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Biomedical subjects

A Jubran

Publications and source records attributed to A Jubran.

42 records · Page 3Linked to original sources
PubMed1992

Experimental polyacrylamide-induced acute injury in rat lung.

We recently reported the first case of accidental aspiration of polyacrylamide occurring in a 26-year-old man. The patient developed severe airway obstruction and parenchymal lung damage and died. Autopsy revealed numerous polyacrylamide particles in his lungs, as well as extensive bronchiolar and alveolar damage. Gas chromatographic and mass spectrometric assessment of the lung tissue failed to reveal polyacrylamide activity, although assessment of the suspending solvent of the polyacrylamide showed a pattern characteristic of an aliphatic hydrocarbon mixture with a prominent dodecane peak. This experimental study was performed to determine the nature and extent of damage to rat bronchial and alveolar epithelia following endotracheal instillation of polyacrylamide, hydrocarbon mixture (petroleum distillate), dodecane (C12H26), or normal saline. The rat lungs were examined grossly and microscopically 10 min and 24, 72, and 96 h after endotracheal instillation, following inflation and fixation with 10 percent buffered formaldehyde. Gross examination revealed congested, mottled visceral pleural surfaces in the rats treated with polyacrylamide and dodecane. There were no pleural exudates or effusions. Microscopically, vascular engorgement, bronchiolitis, and focal pneumonia were observed. Vascular engorgement was most pronounced at 72 to 96 h in rat lungs treated with polyacrylamide and dodecane and was moderate at 24 h in rats treated with petroleum distillate. Focal organizing pneumonia was marked at 96 h in rats treated with petroleum distillate, at 72 h in those treated with polyacrylamide, and at 24 h in those treated with dodecane. The saline-treated control animals showed no change. Our findings suggest that polyacrylamide, dodecane, and petroleum distillate are strong irritants to the airways. However, a direct obstructive/mechanical effect of the polyacrylamide upon the airway has not been excluded. Airway exposure to polyacrylamide may result in lung injury secondary to the polyacrylamide itself, its suspending agents, or both.

Acrylic Resins↗
PubMed1992

The use of mechanical ventilation via a nasal mask in myotonic dystrophy.

A 36-year-old woman with myotonic dystrophy presented with generalized weakness and daytime somnolence. Arterial blood gas analysis revealed significant hypoxemia and hypercapnia, and a polysomnogram revealed additional oxygen desaturation during sleep. For nocturnal ventilatory assistance, the patient received positive-pressure ventilation via a nasal mask. This mode of ventilation produced marked improvement in the patient's nocturnal hypoxemia.

Adult↗
PubMed1990

Reversal of endotoxin-mediated shock by NG-methyl-L-arginine, an inhibitor of nitric oxide synthesis.

Septic shock is a life-threatening condition that results from exposure to bacterial endotoxin. It is manifested by cardiovascular collapse and mediated by the release of cytokines such as tumor necrosis factor. Some of these cytokines cause the release of vasoactive substances. In the present study, administration of 40 microgram/kg of bacterial endotoxin to dogs caused a 33% decrease in peripheral vascular resistance and a 54% fall in mean arterial blood pressure within 30 to 90 minutes. Vascular resistance and systemic arterial pressure returned to normal within 1.5 minutes after intravenous administration of NG-methyl-L-arginine (20 mg/kg), a potent and selective inhibitor of nitric oxide synthesis. L-Arginine reversed the effect of L-NMA and restored the endotoxin-induced hypotension. Although NG-methyl-L-arginine injection increased blood pressure in control dogs, the hypertensive effect was much greater in endotoxemic dogs (24.8 +/- 2.7 mmHg vs 47.8 +/- 6.8 mmHg, p = 0.01, n = 4). NG-Methyl-L-arginine caused only a modest increase in blood pressure in dogs made hypotensive by continuous intravenous infusion of nitroglycerin (17.1 +/- 5.0 mm Hg, n = 3). These findings suggest that nitric oxide overproduction is an important contributor to endotoxic shock. Moreover, our findings demonstrate for the first time, the utility of nitric oxide synthesis inhibitors in endotoxic shock and suggest that such inhibitors may be of therapeutic value in the treatment of septic shock.

Animals↗
PubMed1990

NG-methyl-L-arginine inhibits tumor necrosis factor-induced hypotension: implications for the involvement of nitric oxide.

Clinical assessment of the activity of tumor necrosis factor (TNF) against human cancer has been limited by a dose-dependent cardiovascular toxicity, most frequently hypotension. TNF is also thought to mediate the vascular collapse resulting from bacterial endotoxin. The present studies address the mechanism by which TNF causes hypotension and provide evidence for elevated production of nitric oxide, a potent vasodilator initially characterized as endothelium-derived relaxing factor. Nitric oxide is synthesized by several cell types, including endothelial cells and macrophages, from the guanidino nitrogen of L-arginine; the enzymatic pathway is competitively inhibited by NG-methyl-L-arginine. We found that hypotension induced in pentobarbital-anesthetized dogs by TNF (10 micrograms/kg, i.v., resulting in a fall in mean systemic arterial pressure from 124.7 +/- 7 to 62.0 +/- 22.9 mmHg; 1 mmHg = 133 Pa) was completely reversed within 2 min following administration of NG-methyl-L-arginine (4.4 mg/kg, i.v.). In contrast, NG-methyl-L-arginine failed to reverse the hypotensive response to an equivalent depressor dose of nitroglycerin, a compound that acts by forming nitric oxide by a nonenzymatic, arginine-independent mechanism. The effect of NG-methyl-L-arginine on TNF-induced hypotension was antagonized, and the hypotension restored, by administration of excess L-arginine (100 mg/kg, i.v.). Our findings suggest that excessive nitric oxide production mediates the hypotensive effect of TNF.

Animals↗
PubMed1990

Reliability of pulse oximetry in titrating supplemental oxygen therapy in ventilator-dependent patients.

Pulse oximetry is widely used in the critical care setting, but few studies have examined its usefulness in clinical decision making. One area where pulse oximetry might be useful is in the titration of fractional inspired O2 concentration (FIO2) in ventilator-dependent patients. Unfortunately, documented guidelines for this use do not exist, and in a survey of directors of intensive care units, we found that they employed a wide range of target O2 saturation (SpO2) values. Consequently, we undertook a study to determine if SpO2 could be reliably substituted for measurements of arterial O2 tension (PaO2) when adjusting FIO2 in ventilator-dependent patients. We examined a number of SpO2 target values in 54 critically ill patients aiming for a PaO2 of greater than or equal to 60 mm Hg, while minimizing the risk of O2 toxicity. In white patients, we found that a SpO2 target of 92 percent was reliable in predicting a satisfactory level of oxygenation. However, in black patients, such a SpO2 reading was commonly associated with significant hypoxemia (PaO2 as low as 49 mm Hg), and a higher SpO2 target, 95 percent, was required. In addition, inaccurate oximetry readings (ie, greater than 4 percent difference between SpO2 and direct SaO2 measurements) were more common in black (27 percent) than in white patients (11 percent, p less than 0.05). In conclusion, a SpO2 target of 92 percent was reliable when titrating supplemental O2 in white patients receiving mechanical ventilation; however, in black patients, such a SpO2 reading was commonly associated with significant hypoxemia, and a higher SpO2 target, 95 percent, was required to ensure a satisfactory level of oxygenation.

Black or African American↗