AIA patients showed more intense ADP-induced platelet aggregation and a higher rate of its first wave. The reaction time, the interval from the addition of the aggregation-inducing agent to the maximal change in optical density of the primary aggregation wave, reached 50 s or more in 94.3% of AIA patients, 76.5% (P=0.03) of ATA patients and 54.5% (P<0.001) of controls. The change in light transmittance of the primary aggregation wave was 0.8%/s or greater in 34.3% of AIA patients, 11.8% (P=0.03) of ATA patients and 9.1% (P<0.01) of controls.In ATA patients, the aggregation parameters correlated with a higher excretion of nitrites and nitrates in the daytime (P<0.05). AIA patients did not show such a correlation, indicating the lack of nitric oxide regulation of the platelet functional activity in these patients.
The higher level of nitric oxide produced during the night in AIA patients may have been due to the lack of melatonin control inhibiting the activity of inducible nitric oxide synthase. It is interesting that inducible nitric oxide synthase and N-acetyltransferase (a key enzyme in melatonin synthesis) genes are located in the same chromosome.
The increased production of nitric oxide at night in AIA patients is hypothesized to lead to the generation of per-oxynitrite. This in turn would stimulate platelet aggregation, overcome the beneficial effects of endothelial nitric oxide and prostaglandin I2 and, finally, lead to endothelial injury. Such disturbances in lung microcirculation may be responsible for the precipitation of AIA attacks (Figure 3). If you are looking for most affordable deals and very fast delivery right to your door, you have found the right place for it. This my canadian pharmacy will give you the full range of services and medicine you need, at prices that are very low.
Figure 3 The role of nitric oxide (NO) in lung microcirculation disturbances in acetylsalicylic acid- (ASA) induced asthma (AIA). PGI2 Prostaglandin I2