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The sweat of single sweat glands of healthy individuals and cystic fibrosis patients was analyzed for differences in bicarbonate, lactate, and pH. These values were monitored as a function of sweat rate simultaneously with 1) the electrical potential difference at the duct orifice (with respect to the interstitial fluid) and 2) the concentrations of sodium, potassium, and chloride in surface sweat. Sweat in both groups contained about equal concentrations of lactate and bicarbonate at similar sweat rates. Similarly, the pH of sweat secreted at similar rates in the two populations was not significantly different. Acidification of sweat increased with decreasing sweat rate. In both populations, lactate and bicarbonate may be absorbed passively in the distal sweat duct in their nonionic form and, thus, not influenced by the increased electrical potential difference in the cystic fibrosis sweat duct. The uptake of these ions may involve active proton secretion by sweat duct cells.

Parenchymal cells of exocrine glands have been reported to develop numerous large vacuoles when intensely stimulated either pharmacologically, electrically, or physiologically. We have found that tracheal submucosal glands of the cat form similar vacuoles in response to alpha-adrenergic stimulation. Light and electron microscope examination of tracheal submucosal glands stimulated in vitro with methoxamine (10(-4) M) reveals that only serous cells of the gland acini develop vacuoles. Ductal cells and mucous acinar cells do not form vacuoles. Furthermore, several lines of evidence indicate that within serous cells vacuoles arise from secretory granules, which apparently swell as they accumulate fluid during intense stimulation. The following paper describes some of the factors and characteristics of stimulus-induced vacuolation.

The dye-coupling status of secretory and reabsorptive cells in micro-dissected lengths of human eccrine sweat gland was investigated by means of intracellular microiontophoresis of the fluorescent naphthalimide dye Lucifer yellow CH (Mr 457), which passes through gap junctions. Cells of the reabsorptive duct exhibited complete dye coupling between the apical and basal layers of the epithelium. Conversely, cells of the secretory tubule exhibited selective dye coupling. Of the three cell types present, clear, dark, and myoepithelial, the dark cells were impaled and labeled almost exclusively in the present study. These cells were observed either as single cells or as dye-coupled groups of neighboring dark cells. In no instance were dark cells observed to be dye coupled to clear cells or to myoepithelial cells. Because myoepithelial cells are known to be dye coupled exclusively to neighboring myoepithelial cells, the remaining clear cells must either be uncoupled or show selective dye coupling to neighboring clear cells. The significance of these findings is considered with respect to the regulation and function of the different cell types present in the human eccrine sweat gland.

Mg and PO4 concentrations were significantly higher in unmixed parotid saliva from chronic renal failure (CRF) patients than in controls. No significant differences were noted in the flow, pH or concentrations of Na, K, Cl or Ca; however, the Na/K ratio was significantly lower in CRF patients. No correlation between plasma PTH levels and the concentrations of Ca, Mg, or PO4 in saliva was found. Taken with previous results from elevated divalent ion concentrations in sweat from CRF patients, these findings suggest that the excretion of divalent electrolyte glands may represent a generalized abnormality in exocrine glands in CRF. We hypothesize that the active processes involved in regulating the concentrations of these ions in exocrine secretions are altered so that larger amounts of these elements are excreted in CRF patients.

Human eccrine sweat gland cells grown in culture were found to lose their characteristic shape, becoming flattened and organized into multilayers. The resting membrane potentials of the cultured secretory cells (-35 +/- 2 mV, n = 36) were significantly higher than those measured for cultured duct cells (-22 +/- 1 mV, n = 58, P less than or equal to 0.01). When the cholinergic agonist methacholine (10(-5) or 10(-6) M) was administered, the cultured secretory cells could be distinguished unequivocally by their atropine-sensitive hyperpolarizing response (-20 +/- 2 mV, n = 43), whereas no cultured duct cells responded. When the sodium conductance antagonist amiloride (10(-5) or 10(-6) M) was administered, 44% of cultured secretory cells responded by hyperpolarization (-8 +/- 1 mV, n = 8), whereas 87% of cultured duct cells hyperpolarized (-15 +/- 1 mV, n = 46) and by a significantly greater margin (P less than or equal to 0.01). Substitution of chloride with gluconate in the bathing medium caused membrane potential depolarization in both cultured secretory and duct cell populations, which is consistent with the presence of a chloride conductance in the plasma membrane. The beta-adrenoceptor agonist isoproterenol induced a transient hyperpolarization of 5-10 mV in three out of six cultured secretory cells tested but had no effect on cultured duct cells.

Cl- permeability in the reabsorptive sweat duct (RSD) epithelium from normal subjects was studied using electrophysiological techniques. The average basolateral membrane potential (Vb) of normal ducts was -36.8 +/- 0.8 mV and the average apical membrane potential (Va) was -27.2 +/- 0.8 mV (n = 45). Amiloride in the lumen of microperfused sweat ducts hyperpolarized Va by 34.3 +/- 3.1 mV and Vb by 25.7 +/- 3.1 mV (n = 12) with a small but significant increase in voltage divider ratio (Ra/Rb) from 4.2 +/- 0.8 to 5.0 +/- 0.8 (n = 8). Cl- substitution in the lumen depolarized Va by +37 +/- 4.2 (n = 11) accompanied by a significantly larger increase in Ra/Rb from 4.8 +/- 2.6 (n = 8) to 7.0 +/- 3.1 (n = 8). Bath Cl- substitution depolarized Vb by +24.3 +/- 2.7 mV (n = 15) while decreasing Ra/Rb from 3.2 +/- 0.7 to 1.9 +/- 0.4 (n = 7). These results indicated a significant Cl- permeability in both apical and basolateral membranes. Removing Cl- from the lumen significantly decoupled Va and Vb and restricted the amiloride-induced hyperpolarization to the apical membrane. This result may suggest that intracellular Cl- might be responsible for coupling Va and Vb and that hyperpolarization of Va and Vb by amiloride may result in changes in intracellular Cl-. Alternatively, Va and Vb could be coupled through a Cl- sensitive paracellular shunt. These results are consistent with Cl- permeability in both apical and basolateral membranes of duct cells. However, the question of whether paracellular Cl- permeability is important in Cl- uptake cannot be determined from the present data.

Patients with cystic fibrosis have characteristic disturbances in the electrolyte composition of their sweat, saliva, and pancreatic secretions. We studied the electrical properties of sweat glands in eight patients with cystic fibrosis and in seven normal volunteers to determine the basis of the well-documented inhibition of sodium absorption in this disease. The average electrical potential across 47 sweat glands in the patients was -66.3 +/- 2.1 mV, as compared with -29.8 +/- 3.2 mV for 39 glands in the normal controls (P less than 0.001). The average sweat-secretion rate in 33 glands from six patients was not significantly different from that in 34 glands from six controls, but average concentrations of sodium, chloride, and potassium were significantly higher in sweat droplets from the patients. Calculated rates of both sodium and chloride reabsorption were lower in sweat glands of patients than of normal controls, but chloride reabsorption was more markedly reduced than sodium reabsorption. We conclude that a decrease in epithelial permeability to chloride may explain the characteristic changes in sweat electrolytes in cystic fibrosis and could be a generalized abnormality in the disease.

Techniques available for the measurement of methotrexate (MTX) in biological fluids are reviewed. The importance of measuring MTX in plasma following high-dose MTX treatment is now well recognized and renewed interest in the metabolism and pharmacokinetics of the drug has prompted the development of new techniques of analysis. Results obtained with our radioimmunoassay are presented and compared with results obtained by other methods.

At the present time methotrexate (MTX) is probably the only cytotoxic drug for which therapeutic drug monitoring is important. Radioimmunoassay (RIA), HPLC and enzyme inhibition assays have all been used for this purpose [cf. arts in this vol. by S.H. Curry,#E-3, and J.W. Paxton, #NC(D)-5]. Comparative studies have shown that immunoassay techniques tend to slightly overestimate plasma MTX concentrations especially at late time points [l, 2], although in another study [3] it was concluded that for monitoring purposes any of the techniques was suitable.

A technique is described whereby-volume, self-filling micropipettes can be constructed with minimal time and effort. The delivery volumes of such pipettes may range from several picoliters to more than 100 nl. The delivery of a given pipette of even the smallest volume is precise, generally yielding standard deviations much less than 1% of the mean volume as measured by liquid-scintillation counting of isotope dilutions. The technique offers considerable advantage to previously described techniques for constructing small constant-volume pipettes.

The effect of the loop diuretic bumetanide on Cl- transport in the human reabsorptive sweat duct (RSD) was studied to determine the properties of Cl- transport in this tissue with an emphasis on its role in cystic fibrosis. Bumetanide (10(-4) M) in the bath decreased the NaCl reabsorption rate (+/- SE) from 235 +/- 72 to 77 +/- 24 pmol/min per mm (n = 10). Bumetanide in the lumen decreased the rate of NaCl reabsorption to a lesser extent from 132 +/- 17 to 84 +/- 16 pmol/min per mm (n = 9). At least part of this inhibition appears to be due to the inhibition of a Cl- conductance in the RSD, as evidenced by a significant increase in the specific resistance (Rt) of the tissue from 8.3 +/- 0.6 to 52.7 +/- 19.3 omega/cm2(n = 3) due to bumetanide in the bath. Luminal bumetanide also increased Rt but to a lesser degree [from 9.8 +/- 1.2 to 16.4 +/- 2.0 omega/cm2 (n = 3)]. Bumetanide also affected the transepithelial potential (Vt), hyperpolarizing it from -10.9 +/- 0.8 to -28.6 +/- 2.0 mV (n = 13). In ouabain-inhibited ducts, a threefold dilution of luminal NaCl concentration resulted in a -13.5 +/- 1.7 mV dilution diffusion potential which was abolished by bumetanide in the bath, indicating that bumetanide removed the anion selectivity of the epithelium. Bumetanide hyperpolarized the basolateral membrane potential (Vb) from -33.6 +/- 1.9 to -44.3 +/- 1.4 mV and depolarized the apical membrane potential (Va) from -20.9 +/- 0.9 to 14.0 +/- 1.3 mV. These results suggest that bumetanide inhibits transcellular Cl- conductance with possible additional effects on the paracellular Cl- conductance pathway as well.

Nine hundred twenty-five male progeny from 50 sire families of a commercial sire line were weighed at 14, 28, and 47 days and scored for right ventricular hypertrophydilation at 48 days. Broilers with marked hypertrophy of the right ventricle at processing (298 of 925) were significantly heavier than their more normal contemporaries at 14 and 28 days of age. These results suggest that rapidly growing broilers are more susceptible to increased pulmonary arterial pressure resulting in right ventricular hypertrophy, right ventricular failure, and ascites than slower-growing broilers. Thirty-five (3.5% of 997) broilers died from right ventricular failure and ascites, and 14 (1.5% of 925) has ascites at processing. Two hundred fifty-nine sibs were kept on full feed to 16 weeks of age. Between 7 and 16 weeks, 68 (26.3%) of these cockerels died from right ventricular failure and ascites and a further 27 (10.4%) had marked right ventricular hypertrophy-dilation when processed at 16 weeks. Thus most of the 298 broilers classified as having marked right ventricular hypertrophy at 7 weeks would likely have died from right ventricular failure and ascites if they had been kept on full feed until 16 weeks.

In America, cystic fibrosis (CF) is the most common fatal inherited disease. In the past few years new concepts have evolved regarding the etiology of CF, changing from an almost universal acceptance of the abnormality as a disease of abnormal mucus production to that of a disease of abnormal fluid and electrolyte transport. Although mucus production is increased, this probably occurs as a secondary defense or protection against more primary disturbances in electrolyte transport brought on by a defect in Cl- permeability that affects both fluid absorption and fluid secretion. Here I review the progress that has been made and some of the puzzles uncovered in recent investigations of electrolyte transport in secretory and absorptive processes in cystic fibrosis.

We studied the Cl- permeability properties of apical and basolateral membranes of human reabsorptive sweat duct (RSD) from normal and cystic fibrosis (CF) subjects. In normal ducts, Cl- substitution by impermeant anion gluconate in the lumen increased the voltage divider ratio (VDR) from 4.8 +/- 0.9 to 7.0 +/- 1.1 (n = 8, P less than 0.05), whereas Cl- substitution in the contraluminal bath decreased the VDR from 3.2 +/- 0.7 to 1.9 +/- 0.4 (n = 7, P less than 0.05). These results are consistent with a significant Cl- permeability in both apical and basolateral membranes of normal ducts. Amiloride (10(-4) M) in the lumen of normal ducts resulted in a small increase in VDR from 4.2 +/- 0.6 to 5.0 +/- 0.8 (n = 10, P less than 0.05), whereas the current-induced basolateral membrane voltage deflections (delta Vb) increased from 6.9 +/- 1.3 to 7.7 +/- 1.2 mV, suggesting that inhibition of Na+ permeability decreased basolateral membrane Cl- permeability. In the absence of luminal Cl-, amiloride decreased delta Vb and induced much greater effect on VDR (from 5.2 +/- 1.1 to 10.8 +/- 2.3, n = 9, P less than 0.05) than in the presence of Cl-. Likewise, in the presence of amiloride, Cl- substitution in the lumen had greater effect on VDR (increased from 3.5 +/- 0.5 0.5 to 10.0 +/- 1.5, n = 15, P less than 0.05) than in the absence of amiloride. These results indicate that Na+ conductance in the apical membrane of the normal duct is significantly smaller than Cl- conductance.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to determine if expression of the cystic fibrosis gene can be detected in heterozygotes, we determined sweat responses induced by local stimulation with cholinergic and beta-adrenergic agents for 20 heterozygotes, 19 age- and sex-matched controls, and five subjects with cystic fibrosis. Active sweat glands were counted and sweat droplets were collected in constant bore capillaries and measured optically. Each subject was tested two to six times. The central finding was that the sweat response of carriers was significantly lower than controls to beta-adrenergic stimulation (p = 0.0013, two-tailed t test; p less than 0.02, Mann-Whitney U), while cystic fibrosis homozygotes did not sweat at all. In contrast, the cholinergic sweat responses did not differ between carriers and controls. For both groups the correlation between cholinergic and beta-adrenergic sweating was positive, but a linear regression of beta-adrenergic sweat responses as a function of cholinergic sweat responses yielded slopes that were significantly different for the two groups. The ratio of beta-adrenergic to cholinergic sweating was plotted for each subject; the mean ratio of the carriers was approximately half of the mean for the controls (p = 0.0002 using t test or p less than 0.002 using the Mann-Whitney U). Our results confirm previous studies and provide new evidence that carriers have, on average, a beta-adrenergically stimulated secretory response that is significantly reduced relative to the control response.

Na/K-ATPase sites in both the secretory and reabsorptive epithelia of isolated and microperfused human eccrine sweat glands are localized cytologically. Localization was accomplished through autoradiography of bound 3H-ouabain, a specific inhibitor of the enzyme. Ouabain binding characteristics were determined to ensure maximum specific binding. Enzyme sites are localized only on the basolateral surface of both epithelia in spite of the fact that sodium transport is reversed, i.e., secretory: blood to lumen and reabsorptive: lumen to blood. In view of these findings and in comparison with other recent observations, the role of Na/K-ATPase in secretory electrolyte transport is questioned.

Eccrine sweat is produced by millions of miniscule glands buried in the skin. Eccrine sweating from the general body surface is an extremely important function in human thermoregulation; disturbances either in the control of sweating activity or in the glands themselves can result in problems ranging from minor social embarrassment to fatal hyperpyrexia. A general review of the function and control of normal sweating precedes an overview of sweating abnormalities.

Single equine sweat glands were found to secrete for more than 1 h in vitro in response to pharmacologic secretagogues. The adrenergic agonists epinephrine and norepinephrine evoked maximal sweat rates of 2.0 nl X gland-1 X min-1. However, the concentration of norepinephrine (10(-5) M) required to evoke the maximal response was 10 times higher than that for epinephrine. Maximal sweat rates also were stimulated with the beta 2-adrenergic agonist terbutaline. This stimulation was blocked by the beta-adrenergic antagonist propranolol. Moderate sweating responses were also obtained with the alpha-adrenergic agonists phenylephrine and methoxamine, but these responses also were blocked by propranolol. Neither the muscarinic blocker atropine nor the alpha-adrenergic antagonist phentolamine inhibited any of the pharmacologically induced sweat responses. Unlike most other mammalian exocrine glands, cholinergic agonists were ineffective in stimulating sweat secretion. Therefore equine sweat glands apparently are under predominantly beta-adrenergic control.

The effects of three electrolyte transport inhibitors on the secretory and absorptive function of the human eccrine sweat gland were examined. Amiloride and furosemide at 10(-4) mol/l had no detectable effect on secretion while ouabain at 10(-4) mol/l completely inhibited secretion. In contrast, when amiloride, ouabain and furosemide were applied at 10(-4) mol/l to the luminal surface of the sweat duct by microperfusion, only amiloride blocked Na reabsorption. When the same inhibitors were added to the bathing solution at the same concentration, only ouabain inhibited Na reabsorption detectably. Present findings suggest that the secretory epithelium is permeable to solute and water movement while the duct epithelium is probably impermeable with respect to fluid movement across it.

Summary: The physiological basis for the defect in NaCl reabsorption in cystic fibrosis (CF) sweat glands is not known. We have systematically followed the concentrations of the three major inorganic electrolytes in sweat as a function of single gland sweat rate in patients with CF and normal individuals. The result demonstrates that (1) at low sweat rates, sweat glands of CF individuals can reduce NaCl concentrations to normal levels and (2) that the concentration of organic anions and/or HCO3 in CF sweat is substantially less than in normal sweat. Speculation: Present data and other findings suggest that Na/K transport and a postulated Na/H exchange are normal, but that a postulated anion exchange may be defective in cystic fibrosis sweat glands. These observations suggest an underlying transport genetic abnormality, which might explain observed abnormalities in cystic fibrosis exocrine gland secretions in general.

Several factors affecting the stimulus-induced vacuolation in cat tracheal submucosal glands described in a companion paper [Am. J. Physiol. 241 (Cell Physiol. 10): C18–C24, 1981] were examined. Stimulation with predominantly alpha-adrenergic, beta-adrenergic, and cholinergic agonists at various concentrations and in the presence of appropriate blockers showed that alpha-adrenergic or cholinergic stimulation is more effective in inducing vacuolation than beta-adrenergic stimulation. In addition, Ca- or HCO3- deficient incubation medium or low incubation temperature either blocked or significantly decreased the vacuolation response. Stimulation in the presence of the Na-K-ATPase inhibitor ouabain prevented vacuolation. The known roles of these factors in fluid transport are consistent with the possibility that stimulus-induced vacuolation possibly arises in response to disturbances in cytoplasmic fluid, which are induced in the secretory cell when the fluid component of secretion is intensely stimulated. A model is presented that possibly relates the observed responses to intracellular event and suggests the possibility of ion pumps in the apical membrane.

Summary Radioimmunoassay is a rapid, convenient, specific and sensitive method of measuring methotrexate (MTX) levels in plasma and skin exudate. Chronic users have a delayed peak level compared to recently treated patients. MTX levels in skin exudate approximate to those in plasma. Only 50% of plasma MTX is free, whereas almost all is free in skin exudate.

We demonstrate that electrogenic glucose coupled Na+ absorption accounts for about 20% of the residual, amiloride and Cl- insensitive, Na+ transport in isolated (equine) trachea. Either glucose removal from the mucosal side or addition of 10(-4) M phloridzin, a known pharmacological inhibitor of Na-glucose cotransport in small intestine and kidney proximal tubule, results in depolarization (lumen referenced to bath) of the transepithelial potential difference (Vt) and in a significant decrease of the equivalent short circuit current Ieq by 4 mV and 4 microA/cm2, respectively, without affecting the transepithelial resistance (Rt). Neither glucose removal nor the application of phloridzin on the basolateral side have a significant or consistent effect on the bioelectric parameters.

Experimental conditions affecting tests of atropine-like agents for antagonism of pilocarpine-induced salivation in rabbits have been examined. A simple method of assay of such agents is described. It gave results of fair accuracy and reproducibility, permitted a full statistical analysis, and provided an estimate of the error.

In experiments in which rabbits are to be given atropine or certain atropine-like agents, it is important to select animals whose plasma is deficient in the enzyme tropinesterase (atropinesterase). Three simple procedures for assessing the presence of this enzyme in rabbits in vivo have been examined. It is concluded that a different procedure is needed for albino rabbits than for animals with dark irides. In this way, 95–98% correct assessments of the presence or absence of tropinesterase have been made by simple procedures within 1 hr. Fully reliable assessments could only be made by in vitro methods, two of which (one quantitative and the other qualitative) are described. The latter enabled a reliable all-or-none assessment of tropinesterase activity to be made with only 0·'02 ml of plasma within 1–2 hr.

Seven structurally-related compounds consisting of three antidepressant drugs (imipramine, desmethylimipramine and amitriptyline), three tranquillizing agents (promazine, chlorpromazine and chlorprothixene) and a hybrid, desmethylpromazine, have been examined in a series of tests involving autonomic functions and antagonism of reserpine. Activities of the compounds in antagonizing reserpine-induced ptosis in rabbits and prolongation of alcohol hypnosis in mice give good correlation with their clinical actions, whilst their activities in augmenting excitation of rats by amphetamine and yohimbine toxicity in mice, and in reversing reserpine-induced bradycardia in rats offer further evidence for drug-induced sensitization to adrenergic or tryptaminic mechanisms, which is not however specific for antidepressant agents. No evidence has been obtained to indicate that a central parasympatholytic action is an important component of the antidepressant activity of imipramine and related drugs.

Effects of α-Methyl DOPA and DOPA on the Amphetamine Excitatory Response in Reserpinized Rats

Background The pathological hallmarks of chronic obstructive pulmonary disease (COPD) are inflammation of the small airways (bronchiolitis) and destruction of lung parenchyma (emphysema). These forms of disease arise from chronic prolonged infections, which are usually never present in the normal lung. Despite the fact that primary hygiene and defense of the airways presumably requires a well controlled fluid environment on the surface of the bronchiolar airway, very little is known of the fluid and electrolyte transport properties of airways of less than a few mm diameter. Methods We introduce a novel approach to examine some of these properties in a preparation of minimally traumatized porcine bronchioles of about 1 mm diameter by microperfusing the intact bronchiole. Results In bilateral isotonic NaCl Ringer solutions, the spontaneous transepithelial potential (TEP; lumen to bath) of the bronchiole was small (mean ± sem: -3 ± 1 mV; n = 25), but when gluconate replaced luminal Cl-, the bionic Cl- diffusion potentials (-58 ± 3 mV; n = 25) were as large as -90 mV. TEP diffusion potentials from 2:1 NaCl dilution showed that epithelial Cl- permeability was at least 5 times greater than Na+ permeability. The anion selectivity sequence was similar to that of CFTR. The bionic TEP became more electronegative with stimulation by luminal forskolin (5 μM)+IBMX (100 μM), ATP (100 μM), or adenosine (100 μM), but not by ionomycin. The TEP was partially inhibited by NPPB (100 μM), GlyH-101* (5–50 μM), and CFTRInh-172* (5 μM). RT-PCR gave identifying products for CFTR, α-, β-, and γ-ENaC and NKCC1. Antibodies to CFTR localized specifically to the epithelial cells lining the lumen of the small airways. Conclusion These results indicate that the small airway of the pig is characterized by a constitutively active Cl- conductance that is most likely due to CFTR.

Investigations of biological parameters at increasingly refined levels have sustained interest in methods for analyzing diminishingly small quantities of biological fluids. This report presents a rapid, straight forward procedure for elemental analysis of volumes on the order of 50 picoliters or less using the scanning electron microscope coupled with energy dispersive X-ray analysis. This technique has advantages over previously reported methods in that the preparation is faster, no freeze drying is necessary, and all elements heavier than flouride can be analized simultaneously.

TRACHEAL bronchial submucosal (TBS) glands are thought to supply a significant fraction of respiratory tract fluid (RTF)1, which is critically important in cleaning the airways of the lung. In the cleaning process, cilia in the tracheal bronchial tree continuously sweep the RTF, with debris, out of the lung. But abnormalities in the physicochemical properties of the RTF may impair this clearance, resulting in fluid stagnation, infection and obstruction of the airways. Unfortunately, because of the small size and inaccessibility of TBS glands and the difficulty in collecting their uncontaminated secretions, little is known about their physiology. We have developed methods for collecting and analysing secretions from single TBS glands of the cat in vitro, and we describe here the composition and control of the fluid secreted by these glands. We have found that the composition of the secreted fluids is very similar to that of the extracellular fluid and that secretion flow rates are influenced predominantly by α-adrenergic and cholinergic agonists. In view of the well known exocrinopathy in the lethal genetic disease cystic fibrosis (CF)2, we believe these findings to have implications for pathological changes in the airways in this disease.

Cystic fibrosis is the most common fatal genetic disease affecting caucasians and is perhaps best characterized as an exocrinopathy involving a disturbance in fluid and electrolyte transport. A high NaCl concentration in the sweat is characteristic of patients with this disease; the basic physiological reason for this abnormality is unknown. We have microperfused isolated sweat ducts from control subjects and cystic fibrosis patients, and report here results which suggest that abnormally low Cl- permeability in cystic fibrosis leads to poor reabsorption of NaCl in the sweat duct, and hence to a high concentration of NaCl in the sweat.

A systematic analysis of the vacuum ultraviolet absorption spectra of ClCN, BrCN and ICN, based on measurements of polarised, photofragment fluorescence, has been extended and used to probe the influence of initial state selection on vibrational, rotational (and by energy conservation, translational) energy disposal in the molecular fragments. Measurements have been conducted on channels leading to CN(A2Πi) as well as CN(B2Σ+) and the contrasting behaviour following excitation into intravalence dissociation continua and into predissociated band systems has been characterised. Energy distributions are found to be sensitive to the nature of the photoexcited state rather than simply its energy [though the CN(A) and CN(B) channels exhibit parallel behaviour] and the qualitative utility of the generalised Frank–Condon description of the dissociation process has been confirmed.

Vibrational and rotational energy disposal in CS(A1Π), produced through monochromatic vacuum u.v. photodissociation of CS2, has been studied under effectively collision-free conditions and at considerably higher resolution than in earlier studies by Lee and Judge and Okabe. Vibrational energy disposal in CSe(D1Π) produced from CSe2 has also been studied under similar conditions. The results, which indicate the importance of Franck–Condon considerations, are discussed qualitatively in terms of the formalism developed by Morse et al. Estimates of the overall transition moments, Rv′v″, and Franck–Condon factors for CS(A→X) are presented which confirm recent calculations by Coxon et al. and measurements by Carlson et al. and necessitate a revision of earlier data obtained under lower resolution by Lee and Judge.

New measurements of the photofragment fluorescence excitation spectra of NH2,ND2(A2A1) and NH,ND(c1Π) produced through the vacuum u.v. photodissociation of NH3,ND3 are reported. The spectra, which have been recorded at much higher resolution than previously, eliminate controversy concerning the predissociation of the B and C states and identify a contribution from the totally symmetric stretching mode in the vibronic structure. Measurements of rotational energy disposal in the NH(c1Π) fragment are consistent with a photodissociation threshold at 136.5 ± 0.5 nm and a revised value for ΔH⊖f0(NH)= 322.6 ± 7.1 kJ mol–1.

ISBN : 978-2-84346-352-5 ; 191 p.