by a descending system that involves nucleus raphe magnus (NRM) and adjacent reticular formation. In the studies reported here, the activity of the cells in the PAG was increased by microinjection of glutamate in this area and its effect on both the activity of single cells in the NRM and on a flexion reflex elicited by noxious heat was measured. It is shown that an increase in the firing rate of the cells in the PAG is associated with a raised threshold for flexion and is also correlated with an increase in the firing rate of a majority of the cells in the NRM. This effect on the flexion reflex can be abolished by (a) lesion of the nucleus raphe magnus and a small area of the reticular formation surrounding this nucleus and (b) by nalazone 20 min after its i.v. injection. It is concluded that there is an excitatory connection between the periaqueductal gray and the nucleus raphe magnus and that activation of this system can cause analgesia.

Animals↗
PubMed1979

Morphine presynaptically inhibits a ganglionic cholinergic synapse.

The effects of morphine on synaptic transmission through the inferior mesenteric ganglion (IMG) were studied using intracellular recording techniques. Morphine produced a reversible, dose-dependent reduction in the quantal content of the synaptic potentials with little or no effect on quantal size or the properties of the ganglion cells. This effect of morphine was antagonized by naloxone suggesting the presence of specific preganglionic opiate receptors.

Animals↗