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Biomedical subjects

W M Davis

Publications and source records attributed to W M Davis.

17 recordsLinked to original sources
PubMed1979

Extravasation cyst diagnostic curettement: a treatment. Report of 15 cases and suggested treatment.

Fifteen cases of extravasation lesions of the mandible have been treated. In six cases, the lesions were entered surgically, explored, and directly curetted following preliminary diagnosis by needle aspiration. Healing was uneventful in all cases, and bone regeneration occurred rapidly. Hemorrhage was easily controlled, and the surgery was considered a minor procedure. Nine cases were treated by a combined diagnostic-curettement technique. The entire procedure was quickly performed under local anesthesia. There was little chance of injury to surrounding structures, and there were few postoperative sequelae. The resolution of the lesion and bone regeneration occurred in a time span similar to that of the surgical treatment of lesions.

Adolescent↗
PubMed1979

Reinforcement with intragastric infusions of ethanol: blocking effect of FLA 57.

Suppression of oral intake of ethanol by FLA 57 has been reported for rats and was attributed to an inhibition of dopamine beta-hydroxylase. We have demonstrated the ability of FLA 57 (50 mg/kg, IP) to suppress bar-pressing for intragastric (IG) delivery of doses of ethanol (25 mg/kg). This indicates that the effect on oral intake of ethanol may not be attributed to a taste factor, e.g., a decreased palatability of the ethanol solution. The same dose of FLA 57 did not suppress responding for IG doses of sweet milk. Thus, there was not an impairment of appetitive behavior in general through some nonspecific depressant or toxic action. Furthermore, the primary reinforcing action of ethanol, when used to establish a buzzer as a conditioned reinforcer through repeated pairings, was blocked if FLA 57 was given before pairings. This was evidenced by a failure of such rats to bar-press above the baseline level in a later test of conditioned reinforcement, which contrasted with the increased responding seen for rats receiving saline instead of FLA 57 before ethanol. These data support the previous findings on oral ethanol and confirm that FLA 57 can impair the mechanism by which ethanol produces positive reinforcement in rats.

Animals↗
PubMed1979

Toxic interaction between narcotic analgesics and inhibitors of catechol-O-methyltransferase.

A lethal synergism between morphine and tropolone, an inhibitor of catechol-O-methyltransferase, was previously noted in adult male Holtzman rats. The present research demonstrates that this phenomenon generalizes across factors of sex, age, strain (Sprague--Dawley, Wistar) and species (Swiss albino mice). Acute toxicity was also significantly increased (1.5--1.9 times) in the case of codeine, methadone, meperidine and levorphanol, but to a lesser extent than for morphine (4.0 times) in the S-D strain. Another COMT inhibitor, 3,5-dihydroxy-4-methoxybenzoic acid, interacted with morphine in S-D rats to an equal degree as did tropolone. Post-treatment with 1 mg/kg of naloxone in rats or naltrexone in mice reduced the high lethality associated with morphine plus tropolone. There was a pronounced lowering of whole brain norepinephrine (NE) level after morphine plus tropolone in Wistar rats with doses of each component that alone caused no change in NE. Brain dopamine (DA) was elevated by tropolone and by its combination with morphine. Each drug alone caused slight lowering of brain serotonin. Enhancement by tropolone of the toxicity of (+)-amphetamine in mice and rats was of similar magnitude as for morphine. The possible role of brain NE and/or DA in the sensitivity to acute toxic effects of opioids in rodents is suggested by these data, as well as a parallel in this regard with amphetamine-type stimulants.

Aging↗
PubMed1979

Lethal synergism between morphine or other narcotic analgesics and propranolol.

Interactions of (+/-)-propranolol HCl with various narcotics were determined in albino rats. The 24-h intraperitoneal (i.p.) LD50 of morphine sulfate + saline was 15--16 times greater than for morphine + propranolol in both sexes although morphine was nearly twice as toxic to males as to females. The potency ratios for LD50's with saline vs. with propranolol were: codeine, 1.9, (+/-)-methadone, 6.0; (-)-alpha-acetylmethadol, 2.8 (72 h). The toxicity of levorphanol also was greatly increased with propranolol, but the dose-effect relationship showed non-parallelism vs. levorphanol + saline. Albino mice and mongrel dogs also showed synergism between morphine and propranolol. Mortality after morphine and propranolol was antagonized by naloxone or naltrexone in rats and mice. The potency ratio in rats for morphine + saline vs. morphine + practolol was 3.5. However, the synergism between propranolol and the narcotics probably was unrelated to beta-adrenergic blocking effects of propranolol because of the apparent equivalence of (+)-, (-)- and (+/-)-propranolol in rats for synergism with morphine.

Analgesics, Opioid↗
PubMed1979

Experimental diazepam intoxication in rodents: physostigmine and naloxone as potential antagonists.

The ability of physostigmine and naloxone to reverse the loss of righting reflex (LRR) induced by diazepam was tested in mice and rats. Physostigmine was ineffective under our test conditions, but high doses of naloxone reduced the duration of LRR in both species. However, the LD50 of diazepam in mice was unaltered by 100 or 150 mg/kg of naloxone given 1 hr after LRR to model an antidotal situation. Use of a longer duration narcotic antagonist, naltrexone (172 mg/kg), in the same design likewise failed to elevate the LD50 for diazepam. These data give limited support to prior suggestions for clinical usefulness of naloxone, although not for physostigmine, in the management of intoxication caused by diazepam.

Animals↗
PubMed1979

Morphine lethality in rats: effects of various central receptor blocking agents.

A previous report of a lethal potentiation between sublethal doses of morphine and the beta-adrenergic blocker propranolol was confirmed for Sprague-Dawley rats. An alpha-adrenergic blocker, phentolamine, also showed a lesser but significant potentiation, as did a moderate dose of atropine. No synergism was noted between morphine and methylatropine, haloperidol or methysergide. Phentolamine and a lower dose of atropine, which did not synergize with morphine, both added significantly to the lethality of the combination of morphine and propranolol, whereas methylatropine, haloperidol and methysergide had no significant effect to synergize or antagonize mortality.

Adrenergic alpha-Antagonists↗
PubMed1977

Alcohol-associated conditioned reinforcement.

Research was conducted to examine the ability of alcohol to impart conditioned reinforcement. Rats were allowed to self-administer solutions of either saline or alcohol (25, 50, and 100 mg/kg/infusion) by the intragastric route. Superimposed on the infusion interval was a buzzer (conditioned reinforcing stimulus). Tests during extinction revealed that conditioned reinforcement had been acquired. Results also indicated that as the paired unit dose was increased, potency of the conditioned reinforcer increased. In a second study, the lever-pressing response, which produced saline infusion and the buzzer, became available only subsequent to 5 sessions of pairing the buzzer with infusions of saline or alcohol. The results indicated that lever pressing increased with increasing unit dosage of alcohol infusions in prior pairings.

Animals↗
PubMedDate not supplied

Noradrenergic role in the self-administration of morphine or amphetamine.

The role of brain noradrenergic neurons in mediating the reinforcing properties of small intravenous doses of morphine and d-amphetamine was investigated by pretreatment of rats with the norepinephrine-depleting agents diethyldithiocarbamate and U-14,624, inhibitors of dopamine-beta-hydroxylase (DBH). Such treatment prevented the reacquisition of a self-administration response (bar-press) for morphine (32 mug/kg/injection) or d-amphetamine (15 mug/kg/injection) made available on a CRF schedule. Pretreatment with a DBH inhibitor also prevented the development of a secondary (conditioned) reinforcer based on primary reinforcement assosiated with either drug. Observations indicating that the orienting reflex was intact are taken as evidence that depressant effects of the DBH inhibitors were not severe enough to disrupt the associative process. Therefore, any effect on learning does not seem sufficient to explain the present results. Thus, it is inferred that the mechanisms mediating reinforcement for both morphine and amphetamine were disrupted by the inhibition of central noradrenergic functions.

Animals↗