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Biomedical subjects

M M Cloutier

Publications and source records attributed to M M Cloutier.

At least 19 recordsLinked to original sources
PubMed2001

Diagnosing pediatric asthma: validating the Easy Breathing Survey.

OBJECTIVE: To determine the sensitivity, specificity, and predictive value of a simple, self-administered questionnaire for the diagnosis of asthma in children. STUDY DESIGN: A questionnaire specifically designed to assist primary care providers in making a diagnosis of asthma in children was developed and administered in 4 different primary care and subspecialty clinics, validated, and then used as part of an asthma management program called Easy Breathing. Asthma diagnoses were made according to recommended National Asthma Expert Panel Guidelines. RESULTS: Four questions on the survey were shown to be sensitive and specific for asthma. The sensitivity was greater for all levels (mild, moderate, and severe) of persistent asthma than for mild, intermittent asthma. A positive response to any 1 of the 4 questions was over 94% sensitive for asthma; a negative response to all 4 questions was 55% specific for ruling out asthma. CONCLUSIONS: Patient responses to 4 specific respiratory symptom questions can assist primary care providers in diagnosing asthma in children. Primary care providers serving pediatric populations at high risk for asthma should consider asking patients or their parents these 4 questions regarding asthma symptoms on a regular basis.

Adolescent↗
PubMed2001

Provider adherence to a clinical practice guideline for acute asthma in a pediatric emergency department.

UNLABELLED: Critics of the use of clinical practice guidelines (CPGs) in an emergency department (ED) setting believe that they are too cumbersome and time-consuming, but to the best of the authors' knowledge, potential barriers to CPG adherence in the ED have not been prospectively evaluated. OBJECTIVES: To measure provider adherence to an ED CPG based on National Asthma Education and Prevention Program (NAEPP) recommendations, and to determine factors associated with provider nonadherence. METHODS: Prospective, cohort study of children aged 1-18 years with the diagnosis of an acute exacerbation of asthma who were seen in a pediatric ED and requiring admission, as well as a random selection of children discharged to home following pediatric ED care. The following adherence parameters were assessed: at least three nebulized albuterol treatments in the first hour; early steroid administration (after the first nebulizer treatment); clinical assessments using pulse oximetry and peak expiratory flow (PEF) (for children >6 years old); and use of a clinical score to assess acute illness severity (Asthma Severity Score). Nonadherence was defined as any deviation of the above parameters. RESULTS: Between July 1, 1998, and June 30, 1999, 369 patients were studied. Of these, 38% (139) were discharged to home, 38% (140) were admitted to the observation unit, and 24% (90) were admitted to the inpatient unit. Illness severities at initial presentation to the ED were: 24% (86) had mild exacerbations, 59% (212) had moderate exacerbations, and 17% (62) had severe exacerbations. Sixty-eight percent (95% CI = 63% to 73%) of the patients were managed with complete adherence to the CPG. Of the 32% with some form of nonadherence, most (63%) were children older than 6 years; in this group 64% (48/75) were nonadherent due to lack of PEF assessment. When PEF assessment was disregarded, an 83% (95% CI = 79% to 87%) adherence to the CPG was achieved. Other nonadherence factors included: lack of at least three nebulized albuterol treatments provided timely within the first hour (5%); delay in steroid administration (6%); lack of pulse oximeter use (0.5%); and failure to record clinical score to assess severity (1.1%). Patient age, illness severity (acute and chronic), first episode of wheezing, and high ED volume periods (evenings and weekends) did not worsen adherence. CONCLUSIONS: Clinical practice guidelines can be used successfully in the pediatric ED and provide a more efficient management and treatment approach to acute exacerbations of childhood asthma. With a systematic and concise CPG, barriers to adherence in a pediatric ED appear to be minimal, with the exception of using PEF in the routine ED assessment.

Adolescent↗
PubMed2000

Practice of pediatric pulmonology: results of the Future of Pediatric Education Project (FOPE)

In 1996, the Future of Pediatric Education (FOPE) Project of the American Academy of Pediatrics (AAP) developed surveys to describe the nature of pediatric practices, recent trends in clinical practice, and anticipated workforce needs for both pediatric generalists and pediatric sub-specialists. A survey was specifically developed to describe the features of pediatric pulmonology as self-reported by pediatric pulmonologists. The survey was distributed to members of the AAP Pulmonology Section, the Pediatric Assembly of the American Thoracic Society, and certified pediatric pulmonologists recognized by the American Board of Pediatrics. Of the 535 respondents (67% of those invited to respond), the responses of 388 certified and 94 trained but not board-certified pulmonologists were included in the results. The characteristics of certified and non-certified respondents were the same for most survey questions. Clinical activities occupy 73 +/- 29% of professional time. Most pulmonologists work in urban, inner city, or suburban settings and 85% are affiliated with a medical school. One third are in private practice. As a group, research activities occupy less than 15% of their time. Most pediatric pulmonologists maintain a referral practice and use physician extenders to provide care. Patients with asthma and cystic fibrosis comprise 60-70% of patient volume. Both the volume and complexity of patients are increasing, as is competition for pediatric sub-specialty services. Pediatric pulmonary practices vary in size and in volume of patients that they manage in various settings. Forty percent of respondents identify allergists and other pediatric pulmonologists as sources of competition. Sixty-nine percent of respondents do not believe that there is a current need for additional pediatric pulmonologists in their respective communities. Only 15% of respondents plan to retire in the next decade.

Adult↗
PubMed2000

Factor and subscale structure of a parental health locus of control instrument (parental health beliefs scales) for use in a mainland United States Puerto Rican community.

This study was undertaken to determine whether the subscale structure of an instrument used to measure parental health locus of control is a valid representation of the concept of locus of control in the Puerto Rican community. Ethnocultural differences in values and attitudes may create different conceptualizations of questionnaire items, which may impact on the subscale factor loadings for these items. Four hundred and twenty parents of Puerto Rican ethnicity living in a mainland inner city community in the United States completed the Parental Health Beliefs Scales (PHBS) instrument, which was developed to measure parental locus of control regarding their children's health. Results were subject to exploratory factor analysis. The resultant factor structure was then compared to other published factor structures by confirmatory factor analysis. Exploratory factor analysis results show a new five factor solution. Compared to two previously published factor structures for this instrument, the new five factor structure has a better goodness of fit for this Puerto Rican study sample. Through item analysis, we were able to refine the final structure into a four factor, 15 item instrument. We conclude that the new factor structure for the PHBS creates an instrument with subscales that reflect Puerto Rican cultural beliefs and values, especially as it pertains to locus of control issues (e.g. respect of professionals, collectivism, and the importance of fate). When working with ethnocultural minority groups, the health services researcher needs to be certain that the research instruments used are culturally appropriate and sensitive.

Adult↗
PubMed1998

Byssinosis: role of polymer length on the effect of tannin on the airway beta-adrenergic receptor.

Tannin, isolated from cotton bracts and implicated in the pathogenesis of byssinosis, inhibits isoproterenol and forskolin-stimulated cAMP release from airway cells in part by decreasing cell surface beta-adrenergic receptor number and uncoupling the beta-adrenergic receptor from its stimulatory G-protein (Gs) and in part by inhibiting adenylyl cyclase activity. We have hypothesized that cotton tannin, because of its long polymer length, interacts with the hydrophobic binding pocket of the beta-adrenergic receptor and alters beta-adrenergic receptor binding and Gs coupling. In these studies, tannins of three different polymer lengths and molecular masses were isolated from cotton bracts using sequential Amicon ultrafiltration [molecular mass > 10, 000 (YM10 retentate), 1,000-10,000 (YM10 filtrate), and 1,000-5,000 Da (YM2 retentate)]. The YM10 retentate (25 microg/ml) decreased chloride secretion (Jnet = 1.11 +/- 0.28 (control) to 0.59 +/- 0.18 microEq/cm2.h, p < 0.05, n = 6), decreased cell surface beta-adrenergic receptor number (18.0 +/- 1.8 (control) to 10.6 +/- 0.9 fmol/mg protein, p < 0.02, n = 4), and inhibited forskolin-stimulated cAMP release (5,254 +/- 1,290 (control) to 2, 968 +/- 620 pmol/mg protein, p < 0.01, n = 8). In contrast, neither the YM10 filtrate nor the YM2 retentate had any effect on net chloride secretion, beta-adrenergic cell surface receptor number, or forskolin-stimulated cAMP release. We conclude that polymer length is essential for the effect of tannin on the beta-adrenergic receptor and on adenylyl cyclase.

Animals↗
PubMed1998

Tannin inhibits the cAMP-beta-adrenergic receptor pathway in bovine tracheal epithelium.

Tannin, isolated from cotton bracts, inhibits chloride secretion in airway epithelium. In bovine tracheal epithelial cells, tannin (25 micrograms/ml) blunted isoproterenol (Iso)-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) accumulation. Inhibition was time and dose dependent, with 52 +/- 5% (mean +/- SE, n = 6) inhibition at 60 min and 82 +/- 9% (n = 3) inhibition at 8 h. Inhibition was reversible starting at 4 h. Low-molecular-mass tannin (1,000-5,000 Da) had no effect on Iso-stimulated cAMP accumulation, whereas N-acetylcysteine, which interacts with cysteine residues, blocked the effects of tannin on Iso-stimulated cAMP accumulation. Tannin exposure (25 micrograms/ml for 30 min) had no effect on the dissociation constant (Kd) for [3H]dihydroalprenolol (DHA) (0.41 +/- 0.03 nM, n = 3) but decreased maximal binding from 252 +/- 32 to 162 +/- 36 fmol/mg protein. Using single-point analysis and [3H]CGP-12177, we determined that tannin (25 micrograms/ml for 4 h) decreased surface beta-adrenergic receptor density from 26.4 +/- 4.3 (n = 12) to 11.9 +/- 3.0 fmol/mg protein and that the decrease was dose dependent. Agonist binding affinity by Iso displacement of DHA demonstrated a two-site model (Kd values = 27 +/- 9 and 2,700 +/- 600 nM) and a ratio of high- to low-affinity receptors of 1:1. Tannin (25 micrograms/ml) steepened the curve and shifted it to the right, as did Gpp(NH)p. Gpp(NH)p had no further effect on the shape or position of the displacement curve in the presence of tannin. In contrast, when polymer length was decreased by oxidation, tannin had no effect on the DHA displacement curve. These data demonstrate that tannin reversibly desensitizes bovine tracheal epithelial cells to Iso, decreases beta-adrenergic receptor density, and uncouples the receptor from its stimulatory G protein. These data also suggest that the polymer length of tannin and its interaction with cysteine residues are important for these effects. These studies provide additional evidence for the role of tannin in the occupational lung disease byssinosis.

Acetylcysteine↗
PubMed1996

Tannin stimulates arachidonic acid release from bovine tracheal epithelial cells.

Condensed tannin, isolated from cotton bracts extract (CBE), increases arachidonic acid (AA) release from rabbit alveolar macrophages and inhibits its subsequent reacylation. We determined whether tannin from CBE had any effect upon AA release in bovine tracheal epithelial cells (BTE). [14C] AA release was measured at timed intervals after addition of various concentrations of tannin to BTE cells grown to confluence in the presence of [14C] AA. Tannin caused a time- and dose-dependent release of AA from airway cells, with a maximum release occurring at 1 min in the presence of 100 micrograms/ml of tannin, and was confirmed by high-pressure liquid chromatography. The pattern of release was similar to that observed with bradykinin (2 x 10(-6) M). AA release by tannin was partially inhibited by indomethacin (10(-5) M) but not by 5,8,11,14-eicosatetraynoic acid (ETYA; 10(-5) M. Both of these drugs were effective in inhibiting bradykinin-induced AA release. In addition, AA release was not inhibited by cycloheximide. Endotoxin at 100 pg/ml and higher also caused a time-dependent release of AA that was not inhibitable by indomethacin or ETYA. Tannin-induced AA release was inhibited by pretreatment with pertussis toxin but not by neomycin, an inhibitor of phospholipase C (PLC). Neither pertussis toxin nor neomycin had any effect upon endotoxin-induced AA release. In other experiments, neither tannin nor endotoxin had any effect on [14C]AA uptake by BTE. These data demonstrate that tannin at low concentrations and endotoxin at high concentrations increase AA release by BTE cells. The AA release by tannin is partially metabolized by the cyclooxygenase pathway. We hypothesize that tannin-induced AA release is not mediated by PLC but may be mediated by other phospholipases, including PLA2.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1995

Ethnomedical (folk) remedies for childhood asthma in a mainland Puerto Rican community.

BACKGROUND: Childhood asthma is the most common chronic illness of childhood. The highest prevalence of childhood asthma in the United States occurs in the Puerto Rican community, and there are many traditional beliefs and practices regarding asthma that coexist with biomedical therapies. OBJECTIVES: To describe the ethnomedical treatment practices for childhood asthma in one mainland United States Puerto Rican community and to determine whether any of these practices are effective or potentially harmful. METHOD: Home interview with caretakers of 118 Puerto Rican children with asthma who seek care at two community health clinics in an inner city in the eastern United States. RESULTS: Common home-based ethnomedical practices include attempts to maintain physical and emotional balance and harmony, religious practices, and ethnobotanical and other therapies. Potentially harmful practices are uncommon, and other remedies are only harmful if not taken as directed. Many remedies are not effective from a biomedical standpoint (ie, bronchodilation or antiinflammation), but if analyzed within the ethnomedical explanatory model--which includes the belief that expulsion of mucus and phlegm from the body is beneficial for the treatment of asthma--these remedies bring about the desired effect and are therefore considered effective to the user. CONCLUSIONS: Ethnomedical therapies for asthma in the mainland Puerto Rican community are well known and commonly used. Most practices are not idiosyncratic but fit within a coherent ethnocultural belief system. The health care practitioner can lower the risk for potentially toxic effects of some treatments by discussing these practices with patients and families. Some ethnomedical practices are not discordant with biomedical therapy. Incorporation of these practices into the biomedical plan may help to fit the biomedical therapy into the lifestyle of the patient.

Asthma↗
PubMed1995

Tannin inhibition of protein kinase C in airway epithelium.

Tannin, a polydisperse polyphenol extracted from cotton bracts (CBE), has been implicated in the pathogenesis of byssinosis, a lung disease of mill workers. CBE tannin inhibits chloride secretion in airway epithelial cells by means of an unknown mechanism(s). Activation of protein kinase C (PKC) by PMA (phorbol 12-myristate 13-acetate) in airway cells increases chloride secretion. The effect of tannin on this PKC pathway was examined, using canine tracheal epithelium mounted in Ussing chambers. PMA addition (10 nM) to the mucosal bath resulted in a 0.36 +/- 0.07 microEq/cm2.h (mean +/- SEM, n = 20) increase in short-circuit current (Isc) and a 0.38 +/- 0.17 microEq/cm2.h increase in net chloride secretion (Jnet). The inactive 4 alpha-phorbol had no effect. Tannin addition to the mucosal bath produced a dose-dependent decrease in Isc and Jnet. In tissues pretreated with 2-50 micrograms/ml tannin, and subsequently stimulated with PMA, tannin inhibited PMA stimulation of chloride secretion beginning at a tannin concentration of 10 micrograms/ml (0.09 +/- 0.05 microEq/cm2.h [n = 10] increase in Isc and 0.08 +/- 0.03 microEq/cm2.h increase in Jnet with PMA after tannin pretreatment). At 50 micrograms/ml tannin, the stimulatory effect of PMA was completely abolished. The known PKC inhibitor, H-7 (20 microM), inhibited PMA stimulation, while chelerythrine (2 microM) had not effect on PMA-stimulated Isc and Jnet, and calphostin C was toxic to the airway epithelium. In membrane fragments, 2.5 micrograms/ml tannin inhibited the rate of histone III phosphorylation by PMA from 32.1 +/- 4.4 nmol/mg protein per min to 20.1 +/- 2.7 nmol/mg protein per min (n = 7). In bovine airway cells, tannin pretreatment (2.5 micrograms/ml) decreased the cytosolic activity of PKC but had no effect on PKC translocation to the membrane. We conclude that tannin inhibits chloride secretion in airway epithelial cells in part by inhibiting PKC.

Animals↗
PubMed1995

Pulmonary function abnormalities in Prader-Willi syndrome.

OBJECTIVE: To determine whether individuals with Prader-Willi syndrome (PWS) have abnormalities in pulmonary function as a result of thoracic muscle weakness. DESIGN: Testing of spirometry, flow-volume curves, lung volumes, and static respiratory pressures was performed in patients with PWS who are followed at the University of Connecticut. All tests were performed in triplicate on two or more occasions. Only reproducible tests were accepted. Established normative data were applied for all test results. RESULTS: A total of 18 male subjects (age, 17.9 +/- 10.2 years (mean +/- SD); range, 5-39 years) and 17 female subjects (age, 23.5 +/- 13.0 years; range, 5-54 years) completed the tests. Forced vital capacity and forced expiratory volume in 1 second were reduced; the forced expiratory volume in 1 second/forced vital capacity ratio was normal, total lung capacity was in the low normal range, and residual volume was elevated. Maximum inspiratory (PImax) and expiratory (PEmax) pressures were markedly reduced in 32 subjects tested. Fifteen subjects had PEmax values and 20 subjects had PImax values < 60 cm H2O, respectively. There was a linear correlation between forced expiratory volume in 1 second and both PImax and PEmax (r = 0.71; r = 0.62, respectively), and between forced vital capacity and both PEmax and PImax (r = 0.62 and r = 0.74, respectively). There was an inverse relationship between both PImax and PEmax, and residual volume (r = 0.47 and r = 0.72, respectively). CONCLUSION: Children and adults with PWS have restrictive ventilatory impairment primarily as a result of respiratory muscle weakness. Efforts to improve thoracic muscle strength may be useful in improving pulmonary function in individuals with PWS.

Adolescent↗
PubMed1995

Tannin inhibits adenylate cyclase in airway epithelial cells.

Tannin, isolated from cotton bracts extract and implicated in the pathogenesis of byssinosis, inhibits adenosine 3',5'-cyclic monophosphate (cAMP) production and Cl- secretion in bovine airway epithelial cells in part by inhibiting adrenergic receptor binding. The purpose of this study was to determine whether tannin affected other parts of the adrenergic-cAMP signal transduction pathway by examining the effect of tannin on guanosine 5'-triphosphate (GTP)-regulatory pathways (G proteins) and on adenylate cyclase activity. cAMP production in confluent airway epithelial cells was measured in the presence of cholera toxin (100 micrograms/ml), an activator of GS proteins, and forskolin (0.1-1,000 microM), a direct activator of adenylate cyclase. Cholera toxin stimulated cAMP production; this response, however, was inhibited in cells pretreated with 50 micrograms/ml tannin. Forskolin (100 microM) stimulated cAMP production 13-fold above baseline values. Tannin pretreatment inhibited the stimulatory effect of forskolin on cAMP release in a dose-dependent manner with a tannin concentration causing 50% inhibition of 7.5 micrograms/ml. The stimulatory effect of forskolin on cAMP release was completely inhibited in cells pretreated with 50 micrograms/ml tannin. The inhibition was reversible 3 h after removal of tannin from the solution. Tannin also inhibited forskolin-stimulated adenylate cyclase activity in a dose-dependent, noncompetitive manner. We conclude that forskolin and cholera toxin stimulate cAMP production in airway epithelial cells and that tannin inhibits the production of cAMP in airway epithelial cells by a direct effect on adenylate cyclase activity.

Adenylyl Cyclase Inhibitors↗
PubMed1994

Tannin inhibits cAMP pathways in bovine airway epithelium.

Tannin, isolated from aqueous extracts of cotton bracts, inhibits chloride secretion in airway epithelial cells. The effect of tannin on the epinephrine- and bradykinin-stimulated rise in intracellular free calcium and cyclic adenosine monophosphate (cAMP) was examined using bovine tracheal epithelial cells in suspension and culture. Basal intracellular calcium levels were 33 +/- 11 nM (mean +/- SEM, n = 54) and increased 13- to 15-fold after addition of epinephrine (10(-6) M) or bradykinin (2 x 10(-6) M). Tannin pretreatment blunted the subsequent response to epinephrine beginning at a tannin concentration of 10 micrograms/ml. Pretreatment with 100 micrograms/ml tannin completely inhibited the rise in intracellular free calcium in response to epinephrine but had no effect on the calcium response to bradykinin. In the absence of tannin, both bradykinin and epinephrine increased intracellular levels of cAMP. At a tannin concentration of 10 micrograms/ml, tannin inhibited the rise in intracellular cAMP in cells stimulated with either epinephrine or bradykinin but had no effect on bradykinin-stimulated prostaglandin E2 release. Tannin alone (10 micrograms/ml) increased prostaglandin E2 release. In other studies, tannin inhibited epinephrine binding to airway epithelial cells in a dose-dependent manner. R(o) decreased from 948 +/- 69 fmol/mg protein under control conditions (n = 4) to 587 +/- 131 fmol/mg protein in the presence of 25 micrograms/ml tannin (n = 3). Tannin had no effect upon the Kd for epinephrine binding (132 +/- 12 pM). Tannin had no effect on bradykinin binding to airway epithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Nebulized steroid therapy in bronchopulmonary dysplasia.

The effect of inhaled beclomethasone dipropionate (BEC) was studied in seven infants between 7 and 18 months of age with glucocorticoid-dependent bronchopulmonary dysplasia. Oral glucocorticoid therapy, pulmonary function, growth, daily caloric consumption, blood pressure, blood sugar, blood gases, and immunoglobulins were monitored for 3 months before (control period) and 3 months after (intervention period) instituting inhaled beclomethasone dipropionate (25 micrograms/kg/day divided tid) delivered by Pulmoaide with a DeVilbiss nebulizer. Acute BEC inhalation produced no change in pulmonary function. During BEC treatment, oral glucocorticoid therapy was decreased in all infants, stopped in four infants within 3 months and in the other three infants in 4-5 months. Within 1 month of inhaled BEC the rate of linear growth and weight increased markedly (2.2 +/- 1.8 vs 6.4 +/- 2.4 cm/month - mean +/- SD and 9.3 +/- 6.5 vs 18.2 +/- 7.4 g/day, respectively without change in average daily caloric consumption (113 +/- 16 vs. 110 +/- 15 cal/kg/day). Immunoglobulins also significantly increased during BEC therapy (IgG(Total) 246 +/- 74 vs 463 +/- 111 mg/dL). Pulmonary function revealed moderate obstructive pulmonary disease before BEC. After 3 months of BEC inhalation no significant change occurred although respiratory system resistance decreased and the flow at 25% of tidal volume to peak flow ratio increased more than predicted by intersession variability. In no infant did pulmonary function decline after BEC, nor were any apparent adverse effects noted in this small group of patients. In conclusion, inhaled BEC was effective in decreasing oral glucocorticoid therapy and in modifying glucocorticoid-induced growth suppression in a very small, highly select group of infants with bronchopulmonary dysplasia.

Administration, Inhalation↗
PubMed1993

Congenital cystic adenomatoid malformation.

Congenital cystic adenomatoid malformation is an uncommon congenital anomaly. We present four additional children with CCAM and review the literature. Two of these children had unusual manifestations of CCAM--one presented with a "cavitary lesion" while the other is suspected of having bilateral disease.

Bronchoscopy↗
PubMed1992

p-Aminohippurate transport in airways: competitive inhibition.

p-Aminohippurate (PAH) transport in canine tracheal epithelium occurs by a HCO3- -PAH exchange process that is located on the luminal membrane and is inhibited by stilbene derivatives. The effects of increasing concentrations of other organic anions, including probenecid (10-250 microM), dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP; 10-1,000 microM), phenol red (10-250 microM), and urate (25-500 microM), and the organic cation tetraethylammonium bromide (TEA; 250 microM) on PAH transport were examined in canine tracheal epithelium mounted in Ussing chambers. Neither phenol red, urate, nor TEA had any effect on electrophysiological properties or unidirectional or net PAH fluxes. In contrast, beginning at 10 microM, both probenecid and cAMP produced significant decreases in unidirectional and net PAH absorption without change in unidirectional PAH secretion. The initial change in net PAH absorption occurred in the absence of any change in electrophysiological properties. Higher concentrations of both probenecid and cAMP produced further decreases in net PAH absorption and significant changes in electrophysiological properties. Probenecid and cAMP increased the apparent Michaelis constant for PAH absorption without affecting maximum transport rate. The inhibitory constant for probenecid was 1.01 +/- 0.06 x 10(-4) M (mean +/- SE) and for cAMP was 5.18 +/- 0.20 x 10(-4) M. We conclude that PAH transport in canine tracheal epithelium demonstrates competitive inhibition by other organic anions and substrate specificity. We also conclude that the affinity of the exchange transport system is higher for probenecid than for PAH and cAMP.

Animals↗