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B A McCarty

Publications and source records attributed to B A McCarty.

2 recordsLinked to original sources

Adenosine triphosphate levels in human plasma.

OBJECTIVE: To quantify extracellular adenosine triphosphate (ATP) levels in human platelet-poor plasma as a potential source of synovial fluid ATP, and to determine variables affecting these levels. METHODS: ATP was measured by the specific luciferase method; platelet beta thromboglobulin was determined by radioimmunoassay. The effects of fasting, feeding, venipuncture, and muscular exercise were determined by serial venipuncture in healthy subjects. Diurnal variation was determined by serial sampling through indwelling venous catheters in 3 healthy subjects and 3 women with knee osteoarthritis. RESULTS: Unlike beta thromboglobulin levels, which did not change, an invariable marked (mean 58%) fall in plasma ATP was noted 15 min after the first venipuncture, whether the subject had eaten or not. Indomethacin treatment had no effect on this phenomenon. Exercise of forearm muscles had no effect on plasma ATP. The drop in plasma ATP occurred between 3 and 15 min, with recovery at about 90 min. A diurnal variation in plasma ATP was found with trough levels at noon and at night during sleep. CONCLUSION: The predictable sharp fall in plasma ATP levels induced by venipuncture and the clear diurnal variation suggest that plasma contains ATP independent of platelet dense body release and endothelial cell needle trauma. Synovial plasma flow at peak (600 nM) levels is insufficient to provide more than one-third of the extracellular ATP needed to generate inorganic pyrophosphate in articular tissues.

Adenosine Triphosphate↗

A comparison of the effect of transforming growth factor beta 1 on pyrophosphate elaboration from various articular tissues.

OBJECTIVE: The purpose of this study was to determine the effect of transforming growth factor beta 1 (TGF beta 1) on inorganic pyrophosphate (PPi) elaboration from articular tissues to better understand the pathophysiology of calcium pyrophosphate dihydrate (CPPD) crystal deposition in the joint. METHODS: PPi was measured in the media of adult porcine articular tissue in organ culture and monolayer cultures. RESULTS: TGF beta 1 strongly stimulated PPi elaboration by porcine fibrocartilage and hyaline cartilage. It modestly increased PPi elaboration by ligament, and had no effect on PPi elaborated by synovium. Of all cell types tested in cell culture, only chondrocytes responded to TGF beta 1 by significantly increasing PPi elaboration. CONCLUSION: TGF beta 1 stimulates PPi elaboration from hyaline cartilage, fibrocartilage, and ligament, indicating that there is in situ CPPD crystal formation in these tissues. The ability of tissues to respond to TGF beta 1 by increasing PPi elaboration correlates with the prevalence of CPPD crystal deposition found clinically. The unique response of chondrocyte monolayers to TGF beta 1 reinforces the key role of the chondrocyte in PPi elaboration in the joint. These findings support an etiologic role for responsiveness to TGF beta 1 in CPPD disease.

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