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Biomedical subjects

R W Phillips

Publications and source records attributed to R W Phillips.

At least 109 records · Page 6Linked to original sources
PubMed1984

Persistent hyperinsulinemia due to induced euglycemia in awake endotoxic minipigs.

Transient hyperinsulinemia has been incriminated as a contributing factor to endotoxin-induced hypoglycemia. However, a recent study using endotoxic minipigs noted an increase in the rate of glucose utilization prior to when hyperinsulinemia was seen. Based on this, the "misinformed beta-cell" hypothesis was proposed. If endotoxic pancreatic beta-cells experience an early increase in glucose uptake, they could over-estimate the true glycemic state and release insulin, further contributing to the hypoglycemia. Hypoglycemia would offset increased glucose uptake by the beta-cell and insulin secretion would return to basal rates, explaining the transient nature of the insulin response. According to this hypothesis, maintenance of euglycemia should elicit a sustained rather than transient insulin release. The hypothesis was tested with a euglycemic clamp technique in a group of five endotoxic (Difco 055:B5; 15 micrograms/kg/hr) minipigs (EC) compared to three nonclamped endotoxic minipigs (E). Persistent, profound hyperinsulinemia (15 ng/ml) occurred in the EC group, further supporting the hypothesis. The clamp appeared to be beneficial, since arterial pressure and pH were significantly (P less than or equal to 0.05) higher and arterial lactate levels were lower in EC pigs compared to E pigs. A significant discrepancy was noted between the radioisotope ( [6-3H] glucose)-derived rate of glucose appearance and the rate of exogenous glucose infusion (clamp), which may have been due to unaccounted for changes in glucose pool size and/or futile cycling of glucogenic substrates or glucose through glycogen and lipid.

Acid-Base Equilibrium↗
PubMed1984

Hepatosplanchnic insulin kinetics in awake endotoxemic Yucatan minipigs: the "misinformed B-cell" hypothesis revisited.

Increased pancreatic insulin secretion may be one of the factors associated with the insulinlike activity (ILA) of endotoxemia. While there is little doubt that the prominent hypoglycemia of endotoxicosis is often preceded by systemic hyperinsulinemia, the cause of this increased secretion and its cause-and-effect relationship to the glucose deficit is less obvious. Recently, a "misinformed B-cell" hypothesis was proposed in which it was suggested that increased glucose flux across the pancreatic B-cell early in endotoxemia might lead to a misinterpretation of the existing glycemic state, resulting in increased insulin release. This possibility was based in part on the observation that increased 6-3H-glucose-derived rates of glucose disappearance (Rd) in endotoxic Yucatan minipigs preceded the onset of systemic hyperinsulinemia. Examination herein of the chronological order of events in this group of pigs and three other groups treated with lidocaine, naloxone, or captopril reveals an increase in pancreatic insulin secretory rate most often before increases in systemic Rd. Each of the three therapies were administered as a primed continuous intravenous infusion, 1 hour after the initiation of a continuous intravenous infusion of Difco 055:B5 E. coli lipopolysaccharide at an LD67 dose of 15 micrograms/kg/hr. In those pigs receiving no therapy, lidocaine, or naloxone, significant increases in pancreatic insulin secretion recurred at 40, 40, and 60 min following the onset of endotoxemia respectively. This was followed in 20 min by the first significant increase in relative glucose disappearance rates (%Rd). Captopril-treated pigs experienced a significant increase in %Rd at 60 min, which was followed in 20 min by a significant increase in pancreatic insulin secretion. In all groups, a significant hyperinsulinemia occurred transiently at 80 min postendotoxin, followed in 20 min by the onset of significant hypoglycemia. These observations suggest that increases in %Rd and transient increases in insulin secretion may be simultaneous events at best, and that along with significant increases in absolute levels of hepatic insulin extraction (observed in all groups at 60 or 80 min postendotoxin) may indicate some local effect of insulin release on hepatic glucose.

Animals↗
PubMed1983

Endotoxin dose. I. Hemodynamic, metabolic, and lethal consequences in Yucatan minipigs.

This study was performed in part to establish an endotoxin dosage in miniature swine that would yield reproducible cardiovascular and metabolic aberrations over a specific 6-h sampling period, minimizing lethality during that time. Five groups of three 6-mo-old Yucatan miniature pigs were surgically fitted with jugular vein and carotid artery catheters. One week later they were placed in slings and infused for 6 h with Difco 055:B5 endotoxin at dosages of 0, 2.5, 7.5, 15, and 25 micrograms X kg-1 X h-1. Significant (P less than or equal to 0.05) time-dose interactions were observed in mean arterial pressure, plasma glucose, serum potassium, blood lactate, pyruvate, bicarbonate, pH, PO2, PCO2, and urea nitrogen. Significant (P less than or equal to 0.05) differences were seen in lethality by 5 days postendotoxin: 0 = 0%, 2.5 = 0%, 7.5 = 33%, 15 = 67%, and 25 = 100% lethal. These animals exhibited a sensitive dose response to endotoxin, often at two- or threefold dose differences. The 15 and 25 micrograms X kg-1 X h-1 groups consistently demonstrated the most profound changes in the parameters measured.

Animals↗
PubMed1983

New finishing instruments for composite resins.

The trimming of composite resin restorations encompasses gross finishing, contouring, fine finishing, and polishing. A series of aluminum oxide-coated flexible disks have been marketed and are suitable for that purpose. However, their use is confined to directly accessible convex surfaces. For precise finishing of small delineated areas, and for concave and occlusal surfaces, rigid rotary instruments are necessary. The currently used stones and tungsten carbide burs are ineffective with microfilled composite systems. Thus, a series of finishing burs coated with 40- and 15-microns diamond chips were evaluated because of the superior grinding effectiveness as compared with existing instruments. Surface roughness measurements, and qualitative and quantitative SEM evaluations, indicate that these fine and superfine diamond finishing burs produce surfaces on composite resins as smooth as tungsten carbide burs and stones. At the same time, they cause less surface and subsurface damage or marginal fractures on composite resin restorations. The three-year clinical experience is generally favorable. Further quantitative clinical studies are warranted.

Composite Resins↗
PubMed1983

Effect of salicylates on intestinal secretion in calves given (intestinal loops) Escherichia coli heat-stable enterotoxin.

The inhibitory effect of salicylates on intestinal secretion in 1- to 5-day-old calves given Escherichia coli heat-stable enterotoxin (ST)-induced intestinal fluid response was investigated. Purified ST was diluted in isotonic saline solution to obtain 1:10, 1:25, 1:50, 1:75, and 1:100 dilutions. Each dilution (1 ml) was inoculated into ligated loops in the distal part of the jejunum of each calf. Acetylsalicylic acid (aspirin) given orally (100 mg/kg) at 4 hours before ST was inoculated did not substantially alter the intestinal fluid response to ST. Sodium salicylate (IV) infusion, begun simultaneously when, or at 1 hour after, ST was inoculated, significantly (P less than 0.05) decreased fluid accumulation in those loops inoculated with ST dilutions of 1:25 or greater. The sodium and potassium concentrations of the accumulated fluid did not differ significantly between or within treatment groups. These results indicate that sodium salicylate infusion may be beneficial in treating enterotoxic colibacillosis in calves. Aspirin given orally at the dose used in the present study, would not have any beneficial effect.

Animals↗
PubMed1983

Increased glucose uptake precedes hyperinsulinemia in awake endotoxemic minipigs.

The role of hyperinsulinemia in the development of hypoglycemia was evaluated in awake Yucatan minipigs. Eight adult minipigs were fitted with jugular, portal, and hepatic vein and carotid artery catheters, and hepatic artery and portal vein flow cuffs for determination of transhepatic kinetics and insulin secretion. Three days later they were infused with E. coli endotoxin at 15 micrograms/kg/hr. Transient hyperinsulinemia was preceded by an elevation of the rate of glucose uptake (Rd) determined from [6-3H] glucose-specific activity. This finding suggested that hyperinsulinemia might be caused by, and then be contributory to, increased Rd. If an increase in glucose uptake was also experienced by pancreatic beta-cells, the existing glycemic state could be overestimated and an inappropriate insulin release elicited.

Animals↗