L-NAME prevents in vivo the inactivation but not the down-regulation of hepatic cytochrome P450 caused by an acute inflammatory reaction.

A turpentine-induced inflammatory reaction (TIIR) down-regulates multiple isoforms of hepatic cytochrome P450 (P450) and increases microsomal lipid peroxidation. Since the synthesis of nitric oxide (NO*) is stimulated by inflammatory reactions, and NO* can depress the P450, it was of interest to investigate in vivo whether L-NAME and theophylline, by its anti-inflammatory properties, could prevent the depression of P450 caused by a TIIR. Control and rabbits with a TIIR received L-NAME for 72 h, and the activity of P450 was assessed in vivo and in vitro. In vivo, TIIR reduced theophylline systemic clearance by 50% (p<0.05), P450 total content by 67%, and the amount of CYP1A1/2 proteins by around 60% (p<0.05). L-NAME partially prevented the decrease in theophylline systemic clearance and in P450 total content, as well as the increase in lipid peroxidation; however, L-NAME did not hinder CYP1A1/2 proteins down-regulation. L-NAME did not modify the in vitro ability of the serum of rabbits with TIIR to decrease P450 activity, suggesting that the effect of L-NAME is not associated to a decrease in serum mediators. As assessed by the concentration in seromucoids, theophylline did not modify the severity of the inflammatory reaction, nor did it prevent the decrease in P450 activity. In conclusion, a TIIR down-regulates and reduces P450 activity, decrease that is at least in part mediated by NO*; theophylline does not prevent TIIR-induced P450 decrease in activity.

Hemodynamic effects of intradialytic food ingestion and the effects of caffeine.

Although the hypotensive effects of food ingestion during hemodialysis have been documented, the hemodynamic mechanism is unclear. It could be decreased cardiac output due to splanchnic sequestration or decreased vascular resistance due to splanchnic vasorelaxation. Also, the effects of caffeine, which block postprandial hypotension in the elderly, have not been studied in a dialysis setting. Central hemodynamics were monitored by thoracic electric bioimpedance in 10 dialysis patients who ingested a test meal 1 h into dialysis. All ultrafiltration was done during the initial 2 h. Bicarbonate dialysate was used. Each patient was studied three times in a double-blind (with respect to placebo/caffeine) cross-over trial: placebo/no meal, placebo/meal, and caffeine/meal. Blood pressure decreased sooner and to a great extent in the treatments in which food ingestion accompanied ultrafiltration (e.g., at 30 min after food ingestion, percent change in mean arterial pressure was -12.4 +/- 1.8 versus -2.4 +/- 3.5 mm Hg when food was not ingested; P < 0.05). The hemodynamic mechanism of food-associated hypotension was found to be a fall in systemic vascular resistance (SVRI). Caffeine pretreatment (200 mg), which resulted in intradialytic plasma caffeine levels of about 4 micrograms/mL at time of food ingestion, had no effect on food-associated reductions in blood pressure or SVRI. The results suggest that food ingestion during dialysis causes hypotension primarily because of decreased SVRI. The effects of food ingestion on mean arterial pressure and SVRI are not attenuated by the ingestion of 200 mg of caffeine 1 h before dialysis.

Scanning electron microscopic evaluation of clinically cemented cast gold restorations.

Copper replicas were made of well-fitting, clinically cemented cast gold restorations. The replicas were scanned in the scanning electron microscope to measure the accuracy of fit at the margins. The margin discrepancies observed compared with findings of laboratory studies. Numerous microscopic cracks were found in the cervical enamel of these restored, vital, and asymptomatic teeth.

Parameters that affect in vitro bonding of glass-ionomer liners to dentin.

The purpose of this study was to evaluate the effects of two concentrations of poly (acrylic acid) (10 and 25%), three treatments (untreated, passive conditioning, and active conditioning), and two storage conditions (24 hours in 37 degrees C water and thermal cycling) on the in vitro tensile bond strength of three commercial glass-ionomer liners to human dentin. Bond strengths to untreated dentin after storage for 24 hours ranged from 19.0 to 21.7 kg/cm2 for Glasionomer Base Cement, Cement/Liner, and Ketac-Bond, but dropped to a range of 4.9 to 9.7 kg/cm2 after thermal cycling. Active conditioning with 10% acid resulted in bond strengths after 24-hour storage that ranged from 23.5 to 44.0 kg/cm2, compared with values from 21.7 to 38.0 kg/cm2 with active conditioning using 25% acid. Active conditioning with 10% acid resulted in bond strengths after thermal cycling that were in the range of 15.8 to 27.4 kg/cm2 and were 80 to 320 percent higher than values resulting from passive conditioning under these conditions. Active conditioning with 10% acid for 30 seconds produced a bond strength for Glasionomer Base Cement of 44.0 kg/cm2, compared with a bond strength of 28.7 kg/cm2 for a 10-second active conditioning. Qualitative analysis of scanning electron photomicrographs showed that dentin tubules were opened to a greater extent by active conditioning with 25% acid than by passive conditioning with 10% acid.