Effects of meloxicam on platelet function in healthy adults: a randomized, double-blind, placebo-controlled trial.

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase-1 (COX-1), thereby inhibiting platelet function via blockade of thromboxane A2 (TxA2) formation, and COX-2, the enzyme that mediates inflammatory responses. Meloxicam is a relatively COX-2-selective anti-arthritis drug that shows significant TxA2 inhibition, albeit less than traditional NSAIDs. A randomized, double-blind, placebo-controlled trial was conducted in 79 healthy adults to compare the effects of once-daily therapeutic (7.

Maturational changes in Na(+)-K+ pump activity in guinea pig airway smooth muscle.

The effect of maturation on the Na(+)-K+ pump of airway smooth muscle (ASM) was studied. Na(+)-K+ pump activity of tracheal smooth muscle from immature (1- to 2-week-old) and mature (10- to 12-week-old) guinea pigs was measured as the ouabain-sensitive component of the resting membrane potential and as ouabain-sensitive 86Rb+ uptake (using 86Rb+ as a marker for K+). Maturation resulted in decreases in both the contribution of the Na(+)-K+ pump of the resting membrane potential and in ouabain-sensitive 86Rb+ uptake.

Role of phospholipase C and tyrosine kinase systems in growth response of human airway smooth muscle cells.

The primary culture of confluent human airway smooth muscle (ASM) cells were exposed up to 5 days to human recombinant interleukin (IL)-1 beta in the presence of indomethacin and 1% fetal bovine serum. The proliferation was assessed by a [3H]thymidine incorporation and direct cell count. We found that IL-1 beta significantly increased thymidine incorporation into and cell count of ASM cells in a concentration-dependent manner.

IL-1 beta and IL-6 induce hyperplasia and hypertrophy of cultured guinea pig airway smooth muscle cells.

Guinea pig airway smooth muscle (ASM) cells were maintained in a primary tissue culture (passages 1-3). Cells were exposed to human recombinant interleukin-1 beta (IL-1 beta; 20-100 pg/ml) or interleukin-6 (IL-6; 1-4 ng/ml) in the presence of indomethacin (1 microgram/ml) for up to 5 days. Proliferation of ASM cells was assessed with two techniques, direct counting of cells with a hemacytometer and [3H]thymidine incorporation corrected for total protein content.

Interleukin-1 beta stimulates the proliferation of cultured airway smooth muscle cells via platelet-derived growth factor.

Bronchoalveolar lavage fluid from symptomatic asthmatics contains elevated levels of several proinflammatory interleukins including interleukin-1 beta (IL-1 beta). Biologic activities of IL-1 beta are considered to be critical in the inflammatory process. Since these characteristics include mitogenic properties, we investigated the effect of IL-1 beta on the proliferation of airway smooth muscle (ASM) cells isolated from guinea pig tracheas.