Cutaneous thermal burn and oxidant-mediated acute lung injury: Appearance in serum of lung-related LDH isoenzyme

Previous studies from our laboratory have demonstrated that thermal injury to the skin of rats is associated with the production of oxygen radicals by complement-activated blood neutrophils, resulting in acute lung injury as demonstrated by increases in lung vascular permeability and morphological evidence of vascular endothelial cell damage, interstitial edema, and alveolar hemorrhage. In the present study, the analysis of sera from thermally injured rats reveals an isoenzyme profile for lactate dehydrogenase (LDH;EC 1.1.1.27) that is compatible with origin from lung. The appearance of LDH-4 isoenzyme in serum of thermally injured rats correlates linearly with indices of lung damage, supporting the results of previous studies suggesting that thermal trauma to the skin can cause oxygen radical production by complement-activated blood neutrophils with resultant acute microvascular injury in the lung interstitium. Furthermore, interventions that protect from oxidant-mediated lung injury (catase, scavengers of hydroxyl radical, iron chelators or neutrophil depletion) result in significant reductions in serum levels of the LDH-4 isoenzyme following thermal injury to the skin. Thus, measurements of LDH isoenzyme patterns in serum to be useful in monitoring tissue damage such as oxygen radical-mediated acute lung injury.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25898/1/0000461.pd

The erythromycin breath test as a predictor of cyclosporine blood levels

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/109915/1/cptclpt1990126.pd

Analysis of retinoids by high-performance liquid chromatography using programmed gradient separation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24984/1/0000411.pd

Effects of chronic aminodarone therapy on ventricular tachycardia induced by programmed ventricular stimulation

Several studies have reported upon the inducibility of ventricular tachycardia (VT) with programmed ventricular stimulation (PVS) during chronic amiodarone therapy; however, few studies have systematically described and compared the morphology, duration, and cycle length of VT induced by PVS before and after amiodarone. In this study, 26 patients with symptomatic VT or ventricular fibrillation were evaluated by PVS by means of one to three extrastimuli (ES) before treatment and after 2 months of amiodarone therapy. Before amiodarone, sustained unimorphic VT was induced in 21 patients (group A) and symptomatic, nonsustained VT was induced in five patients (group B). After 65 +/- 8 days of amiodarone (total dose 64.5 +/- 8.9 gm, mean +/- S.D.), 15 of 21 patients (71%) in group A had sustained VT, five patients (24%) had nonsustained VT, and one patient had no VT induced. Four of five patients (80%) in group B had sustained VT and one patient had no VT induced. VT was induced by the same or by fewer number of ES in 79% of cases. When the morphologies of the VT induced before and after amiodarone were compared, the morphology of VT induced after amiodarone was the same in only 8 of 24 patients (33%), unimorphic but different in 14 patients (58%), and polymorphic in the remaining two patients. No correlation was found between the serum concentrations of amiodarone, desethylamiodarone, tetraiodothyronine, triiodothyronine, or reverse triiodothyroinine, and similarities or differences in VT morphology, VT cycle length, or the relative number of ES required to induce VT after treatment with amiodarone. Although VT is ofter still inducible after 2 months of amiodarone therapy, the VT induced is different from the baseline VT in the vast majority of patients.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26864/1/0000429.pd

Interrelationships between serum levels of amiodarone, desethylamiodarone, reverse T3 and the QT interval during long-term amiodarone treatment

The interrelationships between serum levels of amiodarone, desethylamiodarone, and reverse T3, and changes in the corrected QT interval ([Delta]QTc) were examined in 22 patients during long-term treatment with amiodarone. At 1, 3, and 6 months of follow-up, the correlation coefficient between serum levels of amiodarone or desethylamiodarone and reverse T3 ranged from 0.01 to -0.2 (p > 0.4). At the same time intervals, the correlation coefficient between both amiodarone and desethylamiodarone levels and [Delta]QTc ranged from 0.1 to -0.1 (p > 0.6), and the correlation coefficient between reverse T3 and [Delta]QTc also ranged between 0.1 to -0.1 (p> 0.5). Substituting percent [Delta]QTc for [Delta]QTc also did not reveal a significant correlation. These data demonstrate that serum levels of reverse T3 cannot be used as a substitute for serum levels of amiodarone in monitoring patients being treated with amiodarone. The absence of a correlation between serum reverse T3 levels and [Delta]QTc suggests that the delay in repolarization which occurs during amiodarone therapy is not secondary to an amiodarone-induced abnormality in thyroid hormone metabolism.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26433/1/0000521.pd

Pharmacodynamics of intravenous procainamide as used during acute electropharmacologic testing

No previous studies have determined the pharmacodynamics of intravenous procainamide when administered in a dose of 15 mg/kg and at a rate of 50 mg/min, as is common practice during etectropharmacologic testing. In this study, 30 patients received procainamide in this fashion; the right ventricular effective refractory period and the QRS duration at a ventricular pacing rate of 120/minute were then determined every minute for 20 minutes. Ten patients received no maintenance infusion of procainamide (group A), 10 received a 4 [mu]g/min maintenance infusion (group B) and 10 received an 8 mg/min maintenance infusion (group C). Ten additional patients received no procainamide and served as control subjects (group D). The plasma procainamide concentration was measured at 1, 5, 10,15 and 20 minutes after the loading dose was administered. A stable plasma procainamide concentration was not present in group A, B, or C until 15 minutes after infusion of the loading dose. The effective refractory period and QRS duration increased compared with baseline at 1 minute, decreased between 1 and 10 minutes and then remained essentially unchanged between 10 and 20 minutes in all 3 treatment groups. Concentration-effect relation was linear in each treatment group. The plasma procainamide concentrations in group C were significantly greater than in group A; however, the effects on refractoriness and QRS duration were similar in both groups. These findings indicate that with a procainamide dosing method commonly used during electropharmacologic testing, the plasma procainamide concentration decreases significantly during the first 15 minutes after the loading dose is administered; the effects of procainamide on ventricular refractoriness and conduction parallel the changes in the plasma procainamide concentration; and an 8 mg/min maintenance infusion of procainamide results in higher plasma procainamide concentrations without an associated increase in ventricular refractoriness or slowing of conduction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27475/1/0000517.pd