Particulate inhalation during the removal of amalgam restorations.

An aerosol that contains amalgam particles is created when a high-speed hand-piece is used to remove an existing amalgam restoration. Those particles smaller than 10 microns are considered to be fully respirable. This means that a significant percentage of the particles have the potential to travel to the terminal alveoli, where they may become lodged. Long-term exposure to fully respirable particles may compromise a person's respiratory function. Amalgam restorations were placed in the typodont teeth of a mannequin designed to simulate the head and the respiratory tract of a patient. The amalgam restorations were removed under three experimental conditions: dry cut (control), wet cut (water spray) with high-velocity evacuation, and wet cut with high-velocity evacuation and a rubber dam. Particulate exposure was evaluated in the simulated respiratory tracts of the patient and the dentist that were equipped with ambient particle sizing samplers. Use of water spray and high-velocity evacuation significantly reduced patient exposure to particles. The use of a rubber dam, together with water spray and high-velocity evacuation, was responsible for a further significant reduction of exposure to particles when compared with water spray and high-velocity evacuation alone. The dentist, however, was exposed to moderate levels of fully respirable particles for all conditions tested. It is therefore recommended that all dental personnel wear face masks while removing existing amalgam restorations.

Gastrointestinal hormones and the quantitation of spontaneous duodenal motor activity.

This is a survey of the results of recent investigations on gastrointestinal (GI) peptide hormones. In addition to the classical GI hormones (secretin, gastrin, and cholecystokinin-pancreozymin (CCK-PZ], there are at least nine other peptides whose structures and GI effects are known. These include vasoactive intestinal polypeptide (VIP), gastric inhibitory polypeptide (GIP), motilin, pancreatic polypeptide (PP), substance P, neurotensin, somatostatin, enkephalins, and a bombesin-like gastrin-releasing peptide. It is now obvious that the traditional distinctions between hormones, neurotransmitters, and paracrines are rapidly becoming obsolete, as the actions and interactions of these substances within the complex motor system of the GI tract are gradually revealed. The study of perturbed states and toxic effects on the motor function of the small intestine is complicated by the integration of the activity of the small intestine with the activities of the body as a whole. A contemporary approach for evaluating intestinal contractile activity is described that uses computer assistance to measure the intercontractile interval (ICI). This technique may prove useful in assessing the effects of toxicological agents on spontaneous intestinal motor activity in vitro when the agents are delivered to the target sites by physiological mechanisms, in contrast to adding them to the tissue bath.

Comparison of the inhibitory effects of spermine, papaverine and adrenaline upon isolated segments of the rat small intestine.

In the rat isolated duodenal and ileal segments the active baseline force and spontaneous contractile frequency were inhibited by spermine; the relative potencies, estimated as an ED50, were adrenaline papaverine spermine. The changes in baseline force, but not frequency, due to spermine were sensitive to increased calcium. The duodenum was always more sensitive to papaverine and adrenaline, but the relative sensitivities of the duodenum and ileum were essentially equal for spermine. Inasmuch as the gastrointestinal mucosa of most species contains an abundance of polyamines, these results suggest that, in its free form, spermine may subserve a functional role in the inhibition of gastrointestinal motility.

LC50 values for rats acutely exposed to vapors of acrylic and methacrylic acid esters.

Acute exposure studies were conducted using adult male Sprague-Dawley rats to obtain LC50/24 concentrations for the common esters of acrylic and methacrylic acids. The order of acute toxicity was determined to be methyl acrylate greater than ethyl acrylate greater than butyl acrylate greater than butyl methacrylate greater than methyl methacrylate greater than ethyl methacrylate. Four-hour daily exposures (excluding weekends) of young adult male rats to 110 ppm methyl acrylate in air over a period of 32 d failed to produce significant differences in body or tissue weights, blood chemistries, gross metabolic performance, and spontaneous small-intestinal motor activities when compared with a sham-exposed group.

Mechanisms of the secretory and motor responses of the Brunner's gland region of the intestines to duodenal acidification.

The secretory and motor responses of the Brunner's gland region of the duodenum to luminal acidification were examined in rabbits anesthetized with urethan. Isomotic solutions of sodium chloride (pH 7.2) were perfused continuously through adjacent in situ segments. The pH of the perfusate of the proximal segment was changed to 2.0 for 30 min. Perfusion pressure (motor response) and volume and hexosamine concentration (secretory response) of the effluent were recorded for 3 h. The motor and secretory responses to luminal acidification were examined after intravenous (atropine) or intraluminal (lidocaine) pretreatment. Responses to intravenous infusions of serotonin or secretin were determined, also. Both atropine and lidocaine eliminated the initial motor and secretory responses of the proximal segment. Lidocaine eliminated the delayed secretory response of the distal segment. Serotonin caused initial motor and secretory responses, but secretin caused a delayed secretory response only. These results suggest that duodenal acidification elicits a two-phase increase in Brunner's gland secretion, the first being motor-dependent and the second motor-independent. The initial motor response was mediated by a local reflex composed of cholinergic and perhaps tryptaminergic receptors. The delayed secretory response was mediated by local and nonlocal, possibly hormonal, factors. Increased duodenal motility may provide a vehicle for the rapid expulsion of mucus, and thereby serve an important role in the function of the Brunner's glands.

Adrenergic control of somatostatin release.

The effects of adrenergic stimulation and suppression on somatostatin (SS), insulin, and glucagon release were studied in intact dogs. Isoproterenol, a beta-adrenergic agonist, significantly increased portal venous and arterial levels of SS and arterial levels of insulin and glucagon. Propranolol, a beta-adrenergic antagonist, significantly decreased portal venous SS and suppressed the isoproterenol-stimulated increases in the levels of SS, insulin, and glucagon. alpha-Adrenergic stimulation (propranolol plus epinephrine) decreased portal venous SS and arterial insulin. Phentolamine, and alpha-adrenergic antagonist, increased portal venous and arterial SS and arterial glucagon. These data suggest that in intact dogs, stimulation of beta-adrenergic receptors enhances the release of SS, insulin, and glucagon, while stimulation of alpha-adrenergic receptors inhibits the release of SS and insulin without having a definitive effect on glucagon.

Neural and hormonal control of Brunner's gland secretion.

For many years it has been speculated that the physiological function of Brunner's glands was to secrete mucus to protect the proximal duodenum from the corrosive effects of acidified gastric juice. However the control of Brunner's gland secretion remains an enigma. Some evidence exists which indicates both cholinergic and adrenergic innervation of these glands, but current consensus weighs heavily in favor of a hormonal stimulus for glandular secretion. This is based in part on evidence obtained from denervated Brunner's gland pouches following a feeding stimulus. a number of hormones and hormone-like substances have been investigated as possible mediators in this secretory response, however, no specificity was ever demonstrated. The inability to pinpoint a given substance as a common mediator can be attributed to the fact that most active agents employed also affect duodenal motility. We present evidence that Brunner's gland secretion can be observed to be a diphasic response. The initial, transient response is always observed in the presence of increased duodenal motility. The sustained response does not require duodenal motility and is probably hormonally mediated.

Central nervous system effects of methyl methacrylate vapor.

Inhalation experiments were conducted by exposing mature male Sprague-Dawley rats to methyl methacrylate (MMA) monomer vapor in air. The effects upon central neuronal activity associated with acute exposures of chloralose-urethanized rats to monomeric MMA vapor concentrations are summarized in this report. The most remarkable and readily apparent phenomenon was the depression of multiple-unit electrical activity in the lateral hypothalamus and ventral hippocampus of rats which were exposed to 400 ppm of MMA in air for 60 min. In marked contrast, recordings made from the parietal cortex, cerebellum, dorsal hippocampus, medial amygdala, ventral medial hypothalamus, anterior hypothalamus, septum, and mammillary body following comparable exposures showed insignificant changes in multiple-unit electrical activity.

Subacute inhalation toxicity testing with iodoform vapor.

Subacute inhalation experiments were conducted to determine the LC50 value for adult Sprague-Dawley rats exposed to iodoform vapor. Each dose consisted of 5 males and 5 females that were together for a 7-h exposure or sham exposure and then separated for observation over the subsequent 24-h period. The rats were deprived of food and water during actual exposure or sham exposure. Exposures were conducted in a custom-designed 75-l glass chamber. Vapor concentrations were verified in samples taken from the exposure chamber. Under the conditions of the experiments the 7-h LC50 was found to be 183 ppm. The second objective of these experiments was to determine the toxic effect of iodoform vapor on rats exposed for 7 h/d for 7 consecutive days. Three groups of 5 young adult male and 5 female rats were used. One group served as a sham control and the other groups were exposed to 1 and 14 ppm iodoform vapor. No significant differences were noted in food and water intake, urine and feces output, and intestinal transit performance in either exposed group. No remarkable changes were noted in SMA 12/60 blood values for either exposed group. The only histopathological manifestation noted was the presence of mineralized deposits in the medullary renal tubules of some of the rats from the 14-ppm group.

Acute and subchronic toxicity studies of rats exposed to vapors of methyl mercaptan and other reduced-sulfur compounds.

Acute inhalation experiments were conducted to determine 24-h LC50 values for adult Sprague-Dawley rats of both sexes exposed to vapors of methyl mercaptan and other reduced-S compounds for 4 h periods. Using calculated gas concentrations, the following LC50 value for each gas and combination was determined: metyhl mercaptan, 675 ppm; dimethyl sulfide, 40,250 ppm; dimethyl disulfide, 805 ppm; hydrogen sulfide, 444 ppm; and an equimolar mixture of methyl mercaptan, dimethyl sulfide, and dimethyl disulfide, 550 ppm. The effects of body and tissue weights, gross metabolic performance, O2 consumption, systolic blood pressure, various blood parameters, and intestinal transit time associated with 3-mo exposures of young adult male rats to chemically verified concentrations of 2, 17, and 57 ppm methyl mercaptan vapor are summarized in this report. No mortality was experienced by any group. Histopathological findings were essentially nil except for microscopic suggestions of liver damage. The most readily apparent phenomenon was the decrease in body weight. Average values of terminal body weights for all exposed groups were lower than that for the sham control group. This difference was significant in the 57 ppm group and followed a statistically significant dose-related trend.

Site of alpha blockade in the demonstration of nonvagally mediated gastric acid secretion.

Results of previous reports from this laboratory have indicated that electrical centripetal vagal stimulation in the dog that has a bilateral vagotomy evokes mucus secretion from the pyloric antrum and produces an inhibition of motor activities from the stomach to the terminal ileum. We have subsequently observed that electrical central vagal stimulation after the administration of the alpha adrenolytic, phenoxybenzamine to these preparations results in general augmentation of gastrointestinal motor activity. It was also determined that electrical central vagal stimulation, using the same stimulus parameters that were stimulatory for mucus secretion, now resulted in significant increases in both volume and titratable acid secretions. The intact arterial pressor response during periods of electrical central vagal stimulation which enhanced gastric acid output in the dog that had a bilateral vagotomy eliminates the possibility that the mechanism of acid release involves the necessary suppression of the systemic pressor reflex. It is further concluded that the acid-enhancing effect of phenoxybenzamine appears to be limited to the pyloric antrum, even though the acid is secreted from the corpus. This suggests that the neural portion of the acid effect is confined to the antrum. We have successfully demonstrated that the acid-enhancing reflex effect is associated with a definite rise in the concentration of circulating gastrin.

A dual mechanism for intestinal motor effects of methyl methacrylate vapor.

The influence of methyl methacrylate (MMA) vapor on the motor activity of the isolated guinea pig ileum is summarized in this report. MMA vapor was delivered to innervated and denervated strips via the tissue bath air supply at a concentration of 755 +/- 38 ppm. Innervated strips usually showed spontaneous motor activities (sma) which developed shortly after the muscle was mounted. None of the denervated strips exhibited sma. Upon exposure to MMA vapor, there was a rapid and significant decrease in sma and in the contractile responses to electric field stimulation and 0.01 mg acetylcholine administration. Denervated strips demonstrated a similar reduction in response magnitude to electric field and drug stimulation but required a longer time period. The persistence of the MMA-induced inhibitory response of the denervated strips indicates that the inhibitory effect is partly due to a direct action of the agent upon the contractile mechanism of the small intestine.