Ratios of lactulose/mannitol excretion in urine have been signed to assess perturbations of intestinal permeability I • used to assess the extent of intestinal permeability in after burn injury. Seven men with burns ranging from _ various disease and trauma conditions. Reported studies 31% to 78% of the total body surface area (mean 58%) have used this technique to correlate altered gastrointeswere used in this preliminary study to develop our assay (• tinal mucosal permeability totranslocation of bacteria and technique. On the fourth day after the burns were endotoxin, leading to occult sepsis in bum patients.sustained, the patients were given 5 g of mannitol and Enzymatic methods of analysis for urine concentrations of 10 g of lactulose in 100 mL of de-ionized water. A 6-h mannitol and lactulose were used in these studies. We urine collection was initiated after ingestion of the test have found that urine from patients with severe burns solution. We added 1 mL of a 200 g/L chlorhexidine frequently contains compounds that interfere with the solution to the total urine collected. Aliquots of the enzymatic methods. We describe using gas-liquid chrourine samples were frozen at -20 'C until analyses matography to determine mannitol and lactulose simultawere perfbrmed. neously in the urine of burn patients. To avoid the multiple Sample preparation: We added 125 AL of 1 mmoIIL peaks for the anomeric forms of the reducing sugars methylmannopyranoside reagent as an internal standuring precolumn trimethylsilyl derivatization, we condard to 50Al of fivefold-diluted (with de-ionized water) verted the sugars to oximes before the silylation step. The drd ThL of ved-iltedn(withnde ed wer) method gave good recoveries of mannitol and lactulose urine. The sample and internal standard were dried added to burn patients' urine samples. Unlike the enzyunder nitrogen in a heating block at 75 °C. Aftr these matic methods, gas-liquid chromatography eliminates the cooled, we added 100 ML of oxin' solution (25 mg of effect of interfering compounds and allows for the simulhydroxylamine hydrochloride per inilliliter of pyridine), taneous determination of both sugars in urine samples.capped the samples, and incubated them at 75 0C for 30 min. After letting the samples cool, we added 100 AL of Several investigators have proposed that thermal n-trimethylsilyl imidazole reagent (Pierce Chemical, injury alters gastrointestinal mucosal permeability, Rockford, IL 61105-9976) and incubated the solutions causing translocation of bacteria and endotoxin and for 15 min at 75 'C. leading to occult sepsis and multiple organ failure (1-3).Standard preparation: Stock solutions of mannitol (5 Ratios of lactulose/mannitol urine excretion have been mmol/L) and lactulose (0.5 mmol/L) were made in deused to monitor changes in intestinal permeability in ionized water. From the stock mannitol solution, we various disease conditions (4,5). We have found that the pipetted 20, 40, 60, 80, and 100 AL into disposable enzymatic methods commonly used to determine mani...
Background: We previously reported that inhaled nitric oxide (NO) improved pulmonary function following smoke inhalation. This study evaluates the
FObjective: To evaluate the pulmonary effect of treatMain Outcome Measures: Cardiopulmonary variment with N-nitro-L-arginine methyl ester (NAME) with ables and blood gases were measured serially. The muland without inhaled nitric oxide (NO) in a swine model tiple inert gas elimination technique was performed at 3 of endotoxemia.hours. The wet-to-dry lung weight ratio was measured following necropsy. Design: Randomized controlled trial.Results: Administration of LPS resulted in pulmonary Setting: Laboratory.arterial hypertension, pulmonary edema, and hypoxemia with increased ventilation perfusion ratio misInterventions: Following a 20-minute intravenous inmatching. None of these changes were attenuated by fusion of Escherichia coli lipopolysaccharide (LPS) (200 NAME treatment alone but all were significantly pLg/kg), animals were resuscitated with saline solution improved by the simultaneous administration of (1 mL/kg per minute) and observed for 3 hours while meinhaled NO. chanically ventilated (fraction of inspired oxygen [Fio,], 0.6; tidal volume, 12 mLikg; positive end-expiratory presConclusions: Systemic NO synthase inhibition failed to sure, 5 cm HRO). Group 1 (LPS, n=6) received no addirestore hypoxic pulmonary vasoconstriction following LPS tional treatment; group 2 (NAME, n=5) received NAME administration. The deleterious effects of endotoxemia (3 mg/kg per hour) for the last 2 hours; group 3 (NO, on pulmonary function can be improved by inhaled NO n=6) received NAME (3 mg/kg per hour) and inhaled NO but not by systemic inhibition of NO synthase. (40 ppm) for the last 2 hours; and group 4 (control, n=5) received only saline solution without LPS.(Arch Surg. 1994;129:1233-1239 S EPSIS RESULTS in a systemic in-lowing sepsis is a significant comorbid facflammatory response that is tor, therapy aimed at attenuating this mediated by various cytodeleterious process may exert a benefikines and activated leukocial effect on outcome. cytes. Systemic vasodilation Hypoxic pulmonary vasoconstricand hypotension characteristic of sepsis tion is a mechanism that modulates pulhave been hypothesized to occur secondmonary gas exchange by matching the disarily to endogenous overproduction of nitribution of blood flow to ventilation. 7 ,8 tric oxide (NO).',' In contrast to the sysHowever, the cellular mechanisms that initemic vasodilatory response, pulmonary tiate and maintain HPV remain poorly un-
Selectin blockade attenuated lung injury after smoke exposure. These data support the hypothesis that neutrophils play a pivotal role in smoke inhalation injury.
Abstract. Several fluorescent substances are present in the supematants of acidprecipitated whole blood or plasma from burned patients. Perchloric acid supematants of sera from infected, but not uninfected, burned rats contained a fluorescent substance with maximum emission at 420 nm at 355-nm excitation (355 ex/420 em). In this study Mm of serum from burned human patients, several fluorescent substances were resolved Ami by reverse-phase high-pressure liquid chromatography. One of these fluorescent comnponents had an high-pressure liquid chromatography retention time and fluorescent m " characteristics Identical to those of neopterin. The identification of this component as neopterin was verified by thormospray mass spectrometry. Serum neopterin concentra--tions were then determined in supernatants of patient serum samples having various '21M levels of 355 ex/420 em fluorescence. A correlation was found between the concentrations of neopterin determined by high-pressure liquid chromatography and the presence -of bacteremia in burned patients. These findings suggest that neopterin, which is a useful indicator of infection in other clinical settings, may also be an indicator of infection in burned patients.[P.S.E. B.M. 1992, Vol 199] Infect i on poses a serious threat to all severely burned chemical indices specific to the invading species are patients and is a persistent obstacle to successful desirable, the spectrum of microbes to be differentiated therapy. Prompt diagnosis of infection is crucial and their low levels in the blood early in infection limit for timely treatment and for patient survival. Systemic the likelihood of developing such indices. As an alterchanges induced by burn injury, such as ieukocytosis native, a biochemical change in serum or blood specific and fever, hamper the early detection of sysLmic infecto infection itself would permit early identification of tion and make its diagnosis difficult in such patients.this state, and might have diagnostic utility. Rapid biochemical detection of the presence of infecWe have purified and biochemically characterized tion, if reliable, could provide diagnostic verification substances from the blood of burned patients in which more promptly than is currently possible with standard 420-nm fluorescence emission at 355-nm excitation microbiologic techniques.(355 ex/420 em) was detected in perchloric acid (PCA) Abnormal levels of hormones (1, 2), acute phase supernatants. These substances offer some promise as proteins (3, 4), and fluorescent substances (5) incubating for 10 min at 4"C, the mixture was centrifuged at 4°C for 10 min at 3,000g; the supernatant was
Smoke inhalation is a significant comorbid factor in thermal trauma. The effect of inhaled nitric oxide (NO) on smoke inhalation injury was evaluated in an ovine model. Following smoke exposure, group 1 animals (n = 9) spontaneously breathed room air, and group 2 animals (n = 8) breathed 20 parts per million of 47e NO in air for 48 hours. Cardiopulmonary variables and blood gases were serially measured; bronchoalveolar lavage (BAL) was performed and wet-to-dry lung weight ratios (W/D) determined at 48 hours. Pulmonary vasoconstriction following smoke inhalation was significantly attenuated by inhaled NO (p < 0.05), which exerted no apparent effect on the systemic circulation. In group 2, the serial decline in pulmonary oxygenation was less than in group 1, consistent with a smaller physiologic shunt (p < 0.05). There were no significant differences in W/D, lung compliance, BAL fluid analysis results, or histologic evaluation findings between the two groups. These results suggest that inhaled NO exerted beneficial effects on pulmonary arterial hypertension and oxygenation following smoke inhalation without apparent amelioration of airway inflammation. SMOKE INHALATION causes acute airway inflam-mune function, and inflammation induced by cytomation and subsequent pulmonary edema that are par-kines.' 5 's tially mediated by activated leukocytes and various Inhaled nitric oxide (5-150 ppm) has been recently inflammatory cytokines.1 These changes impair pul-reported to act as a selective pulmonary vasodilator monary function by increasing ventilation-perfusion without causing systemic vasodilation. Pulmonary mismatching and ultimately enhancing susceptibility vasodilatation following inhalation of nitric oxide has to pulmonary infection, which increases both morbidity been demonstrated in animal models of pulmonary arand mortality in patients with thermal injury.2 ' 3 terial hypertension induced by a thromboxane analog, Medical interventions that attenuate this deleteri-heparin-protamine treatment, hypoxemia, and sepous process may exert a beneficial effect on outcome. sis.9-11 Beneficial effects of inhaled nitric oxide have Nitric oxide, an endothelial-derived relaxing factor, been reported in patients with pulmonary hypertenis generated from L-arginine in mammalian tissues. 4 sion, adult respiratory distress syndrome (ARDS), conNitric oxide is a lipophilic free radical with a short half genital heart failure, chronic obstructive lung disease, life, which appears to act through a signal transduction and pneumonia. 12-16 event on local cells.5 Nitric oxide activates the syntheTo our knowledge, the effect of inhaled nitric oxide sis of intracellular guanosine 3',5'-cyclic monophos-on chemically induced lung injury has not been examphate (cGMP) and reduces intracellular free calcium ined. This study evaluated the effects of inhaled nitric concentration, leading to smooth muscle relaxation as oxide on smoke inhalation injury in an ovine model. well as inhibition of platelet aggregation and adhesion. '7 In addition, n...
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