Monitoring pulmonary vascular permeability using radiolabeled transferrin.

G S Basran; J G Hardy

doi:10.1097/00005382-198807000-00009

Home/Archive/PubMed

PubMed · 3392761

Monitoring pulmonary vascular permeability using radiolabeled transferrin.

G S Basran·J G Hardy

View original source ↗Export metadata ↓

Abstract

A simple, noninvasive technique for monitoring pulmonary vascular permeability in patients in critical care units is discussed. High vascular permeability is observed in patients with clinically defined adult respiratory distress syndrome (ARDS) but not in patients with hydrostatic pulmonary edema or in patients with minor pulmonary insults who are considered to be at risk of developing ARDS. The technique has been used in the field of therapeutics and pharmacology to test the effects of the putative antipermeability agents methylprednisolone and terbutaline sulfate. There appears to be a good correlation between the acute inhibitory effect of either drug on transferrin exudation and patient prognosis. Thus, a byproduct of such drug studies may be an index of survival in patients with established ARDS.

Explore related subjects

Burns, Inhalation Capillary Permeability Erythrocytes Humans Indium Radioisotopes Lung Methylprednisolone Monitoring, Physiologic Pulmonary Edema Respiratory Distress Syndrome Technetium Transferrin Wounds and Injuries Case Reports Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

G S Basran, J G Hardy. 1988. Monitoring pulmonary vascular permeability using radiolabeled transferrin.. https://doi.org/10.1097/00005382-198807000-00009

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

[Which therapy options are reliable in smoke inhalation?].

Explore the source record for details and available documents.

Burns, Inhalation↗

PubMed2006

Lung injury from smoke inhalation.

Significant morbidity and mortality from smoke inhalation occurs in victims of fire. Lung injury can be caused by chemical and thermal insults. A variety of noxious gases, irritants and asphyxiants are generated depending on the material burnt. Carbon monoxide is the predominant cause of death among fire victims. Treatment should be directed at reversing hypoxaemia as a result of asphyxia or carbon monoxide poisoning. There is no evidence that the routine use of corticosteroids or prophylactic antibiotics is beneficial. Through a better understanding of the pathophysiology of smoke-induced lung injury, the effects of exogenous surfactant, leukotriene inhibitors, antioxidants, nitric oxide synthase inhibitors and fibrinolytics suggest that these compounds may have a future therapeutic role in smoke-induced injury. Studies are needed to evaluate the safety and efficacy of these potential therapies before they are used clinically.

Burns, Inhalation↗

PubMed2006

Theoretical evaluation of burns to the human respiratory tract due to inhalation of hot gas in the early stage of fires.

A transient two-dimensional mathematical model for heat and water vapor transport across the respiratory tract of human body was established and applied to predict the thermal impact of inhaled hot gas to the nasal tissues during the early stage of fires. Influences of individual's physiological status and environment variables were comprehensively investigated through numerical calculations. Burn evaluation was performed using the classical Henriques model to predict the time for thermal injury to occur. It was shown that decreasing the air velocity and increasing the respiratory rate is helpful to minimize the burn over the respiratory tract. The effect of relative humidity of surrounding dry hot air could be ignored in predicting burns for short duration exposures. Due to evaporation cooling on the mucousal membrane, the burn often occurs at certain positions underneath the skin of the tract near the inlet of the respiratory tract. Most of the tissues near the surface suffer injury immediately after exposure to fire, while in the deeper tissues, serious damage occurs after a relatively longer time period. The method presented in this paper may suggest a valuable approach to theoretically evaluate the injury of hot air to the human respiratory tract under various fire situations.

Burns, Inhalation↗