Identification of Cigarette Smoke Components: RESULTS(3)

RESULTS(3)

Effect of KCN on OPR

Only KCN was studied in the OPR experiments since cyanide was the only smoke component tested that was present in smoke solutions in high enough concentration to account for an effect on CBF. The following experimental design was used. Infundibula were first incubated in EBSS-HA, challenged with one of three doses of KCN, then allowed to recover in EBSS-HA after washout of the test medium. OPR measurements were made after 10 min in control medium (EBSS-HA), after 10, 25, and 40 min in KCN, and after 10 min in washout medium (EBSS-HA). ventolin inhalers

Two control experiments were first performed. To determine whether flushing the chamber affected OPR, EBSS-HA only was perfused into chambers using the above protocol, and no effect on OPR was observed (not shown). To eliminate the possibility that potassium could effect OPR, 50 |xM or 100 (jlM KC1 was perfused in the second control experiment. Again no effect was observed on OPR (not shown), indicating that neither potassium nor chloride decreased OPR at these concentrations. In contrast, when KCN was perfused into chambers, OPR was inhibited in a dose-dependent manner, and at concentrations of 15 and 50 (jlM, KCN produced significant inhibition of OPR as compared to control rates (Fig. 5). Most inhibition of OPR by cyanide occurred within the first 10 min of exposure. However, at 50 |jlM KCN, inhibition was also time-dependent, and OPR decreased significantly between 10 and 40 min of exposure to KCN. The effect of cyanide on OPR was partially reversed by washout; however, rates following washout were still significantly below starting control values.
Fig4Identification of cigarette
FIG. 4. The effect of KCN on CBF. CBF is plotted for incubations in control medium (EBSS-H), four concentrations of KCN, and washout medium (EBSS-H). Concentrations of 50 p,M and 100 |xM KCN significantly inhibited CBF as compared to control values in EBSS-H alone (p = 0.035, p = 0.001 respectively). Beat frequency recovered to control values during washout. Values indicated by * (p < 0.05) and ** (p < 0.01) are significantly different from the control. Each bar is the mean ± SD of four experiments.

Fig5Identification of cigarette
FIG. 5. Effect of KCN on OPR in vitro. OPR (|xm/sec) is plotted as a function of KCN concentration. For each KCN concentration tested, OPR is first shown in control medium (EBSS-HA), then after 10 (E10), 25 (E25), or 40 (E40) min of exposure to KCN, then 10 min after washout with EBSS-HA. OPR decreased significantly compared to that of the EBBS-HA control at KCN concentrations of 15 and 50 |iM. At 50 |j,M, OPR also decreased significantly between 10 and 40 min of exposure to KCN. During washout, OPR partially recovered, but remained significantly lower than the control. Values indicated by * (p < 0.05) and ** (p < 0.01) are significantly different from the EBSS-HA control. Bars for each dose are the means ± the standard deviation of five experiments.

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