Перегляд вихідного коду сторінки Weird Yet Somehow Workable Ficain Tactics

After a breath of 100% N2, end-tidal fell precipitously (P?[http://www.selleckchem.com/products/CAL-101.html Akt inhibitor] N2. All subjects reported light-headedness after a breath of 100% N2 and more severe light-headedness after a breath of 10% CO2 in 90% N2. As expected, relative to the duration of apnoea following a breath of room air, the apnoeas were significantly shorter following a breath of N2, and shorter still following a breath of 10% CO2 in 90% N2. These values are reported in Table?1. The same was true for the latencies at which the asphyxic sympathetic bursts occurred; with increasing chemical drive, the bursts occurred earlier. There were no differences in the duration of the inhibition of MSNA following inhalation of any of the gases. However, following the resumption of breathing at the second asphyxic break point, the period of sympathetic inhibition was significantly longer (Table?1). During the end-expiratory apnoea the blood pressure increased progressively up to the first asphyxic break point, in line with the increase in MSNA. As illustrated in Fig.?3, following the single breath of either 100% N2 or 10% CO2 in 90% N2 at the asphyxic [http://en.wikipedia.org/wiki/Ficain Ficain] break point, there was a sudden rapid fall in blood pressure, which lasted for the majority of the second breath-hold period. However, blood pressure did increase as the subject approached the second asphyxic break point; this was presumably due to the asphyxically generated sympathetic bursts that occur during this period, causing blood pressure to rise above baseline levels at the start of the recovery period. Average changes in systolic and diastolic pressures for both 100% N2 and 10% CO2 in 90% N2 are shown in Table?2. During the inflation phase of an inspiratory-capacity [http://www.selleckchem.com/small-molecule-compound-libraries.html Selleckchem Small molecule library] apnoea a short period of sympathetic inhibition, followed by a sustained increase in MSNA, was observed as described previously and illustrated in Fig.?. Table? shows that the inspiratory-capacity apnoeas were significantly shorter when subjects inhaled 100% N2 at the beginning of the manoeuvre, and shorter still when subjects inhaled 10% CO2 in 90% N2, although these gas mixtures were assessed in only three subjects. However, the duration of inhibition of MSNA during the inflation phase was identical for all gases (Table?), and was shorter than that seen after a single breath of any gas following an end-expiratory apnoea. The purpose of this study was to determine whether lung inflation per se, rather than the relief from hypoxia and hypercapnia, is responsible for the inhibition of MSNA after an end-expiratory apnoea.