Non-cladding optical fiber is available for detecting blood or liquids.

OBJECTIVES: Serious accidents during hemodialysis such as an undetected large amount of blood loss are often caused by venous needle dislodgement. A special plastic optical fiber with a low refractive index was developed for monitoring leakage in oil pipelines and in other industrial fields. To apply optical fiber as a bleeding sensor, we studied optical effects of soaking the fiber with liquids and blood in light-loss experimental settings. METHODS: The non-cladding optical fiber that was used was the fluoropolymer, PFA fiber, JUNFLON™, 1 mm in diameter and 2 m in length. Light intensity was studied with an ordinary basic circuit with a light emitting source (880 nm) and photodiode set at both terminals of the fiber under certain conditions: bending the fiber, soaking with various mediums, or fixing the fiber with surgical tape. The soaking mediums were reverse osmosis (RO) water, physiological saline, glucose, porcine plasma, and porcine blood. The light intensities regressed to a decaying exponential function with the soaked length. RESULTS: The light intensity was not decreased at bending from 20 to 1 cm in diameter. The more the soaked length increased in all mediums, the more the light intensity decreased exponentially. The means of five estimated exponential decay constants were 0.050±0.006 standard deviation in RO water, 0.485±0.016 in physiological saline, 0.404±0.022 in 5% glucose, 0.503±0.038 in blood (Hct 40%), and 0.573±0.067 in plasma. The light intensity decreased from 5 V to about 1.5 V above 5 cm in the soaked length in mediums except for RO water and fixing with surgical tape. CONCLUSIONS: We confirmed that light intensity significantly and exponentially decreased with the increased length of the soaked fiber. This phenomena could ideally, clinically be applied to a bleed sensor.

Paraquat-induced oxidative stress and dysfunction of the glutathione redox cycle in pulmonary microvascular endothelial cells.

Oxidative stress and changes in the antioxidant defense system that include the glutathione redox cycle in cultured pulmonary microvascular endothelial cells after exposure to paraquat at 0.1 and 0.5 mM were examined as a function of time. Cell viability was substantially lost 72 h after exposure to 0.5 mM paraquat, but not 0.1 mM paraquat. Viability loss was accompanied by increased glutathione-protein mixed disulfide formation, as well as a loss in glyceraldehyde-3-phosphate dehydrogenase activity, indicating a low defense potential. At 4 h after exposure to paraquat at both doses, however, a marked loss in NADPH was found, together with a decrease in aconitase activity. With 0.5 mM paraquat, increased NADP(+) accompanied by NADPH loss diminished constantly after 48 h without recovery of lost NADPH, suggesting destruction of pyridine nucleotides under oxidative stress. NAD(+) decreased 72 h after exposure to 0.5 mM paraquat, but NADH was not influenced. 3-Aminobenzamide did not protect the loss in NADP(+) or NAD(+) and cell viability. Although oxidized glutathione did not increase by exposure to paraquat at both doses through a 96-h exposure period, reduced glutathione increased at 48 to 72 h, with an increase in glutathione disulfide reductase activities. In contrast, a marked loss in glutathione peroxidase activity was produced 48 h after exposure to 0.5 mM paraquat, preceding cell injury. Mercaptosuccinate, an inhibitor of glutathione peroxidase, distinctly hastened viability loss by paraquat. These results indicate that the reduced ability of the glutathione redox cycle, leading to high oxidative stress, is closely associated with paraquat-induced cytotoxicity.