Experiences of Kidney Transplant Recipients as Patient Navigators.

BACKGROUND AND OBJECTIVE: The use of trained kidney transplant recipients as patient navigators resulted in increased completion of the steps in the transplant process by dialysis patients. We sought to understand the experiences of these patient navigators. SETTING AND PARTICIPANTS: Six kidney transplant recipients were hired and employed by transplant centers in Ohio, Kentucky, and Indiana. The transplant navigators received formal training as peer educators, met with dialysis patients on a regular basis, and provided tailored education and assistance about transplantation to each patient. They worked closely with the pretransplant coordinators and social workers to learn the details of each patient's transplant work-up. METHODOLOGY: We queried navigators using open-ended questions to learn about their experiences. Navigator responses were coded and common themes identified. A thematic auditor reviewed and refined the coding. RESULTS: Two primary categories of themes emerged about the navigator experience: 1. practical comments that supported programmatic or implementation observations of the navigators, and 2. affective comments that reflected a shared experience among the navigators and patients. The navigators were able to fill voids in the transplant process that were not fulfilled by other caregivers. This was accomplished by a natural bond based upon a shared experience (of dialysis and kidney failure) between the navigator and the patient. The patient and navigator became experiential partners. CONCLUSION: Kidney transplant recipients trained as patient navigators fill the role of a nontraditional medical provider, offer support during the transplant process, and provide an added benefit to complement routine dialysis and nephrology care.

Paranasal sinus ventilation in healthy subjects and in patients with sinus disease evaluated with the 133-xenon washout technique.

Ventilation of the paranasal sinuses is of great importance in sinus pathophysiology. Therefore, methods of measuring sinus ventilation are important for the evaluation of patients with sinus disease. In the present study, a 133-xenon washout technique was used to evaluate the ventilation of the paranasal sinuses in 34 healthy subjects and in 13 subjects with sinus disease (5 patients with nasal polyposis and 8 patients with chronic sinusitis). For this purpose, a 133-xenon-air mixture was insufflated in each nostril and the washout of the radioactive gas from the paranasal sinuses was monitored with a dynamic single-photon-emission computed tomography camera. The half-time (+/-SD) was found to be 18 +/- 18 minutes for the maxillary sinus, 10 +/- 8 minutes for the frontal sinus, and 18 +/- 23 minutes for the posterior ethmoid and sphenoid sinuses in the healthy subjects. Repeated measurements in 18 of the healthy subjects indicated that the method had acceptable reproducibility according to a Bland-Altman plot. The 133-xenon washout was not influenced by insufflation pressure, nasal patency, or body position. The subjects with sinus disease exhibited half-times of 77 +/- 101 minutes for the maxillary sinus, 91 +/- 124 minutes for the frontal sinus, and 60 +/- 60 minutes for the posterior ethmoid and sphenoid sinuses. For patients with nasal polyposis, the half-time was significantly longer than that in healthy subjects, while patients with chronic sinusitis did not differ from healthy subjects in this respect.

Factors influencing 133-xenon washout in a nose-sinus model.

The 133-xenon washout technique is a non-invasive method for the evaluation of ventilation of the paranasal sinuses. The half-time of 133-xenon washout (T(1/2)) is considered to reflect sinus ostial function and sinus ventilation. However, it is not known how morphological and physiological factors affect the washout from the paranasal sinuses. The aim of the present study was to evaluate how sinus volume, ostial diameter and nasal ventilation influence 133-xenon washout in a nose-sinus model. This is important for the interpretation of measurements of 133-xenon washout from paranasal sinuses in healthy subjects and in subjects with sinus disease. The 133-xenon washout was measured with a scintillation camera. The statistical analysis of the results showed that the logarithm (to the base 10) of the half-time of 133-xenon washout is linearly related to the ostial diameter, the sinus volume and the nasal ventilation in the model. In a multiple linear regression model, the most important factor contributing to 133-xenon washout was found to be the ostial diameter, which explained 76% of the variation in log T(1/2). In the same statistical model the sinus volume explained 7.5% and the ventilation 5.3% of the variation in log T(1/2). Calculations of the functional ostial diameter in healthy subjects were made, based on the results of the model study. The mean functional ostial diameter was found to be 3.5 mm (range 0.5-7.5 mm). The results obtained with the present model experiments may be of importance for the correct interpretation of the results of measurements of 133-xenon washout in healthy subjects and patients.

Cyclic adenosine monophosphate stimulation of mucociliary activity in the upper airways in vivo.

Xanthine derivatives are known to accelerate mucociliary transport in the lower airways, probably by preventing degradation of cyclic adenosine monophosphate (cAMP) and thereby increasing its intracellular concentration. The purpose of this study was to investigate the effects of cAMP on mucociliary activity in the upper airways. The effect on the mucociliary activity in the rabbit maxillary sinus of the xanthine derivatives theophylline and enprophylline was compared to that of the cAMP analog dibutyryl cAMP. The compounds were administered into the maxillary artery, and the response was recorded with a photoelectric technique. Infusions of theophylline (1.0 and 10 mg/kg) increased mucociliary activity (22.8% +/- 5.9%, n = 6, and 21.6% +/- 4.9%, n = 7, p < .05, respectively). Infusions of enprophylline (1.0 and 10.0 mg/kg) accelerated mucociliary activity (at the highest dosage tested, 24.3% +/- 4.1%). Infusions of dibutyryl cAMP (0.1 and 1.0 mg/kg) stimulated mucociliary activity, with the maximum increase (20.1% +/- 3.0%, n = 13, p < .05) being observed at a dosage of 0.1 mg/kg. The infused substances increased mucociliary activity within 1 minute after the start of the infusion, the duration of the response being approximately 20 minutes for theophylline, 22 minutes for enprophylline, and 12 minutes for dibutyryl cAMP. The present results support the view that cAMP is involved in regulating mucociliary activity in the upper airways. It remains to be elucidated whether xanthines such as theophylline and enprophylline are beneficial in upper airway disease in which mucociliary function is impaired (eg, chronic sinusitis).

Effects of inflammatory mediators on ciliary function in vitro.

Prostaglandins and histamine released during inflammatory and allergic reactions can affect the mucociliary system in different ways. By studying the effect of these mediators on ciliary beat frequency (CBF) with a photo-electrical technique in airway explants from different species, i.e. guinea-pig trachea, rabbit maxillary sinus, and human adenoid, the mechanisms underlying the effects of prostaglandin and histamine were further elucidated. Prostaglandin E1 (PGE1) produced a modest increase in CBF in preparations from guinea-pig trachea. The maximum response was 12.9 +/- 3.4% for the dose of 0.1 micrograms/ml, corresponding with 0.28 microM. Prostaglandin E1 produced a dose-dependent increase in explants from rabbit maxillary sinus, the maximum effect was 35.9 +/- 14.1% at a dose of 1.0 micrograms/ml. PGE1 produced a lesser increase in CBF in explants from human adenoids. A maximum increase of 4.1 +/- 1.6% was observed at a dose of 0.1 mg/ml. Histamine produced a moderate increase in CBF in explants from human adenoid at concentrations of 0.01-0.1 mM, corresponding with 1.84-18.4 micrograms/ml. In contrast, histamine did not significantly alter CBF in explants from the rabbit maxillary sinus or guinea-pig trachea. These results indicate that there are interspecies differences in the responsiveness to prostaglandins, and that PGE1 seems to have more powerful effects on CBF in the upper than in the lower airways.(ABSTRACT TRUNCATED AT 250 WORDS)

NK1 receptors mediate the increase in mucociliary activity produced by tachykinins.

The mucociliary activity of the rabbit maxillary sinus is increased after exposure to airway irritants such as cigarette smoke and capsaicin. This effect is partly due to a cholinergic reflex but involves an atropine-resistant response probably mediated by the release of tachykinins such as substance P or neurokinin A from sensory nerve endings. The aim of the present investigation was to evaluate the type of tachykinin receptor which mediates this increase in mucociliary activity. The mucociliary activity of the rabbit maxillary sinus was studied photoelectrically in vivo. It was found that a selective NK1 receptor agonist, [Sar9,Met(O2)11]substance P, dose dependently stimulated mucociliary activity, the maximum increase being 43.74 +/- 6.07% at a dose of 1 nmol/kg. A selective NK2 receptor agonist, [Nle10]neurokinin A-(4-10), produced a much weaker response, the maximum increase being 15.23 +/- 3.86% at a dose of 10 nmol/kg, whereas an NK3 receptor agonist, [Pro7]neurokinin B, was without effect. When the effects of the selective agonists were compared with the responses elicited by naturally occurring tachykinins at a dose of 1 pmol/kg, the order of the magnitude of the responses was [Sar9,Met(O2)11]substance P > substance P > neurokinin A. At this dosage the NK2 and NK3 receptor agonists did not have a significant effect. Pretreatment with the endopeptidase inhibitor phosphoramidon did not influence the magnitude of the responses but increased their duration. It is concluded that the NK1 receptor is responsible for the increase in mucociliary activity elicited by tachykinins released from sensory afferents in the upper airways.

Histamine stimulation of mucociliary activity in the rabbit maxillary sinus.

The in vivo effect of histamine on mucociliary activity in the rabbit maxillary sinus was investigated by injecting histamine into the maxillary artery and recording the responses with a photoelectric technique. Histamine stimulated the mucociliary activity dose-dependently in the dose range 10 to 1,000 micrograms/kg. The maximum response was 31.6% +/- 3.7% at a dose of 50 micrograms/kg. The histamine-induced stimulation of the mucociliary activity was characterized by a short latency with a peak response within 1 to 2 minutes and a slow decline lasting about 5 minutes. The response displayed tachyphylaxis. Cholinergic blockade with atropine did not affect the response to histamine. Blockade of H1 receptors with pyrilamine abolished the response to histamine, whereas blockade of H2 receptors with cimetidine was without effect. The H2 agonist dimaprit failed to stimulate the mucociliary activity. It is concluded that histamine stimulates the mucociliary activity in the rabbit maxillary sinus via H1 receptors.

Mucociliary activity and the diving reflex.

It has previously been shown that mucociliary activity in the rabbit maxillary sinus is immediately increased after short-term exposure to such airway irritants as cigarette smoke and ammonia vapor. This increase is mediated through the stimulation of capsaicin-sensitive nerve endings. Besides producing the mucociliary effect, these irritants inhibit breathing, a response characteristic of the diving reflex in mammals. Whether an increase in mucociliary activity is part of the diving reflex was investigated by injecting 0.5 mL water into the nasopharynges of anesthetized rabbits. Mucociliary and respiratory responses were compared with the effects of mechanical stimulation (ie, rotating an intranasal catheter until sneezing occurred). Water challenge produced an increase in mucociliary activity of 21.6% +/- 2.4%, a response that began approximately 10 seconds after injection. Mucociliary acceleration was completely blocked by atropine, indicating a cholinergic mechanism, but was unaffected by pretreatment with capsaicin. The respiration rate was inhibited by about 45% after challenge with water. Pretreatment with atropine and capsaicin had no effect on this reduced respiratory rate. Mechanical stimulation of the nasal mucosa accelerated mucociliary activity. This response appeared approximately 4 seconds after stimulation was begun, and occurred simultaneously with the onset of sneezing. The peak increase was 22.0% +/- 2.1%. Sneezing was followed by an increase in the respiration rate of about 40%. Pretreatment with atropine or capsaicin had no effect on respiratory responses, but did inhibit mucociliary acceleration, suggesting that the response is mediated through cholinergic effector neurons after activation of capsaicin-sensitive nerve endings.(ABSTRACT TRUNCATED AT 250 WORDS)

Prostaglandin E1 enhances the histamine induced stimulation of the mucociliary activity in the rabbit maxillary sinus.

Inflammatory mediators are released in the airways during both inflammatory and allergic reactions, and many of these mediators affect mucociliary activity. To discover whether mucociliary activity is changed by a combination of mediators, the interaction between prostaglandins and histamine or methacholine was studied in vivo in the rabbit maxillary sinus. We used a photoelectric technique and recorded frequency changes induced by tested substances. Prostaglandins E1 and F2 alpha (PGE1 and PGF2 alpha) were given as ia. infusions followed by bolus injections of histamine or methacholine. Infusion with PGE1 (0.1 microgram.kg-1) enhanced the stimulating effect of a subsequent injection of histamine (10 micrograms.kg-1), maximum stimulation being 33 +/- 6% compared to 14 +/- 4% after histamine alone (p = 0.02). When the histamine injection was given 20 min after PGE1 no enhancement was observed. PGE1 did not enhance the stimulating effect of methacholine. In contrast to PGE1, PGF2 alpha failed to enhance the effect of histamine. It is proposed that a role of PGE1 is to modify the mucociliary response to other mediators released during inflammatory and allergic reactions.

The influence of leukotrienes and platelet activating factor on mucociliary activity in the rabbit maxillary sinus.

Inflammatory mediators released in the airways during allergic reactions can affect the mucociliary system. Leukotrienes and platelet activating factor have been shown to affect the mucociliary activity in various cell preparations. The in vivo effects of these inflammatory mediators on mucociliary activity in rabbit maxillary sinus were investigated using a photoelectric technique. Leukotrienes C4 and D4 in the dose range 0.01-10.0 nmol/kg did not alter mucociliary activity significantly, either when given as bolus injections or as intraarterial infusions. Platelet activating factor had no effect in the dose range 0.001-0.1 nmol/kg. A dose of 1.0 nmol/kg increased mucociliary activity by 20.2 +/- 5.5% but produced adverse respiratory and circulatory effects at the same time. It is concluded that the inflammatory mediators leukotrienes C4, D4 and platelet activating factor have no essential regulatory influence on mucociliary activity in the upper airways of the rabbit.

Cholinergic and C-fibre mediated mechanisms in the stimulation of mucociliary activity induced by prostaglandins and histamine.

The involvement of cholinergic and C-fibre mediated mechanisms in the stimulation of mucociliary activity induced by prostaglandins and histamine was investigated in vivo in the rabbit maxillary sinus with a photoelectric technique. The prostaglandins E, (PGE,) and F2(2) alpha (PGF2 alpha) in dose of 0.1 microgram/kg and 10 micrograms/kg respectively stimulated the mucociliary activity in a biphasic fashion, with a small initial response during the first 1-2 min and a later maximum response after 3-4 min. These effects were resistant to atropine and to the SP antagonist (D-Pro2, D-Trp7,9)SP. The small initial response was blocked by pretreatment with high doses of capsaicin (13 mg i.a.), while the maximum response was unaffected. This indicates that the mucociliary responses induced by PGE, and PGF2 alpha involve capsaicin-sensitive C-fibres but that neither acetylcholine nor substance P were responsible. Histamine (50 micrograms/kg) stimulated mucociliary activity in the rabbit maxillary sinus and the effect was abolished by pretreatment with high doses of capsaicin and reduced by the SP antagonist (D-Pro2, D-Trp7,9)SP. This indicates that the histamine-induced stimulation of mucociliary activity involves capsaicin-sensitive C-fibres and that the effect might be mediated by substance P.

The effects of prostaglandins E1, E2 and F2 alpha on mucociliary activity in the rabbit maxillary sinus.

The in vivo effects of prostaglandins E1, E2 and F2 alpha on mucociliary activity in the rabbit maxillary sinus were investigated using a photoelectric technique. Prostaglandins E1 and F2 alpha both accelerated the mucociliary wave frequency in a dose-dependent fashion. For prostaglandin E1 the maximum increase was 17.4 +/- 2.6% (0.1 micrograms/kg), for prostaglandin F2 alpha it was 24.1 +/- 3.0% (10 micrograms/kg). The effects of prostaglandin E2 was inconsistent. Although some doses stimulated mucociliary activity, the effects were not reproducible. Inhibition of phosphodiesterase with theophylline did not alter the response to exogenous prostaglandin E1, nor did inhibition of endogenous prostaglandin synthesis with indomethacin affect the basal mucociliary activity or the response to exogenous prostaglandin E1. The present findings suggest that the tested prostaglandins are of minor importance for regulating mucociliary function in the rabbit maxillary sinus.

Nasal exposure to airway irritants triggers a mucociliary defence reflex in the rabbit maxillary sinus.

The effect on mucociliary (m.c.) activity in the rabbit maxillary sinus of cigarette smoke and ammonia (NH3) vapour delivered through a tracheal cannula or as nasal challenges was investigated by a photo-electric technique, and compared with simultaneously induced changes in the respiratory rate. Neither irritant had any effect on m.c. activity in the sinus after tracheo-bronchial exposure. However, the respiration rate was increased by NH3 vapour (2.5 ml, diluted 1:1 with room air) and neat cigarette smoke (10 ml) by 76.9% and 24.3% respectively (median values). In contrast, nasal challenges with both irritants increased m.c. activity by 24.1% (NH3) and 19.1% (cigarette smoke), and reduced the respiration rate by 31.0% (NH3) and 28.4% (cigarette smoke) (median values). NH3 vapour sometimes produced an apnea proper. Identical results were obtained in laryngectomized rabbits, indicating that laryngeal afferents were not involved in the responses. Moreover, topical application of the C-fibre stimulant capsaicin mimicked the effects produced by the airway irritants. It is concluded that nasal exposure to irritants triggers at least two different protective reflexes. One is the increase of m.c. activity in the upper airways involving sensory C-fibres and the other the apneic reflex of Kratschmer.

The role of neurokinin A and calcitonin gene-related peptide in the mucociliary defence of the rabbit maxillary sinus.

Substance P (SP) released from sensory C-fibres in the airways increases the mucociliary (m.c.) activity in the rabbit maxillary sinus. The purpose of the present study was to investigate the m.c. effects of two other neuropeptides, coexisting with SP in sensory neurones, neurokinin A (NKA) and calcitonin gene-related peptide (CGRP). NKA increased the m.c. activity dose-dependently (dose range 0.1-5.0 micrograms/kg) the maximum increase being 33.6 +/- 6.0%. The effect was inhibited by pretreatment with the tachykinin antagonist (D-Pro2, D-Trp7,9)SP, but not with atropine or hexamethonium. Thus NKA released from sensory C-fibres may contribute to the non-cholinergic increase of m.c. activity observed after C-fibre stimulation. In contrast CGRP did not influence the m.c. activity. Neither did it influence the responses to NKA or SP. It is concluded that CGRP is unlikely to be involved in the control of m.c. function.

Stimulation of C fibers by ammonia vapor triggers mucociliary defense reflex.

The neuropeptide substance P (SP) released from airway sensory C fibers accelerates mucociliary activity, and C fibers in the airways are stimulated by various irritants including ammonia (NH3) vapor. The short-term effects of NH3 vapor on mucociliary function in the in the maxillary sinus of rabbits anesthetized with urethane were investigated by a photoelectric technique. Challenges with 1.5 ml NH3 increased mucociliary activity dose-dependently, the maximal response being 26.6 +/- 1.6%. The increase appeared within 1.3 +/- 0.3 s after exposure. Atropine and hexamethonium decreased the effect of NH3, indicating that part of the response was mediated by cholinergic effector neurons, but a noncholinergic effect clearly remained. Pretreatment with large doses of capsaicin (13 mg i.a.) abolished the response, whereas the SP antagonist (D-Pro2, D-Trp7,9) SP inhibited the noncholinergic response. Challenges with NH3 vapor also decreased the respiratory rate. An identical response was noticed during injections with the C fiber stimulant capsaicin. Together these results indicate that NH3 vapor triggers a mucociliary protective reflex in the airways, involving capsaicin-sensitive C fibers. The recorded increase of mucociliary activity is probably due to the combined effect on the mucociliary system of both SP and acetylcholine released from the afferent and efferent part of the reflex arc, respectively.

Effects of neurokinin A and calcitonin gene-related peptide on mucociliary activity in rabbit maxillary sinus.

Substance P (SP) released from sensory C-fibers in the airways increases the mucociliary (m.c.) activity in the rabbit maxillary sinus. The purpose of the present study was to investigate the m.c. effects of two other neuropeptides, coexisting with SP in sensory neurones, neurokinin A (NKA) and calcitonin gene-related peptide (CGRP). NKA increased the m.c. activity dose-dependently (dose range 0.1-10.0 micrograms/kg, 88 pmol to 8.8 nmol/kg), the maximum increase being 41.9 +/- 2.6%. The effect was inhibited by pretreatment with the tachykinin antagonist (D-Pro2,D-Trp7,9)SP, but not with atropine or hexamethonium. Thus NKA released from sensory C-fibers may contribute to the non-cholinergic increase of m.c. activity observed after C-fiber stimulation. In contrast CGRP did not influence the m.c. activity. Neither did it influence the responses to NKA or SP. It is concluded that CGRP is unlikely to be involved in the control of m.c. function.