P-10--its potential as a posterior composite.
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Composite Resins↗
Biomedical subjects
R W Phillips
Publications and source records attributed to R W Phillips.
Fluid therapy for diarrheic calves. What, how, and how much.
The pathophysiologic consequences of neonatal diarrhea in calves are presented. A brief discussion of intestinal function, nutrient absorption, and osmolar effects follows. A rationale for appropriate fluid therapy is presented, and comparison of some currently marketed products are made.
Animals↗
Malabsorption due to selected oral antibiotics.
This article represents an overview of recent research conducted on antibiotic-induced malabsorption in calves. The authors feel strongly that this work identifies a serious and ill-defined problem in the management of neonatal calves. Too often the solution utilized by veterinarian and stockmen for controlling neonatal diarrhea has been to administer oral antibiotics. In many cases, this has been done on the basis of antibiotic sensitivity testing, an approach that seems appropriate. Unfortunately, little consideration has been given to the relative sensitivity of the neonatal intestinal mucosa, with its very rapid turnover, to the potentially detrimental effects of oral antimicrobial therapy. The data that we have collected over the past 3 years conclusively demonstrate that high levels of four commonly used oral antibiotics, especially neomycin and chloramphenicol but also tetracycline and ampicillin, can cause a malabsorption diarrhea in normal calves. This action is not due to viral agents or overgrowth of resistant microbes but is the result of direct modification of the intestinal mucosa. Extrapolation of these data to different dose levels may not be accurate. Oral antibiotics may be of value in treating neonatal enteritis. Conversely, there can be too much of a good thing, and many cases of chronic diarrhea following use of oral antibiotics may be the result of an overenthusiastic and prolonged dosage regimen. Be cautious!
Animals↗
Milk replacers for the neonatal calf.
A rather long list of broad generalizations exist regarding milk replacers for calves. At least two more general statements should be added to that list. Most broad generalizations regarding milk replacers should be applied cautiously; and if young calves (less than 2 to 3 weeks) are to be fed milk substitutes, the products should be of high quality. Our primary goal in feeding baby calves should be health oriented--that is, not to pre-dispose to or cause diarrhea through diet. This means using milk-source ingredients in milk substitutes targeted for young calves. The preponderance of data presented in this article underscores that statement. Milk replacers containing nonmilk sources of major nutrients are better fed to older calves.
Animal Feed↗
Effects of various agents in cleaning cut dentine.
The effectiveness of various agents in cleaning cut dentine surfaces was investigated. Attempts to remove the smeared layer of dentine after the preparation of a cavity showed that a polyacrylic acid (Durelon liquid) gave the best result, flour of pumice or a prophylaxis paste (Prevodontic) used with a rubber cup were effective, but 3% hydrogen peroxide and a cavity cleaner (Cavilax) were not. The only effective agents following the use of a zinc oxide eugenol temporary cement were the flour of pumice and prophy paste.
Acetates↗
Properties of microfilled composite resins as influenced by filler content.
Two series of composite resins were prepared with a light-cured urethane dimethacrylate matrix to which varying amounts of two types of silanated silica particles were added. One series contained volume fractions ranging from 15.8 to 28.8% silica particles of 20 nm in diameter (Type I filler) and the other series volume fractions of from 24 to 49.4% of an agglomerated silica particle of 40 nm in diameter (Type II filler). Tests were conducted to determine the effect of filler level on: depth of cure as determined by hardness measurements; color stability in both UV light and water; water sorption with time; hardness; compressive strength; strain behavior in slow compression; and resistance to toothbrush abrasion and wear by hydroxyapatite. Analysis of the data obtained for these two microfilled series indicate that increased filler levels result in trends for increased depth of cure, color stability, hardness, compressive strength, and stiffness, while water sorption and resistance to both toothbrush abrasion and wear by hydroxyapatite were reduced. These trends were more pronounced for the Type II filler series than for the Type I filler series. However, there was a greater differential in filler levels within the Type II series than within the Type I series.
Acrylates↗
Effect of filler content and size on properties of composites.
Two series of dental composites, along with the unfilled resin matrix, were examined to determine the effects of filler level and size on selected properties. Both series were prepared by incorporating a silanated barium borosilicate filler into a visible-light-activated polyphenylene polymethacrylate resin matrix. One series had a filler particle size of 2 microns, with filler levels of 20, 40, 45, 50, and 53% (vol). The second series contained a 15-microns filler in amounts of 20, 40, 50, 60, and 65% (vol). Tests conducted included: depth of cure as evaluated by hardness, water sorption, compressive strength, stress-strain behavior under slow compression, toothbrush abrasion, and wear by hydroxyapatite. Analysis of the data indicated that increased filler levels resulted in increased hardness, compressive strength and stiffness, and decreased water sorption. Also, there was a slight trend toward improved depth of cure. Incorporation of the 2-microns filler decreased the abrasion resistance of the resins to toothbrushing as compared with the unfilled resin, while addition of the 15-microns filler improved resistance. All filled resins exhibited a significant improvement in resistance to wear by hydroxyapatite as compared with the unfilled resin. There was a trend for increased wear with increased filler level. The particle size of the filler appeared to have a moderate influence on the properties. When compared with 15-microns filled resins of the same filler levels, the 2-micron filled series appeared to have inferior properties in terms of depth of cure, compressive strength, water sorption, and resistance to toothbrush abrasion. Properties which were less affected by particle size were hardness, stiffness, and wear resistance to hydroxyapatite.
Chemical Phenomena↗
Hyperosmotic oral replacement fluid for diarrheic calves.
Twenty-five diarrheic neonatal calves, none of which was recumbent, were used to determine oral efficacy of a commercial product for fluid replacement, either by suckle or intubation. Changes in plasma protein, glucose, sodium, potassium, and osmolality as well as blood lactate and PCV were measured. Core body temperature and surface temperature at the hock and fetlock were monitored. Data were analyzed for interaction with time and response according to clinical condition. Significant differences (P less than 0.05) following therapy were restricted to glucose and potassium changes. Beneficial posttreatment trends were observed in cutaneous temperature, blood lactate, plasma protein, and PCV values.
Animals↗
Report of the Committee on Scientific Investigation of the American Academy of Restorative Dentistry.
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Adult↗
Resistance of calcium hydroxide preparations to solubility in phosphoric acid.
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Calcium Hydroxide↗
Naloxone therapy in awake endotoxemic Yucatan minipigs.
Twelve Yucatan miniature pigs were fitted with jugular, portal, hepatic vein, and carotid artery catheters, and hepatic artery and portal vein flow cuffs to quantitate portosystemic and transhepatic kinetics. Seventy-two hours later they were placed in slings, and following a 3-hr control period were infused with Escherichia coli endotoxin at 15 micrograms/kg/hr for 6 hr. Eight were controls and 4 received a primed (2 mg/kg) continuous infusion (2 mg/kg/hr) of naloxone 1 hr after initiation of endotoxin. In the naloxone group, arterial hypotension developed by 60 min. Arterial pressure increased to 125 mm Hg by 80 min (20 min post naloxone) and maintained this level for 3 hr. [6-3H]Glucose-derived rate of disappearance (Rd) values were increased above their own control period at 60 and 80 min, but were approximately 55% lower than untreated controls. Rate of appearance (Ra) values remained unchanged in the naloxone group resulting in a net glucose deficit. After 1 hr of endotoxin, blood pyruvate increased from 1.0 to 1.8 mg%, reached 3.3 mg% at 80 min, and remained elevated. Blood lactate similarly increased from 11 to 35 mg% by 60 min, increasing further to 82 mg% 20 min after naloxone infusion, in concert with signs of severe distress. Portal and hepatic total O2 decreased by 60 min and 100 min, respectively, reflecting depressed hepatic O2, input. Lethality was 75% in naloxone-treated pigs by the end of the experiment, vs 0% in untreated animals. Naloxone improves some hemodynamic parameters. However, in these conscious postsurgical patients, naloxone blocked some beneficial effects of endogenous opiates resulting in severe metabolic derangements and increased mortality.
Animals↗
Intestinal metabolism of orally administered glucose and fructose in Yucatan miniature swine.
Absorption rates and metabolism of orally administered glucose and fructose were quantitated in conscious, overnight-fasted, Yucatan miniature swine. The pigs were surgically prepared, with catheters in the portal vein and a carotid artery. A continuous wave Doppler flow cuff was placed around the portal vein. Four to 7 days after surgery, arterial and portal venous blood samples were obtained in the basal state and at 15-minute intervals for 4 hours following oral administration of glucose or fructose (1.5 g/kg body weight). Absorption rates and intestinal metabolism were calculated from portal blood flow and arterio-venous concentration differences for glucose, fructose and lactate. Oral fructose administration was accompanied by a rise in intestinal lactate production, which correlated significantly with the fructose absorption rate. Intestinal lactate output during fructose absorption could account for 12% of the fructose absorbed or metabolized. A small rise in glucose output from the gut was also observed. In contrast, after oral glucose administration, only a modest rise in intestinal lactate output was noted. It could account for only 2% of the glucose absorbed or metabolized. No correlation between glucose absorption rate and intestinal lactate output was observed. These studies indicate that a significant portion of oral fructose is converted to lactate during absorption but that the major part enters the portal vein as fructose. Only minimal intestinal metabolism of ingested glucose occurs.
Administration, Oral↗
Long-term F release from glass ionomer cements.
Fluoride release from three commercial glass ionomer filling cements and three glass ionomer luting cements was measured in the laboratory over a 12-month period. Fluoride release from these glass ionomer cements was compared with that released from a silicate, silicophosphate, and a fluoride-containing polycarboxylate cement. The fluoride released from the glass ionomer cements throughout the one-year period was similar, both in quantity and pattern, to that released by the silicate cement. The silicophosphate cement tended to release fluoride in somewhat lesser amounts, while the amount of fluoride released by the polycarboxylate was negligible after the first few days. Analysis of these data indicates that these glass ionomer cements probably possess anticariogenic properties similar to those of silicate cement.
Chemical Phenomena↗
In vivo and in vitro wear of potential posterior composites.
The influence of cavity size, material composition, and curing mechanism on wear resistance of Class II MOD resin restorations was analyzed quantitatively. Wear resistance tends to increase both as cavity size decreases, and also from chemical- to light- to heat-cured. As to wear, among the composite resins tested, there was no acceptable resin-based amalgam substitute.
Chemical Phenomena↗
Effects of captopril on hemodynamic and metabolic parameters in awake endotoxemic Yucatan minipigs.
Angiotensin II (AII), a potent vasoconstrictor, contributes to ischemic and decompensatory phases of shock. Captopril may benefit vital organ and tissue perfusion by inhibiting AII formation. We fitted 13 approximately 50-kg pigs with jugular, portal, hepatic vein, and carotid artery catheters, and hepatic artery and portal vein flow cuffs to quantitate portosystemic and transhepatic kinetics. We placed them in slings 72 hr later and following a 3-hr control period, they were infused with E. coli endotoxin at 15 micrograms/kg/hr for 6 hr. We kept eight as controls and five received a primed (2 mg/kg) continuous infusion (2 mg/kg/hr) of captopril 1 hr after initiation of endotoxin. Arterial hypotension developed by 60 min and hypoglycemia by 100 min in both groups; captopril had no effect on these parameters. Blood lactate increased from 7.8-32.1 mg/dl 80 min postendotoxin, and for the third to fifth hours of endotoxin infusion was significantly higher than those of the control group. 6-3H-glucose-derived appearance (Ra) values remained at 1.88-2.35 mg/kg/min throughout the experiment. Glucose disappearance (Rd) values were elevated from 60-120 min of endotoxin, increasing to 2.68-3.13 mg/kg/min versus 1.86 mg/kg/min preendotoxin. These changes corresponded to those in lactate, and incurred only a brief significant net glucose deficit (%Rd-%Ra) that peaked at 61.1% at 100 min. For 140-360 min postendotoxin, glucose balance was at most 8.3% in deficit (200 min) and 13.6% in positive balance (280 min) versus a net deficit of up to 25.4% (220 min) for the untreated group for much of the experiment. Portal and hepatic venous blood flow in captopril-treated pigs was lower than that in untreated pigs before endotoxin (8.2 and 10.0 ml/kg/min versus 12.9 and 17.9 ml/kg/min, respectively), but was not depressed following endotoxin infusion, versus 50% reductions in the untreated pigs, postendotoxin. Captopril maintained hepatosplanchnic blood flow and effected modest improvements in glucose kinetics.
Animals↗
Lidocaine therapy in awake endotoxemic Yucatan minipigs. I. Metabolic parameters and glucose biokinetics.
Cellular membrane destabilization induced by endotoxin and endogenous inflammatory mediators contributes significantly to the progression of metabolic and hemodynamic dysfunction in endotoxemia. Owing to its membrane-stabilizing properties, lidocaine may prove beneficial in the treatment of endotoxic shock. Twelve 50-kg pigs were surgically fitted with jugular venous and carotid arterial catheters. Seventy-two hours later they were placed in restraint slings, and following a 3-h control period, were infused with Escherichia coli endotoxin (Difco 055:B5) at 15 micrograms/kg for 6 h. Eight were controls and four received a primed (2 mg/kg) continuous infusion (2 mg/kg/h) of lidocaine 1 h following the initiation of endotoxin infusion. In the lidocaine-treated group, arterial hypotension (113 mmHg) developed by 60 min, continued to fall to 104 mmHg by 200 min and rose terminally to 118 mmHg. These values were higher than the control group, but were below those of the control period of the lidocaine group. Six -3H-glucose-derived Rd values were increased above their own control period at 60 min, but were approximately 55% lower than in the untreated group. Ra values were not significantly changed in the lidocaine-treated group resulting in a net glucose deficit which was more profound than in untreated pigs, whose Ra values did increase. The degree of hypoglycemia was more profound in lidocaine-treated pigs from 100-260 min, stabilizing at 29-37 mg/dl. Blood lactate (70 mg/dl) was above those of the control pigs (44 mg/dl) from 160 to 220 min. U-14C-glucose-derived glucose recycling was increased above the lidocaine group's preendotoxin control period and reached values twice those of the untreated pigs' endotoxin infusion period. Compared to their own control period and the untreated group's endotoxin infusion period, percentage lactate/glucose was decreased from 40 min on. Lidocaine treatment elicited modest improvements in systemic arterial blood pressure and reduced relative glucose utilization and gluconeogenesis, but in itself, was not a sufficient therapy for endotoxic shock in this model.
Acid-Base Equilibrium↗
Lidocaine therapy in awake endotoxemic Yucatan minipigs. II. Hepatosplanchnic metabolism.
Reductions in hepatosplanchnic blood flow and oxygen delivery contribute to the hepatic metabolic dysfunction observed in endotoxemia. Through its membrane-stabilizing activity, systemic lidocaine therapy may modify visceral hemodynamics and preserve hepatocellular metabolic function in endotoxic shock. Twelve 50-kg pigs were surgically fitted with jugular, portal, hepatic venous and carotid arterial catheters, and hepatic arterial and portal venous flow cuffs to quantitate portosystemic and transhepatic kinetics. Seventy-two hours later they were placed in slings, and following a 3-h control period were infused with Escherichia coli endotoxin (Difco 055:B5) at 15 micrograms/kg/h for 6 h. Eight were controls and four received a primed (2 mg/kg) continuous infusion (2 mg/kg/h) of lidocaine 1 h following the initiation of endotoxin infusion. Hepatosplanchnic blood flow was relatively unaffected by lidocaine infusion. In both untreated and treated pigs, hepatic arterial flow decreased by 25-30%, portal venous flow fell by approximately 60%, and hepatic venous flow was reduced by 50%. Following 2 h of endotoxin infusion, net splanchnic glucose uptake was increased significantly in lidocaine-treated pigs, but not in untreated endotoxemic animals. Transhepatic lactate kinetics were unaffected by treatment, but net hepatic pyruvate uptake in the lidocaine-treated group increased as compared to the untreated group by 140 min postendotoxin, being significantly greater at 220, 280, and 320 min. Hepatic oxygen input was significantly reduced by 25-30% in both groups within 1 h of the onset of endotoxemia, but hepatic oxygen extraction efficiency increased two-to-three-fold, thereby maintaining net hepatic oxygen uptake. Despite the maintenance of hepatic oxygen uptake and improved hepatic pyruvate extraction in lidocaine treated endotoxemic pigs, no significant improvements in glucose homeostasis were incurred, leading to the conclusion that lidocaine therapy offered few significant advantages in the treatment of overall metabolic derangements during acute endotoxemia.
Animals↗