The effect of cyclazocine on the cardiovascular responses to pressor and depressor amines in the rat

In anesthetized rats, cyclazocine potentiated the pressor responses to norepinephrine, epinephrine, tyramine and phenylephrine. Neither the depressor responses to isoproterenol nor the pressor resposes to angiotensin were potentiated by cyclazocine. In pithed and adrenalectomized rats, cyclazocine potentiated the pressor responses to norepinephrine. Chemical sympathectomy abolished the cyclazocine-induced potentiation of pressor responses to norepinephrine. In isolated rat atria, cyclazocine potentiated the chronotropic action of norepinephrine but did not alter the response to isoproterenol. It is suggested that cyclazocine causes potentiation of the agonistic properties of the various amines by interacting with the sympathetic nervous system, possibly by inhibiting the uptake of the amines into adrenergic nerve terminals.     

Cyclazocine and norepinephrine uptake, metabolism, and turnover in the rat brain

The effects of cyclazocine, a narcotic agonist/antagonist, on the uptake, metabolism, and turnover of norepinephrine in rat brains were studied. Cyclazocine significantly depressed the accumulation of intracisternally administered [3H]norepinephrine and the formation of 3,4-[3H]dihydroxymandelic acid but did not alter the formation of [3H]-normetanephrine. Comparatively, imipramine reduced the uptake of [3H]norepinephrine, decreased the formation of 3,4-[3H]dihydroxymandelic acid, and increased the formation of [3H]normetanephrine. Moreover, cyclazocine increased the formation of endogenous 3-methoxy-4-hydroxyphenylethylene glycol and produced a fall in endogenous norepinephrine. It is suggested that cyclazocine reduces the accumulation of [3H]norepinephrine, decreases endogenous norepinephrine levels, and increases the formation of 3-methoxy-4-hydroxyphenylethylene glycol by interacting with brain adrenergic nerves, presumably by inhibiting neuronal uptake and facilitating norepinephrine turnover.     

Effects of sinus surgery in patients with cystic fibrosis after lung transplantation: a 10-year experience

Chronic infectious rhinosinusitis with Pseudomonas aeruginosa is common in cystic fibrosis and may result in allograft infection after lung transplantation. Sinus surgery followed by nasal care may reduce these adverse effects. Sinus surgery was performed in 37 patients with cystic fibrosis after transplantation. Bacteriology of sinus aspirates (n=771) and bronchoalveolar lavage (BAL) (n=256) was correlated with clinical data. Sinus surgery was successful in 54% and partially successful in 27% of patients. A significant correlation between negative sinus aspirates and negative BAL and between positive sinus aspirates and positive BAL (P<0.0001) was found. Successful sinus management led to a lower incidence of tracheobronchitis and pneumonia (P=0.009) and a trend toward a lower incidence of bronchiolitis obliterans syndrome (P=0.23). Sinus surgery followed by daily nasal douching may control posttransplant lower airway colonization and infection. In the long term, this concept may lead to less bronchiolitis obliterans syndrome by decreasing bronchiolar inflammation.     

Variability of inspiratory conductance quantifies flow limitation

In the present study, our aim was to investigate whether the variability of conductance over the course of inspiration reflects flow limitation. Pressure/flow conditions in the upper airway were modelled by a collapsible tube within a rigid chamber and a pump simulating respiration. Instantaneous conductance was estimated every 20 ms as flow/resistive pressure, and its variability during inspiration expressed as the 90th/50th percentile ratio. Accuracy of this ratio to quantify flow limitation was evaluated by observing whether it changed predictably with adjustments of model parameters. To illustrate the potential of this ratio to quantify flow limitation in a clinical setting, we recorded pneumotachographic airflow and oesophageal pressure in 11 patients with obstructive sleep apnoea during nasal continuous positive airway pressure (CPAP) ventilation, and observed changes in the 90th/50th percentile ratio of inspiratory lung conductance induced by mask pressure titration. Rising pressure surrounding the collapsible tube from subatmospheric to positive values induced progressive inspiratory collapse and increased 90th/50th percentile ratios of inspiratory conductance as predicted. Changes in flow limitation induced by other model modifications were also correctly tracked by the 90th/50th conductance percentile ratio. Increasing mask pressure during CPAP ventilation in sleep apnoea patients from subtherapeutic to therapeutic pressure levels was associated with the expected decrease in the 90th/50th percentile ratio of inspiratory lung conductance from a mean of 6.5+/-3.1 to 1.6+/-0.3 ( P <0.001). We conclude that variability of inspiratory conductance quantified by the 90th/50th percentile ratio may serve as a measure of flow limitation that is independent of the absolute value of conductance.