Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Fluids and Secretions”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed1988

Freezing avoidance and the distribution of antifreeze glycopeptides in body fluids and tissues of Antarctic fish.

The distribution of antifreeze glycopeptides (AFGPs) in the body fluids and tissues of antarctic notothenioid fish was determined. In Dissostichus mawsoni (Norman), the peritoneal, pericardial and extradural fluid, like the blood, contained all eight AFGPs and in concentrations sufficient to depress freezing points below that of sea water (-1.9 degree C). Secreted fluids including urine, endolymph and aqueous and vitreous humour either lack all AFGPs or have very low concentrations of only the low molecular weight forms and have freezing points of about -1.0 degree C, and are therefore undercooled with respect to environmental temperature. Fluids with high concentrations of AFGPs also contain high levels of proteins similar to plasma proteins. Systemic administration of tritiated AFGPs in the closely related species Trematomus bernacchii (Boulenger) yielded a distribution pattern similar to that of the native AFGPs in D. mawsoni. This suggests passive distribution of AFGPs into the various fluid compartments following secretion from the liver; a pattern typical of secreted blood proteins. Tissue distribution of AFGPs was determined by comparison with that of the extracellular space marker [14C]polyethylene glycol. AFGPs were found in the interstitial fluid of all body tissues examined except brain tissue. No tissue showed any intracellular accumulation of tritiated AFGPs from the blood.

Animals↗
PubMed2003

CFTR and bicarbonate secretion by [correction of to] epithelial cells.

Defective HCO(3)(-) and fluid secretion are hallmarks of the pathophysiology of the pancreas of cystic fibrosis patients. Recently, impaired HCO(3)(-) secretion has been shown in most tissues known to express the cystic fibrosis transmembrane conductance regulator (CFTR). New results suggest that CFTR plays an important role in the transcellular secretion of HCO(3)(-).

Bicarbonates↗
PubMed1998

Response of the parotid gland of the brushtail possum, Trichosurus vulpecula, to adrenergic stimulation.

Adrenergic stimulation of parotid secretion was investigated in anaesthetised brushtail possums to ascertain fluid secretion rates and salivary composition. Because neither alpha- nor beta-adrenergic stimulation evoked saliva output, infusion of the adrenergic agonists was superimposed on a pre-existing bethanechol-stimulated flow. Isoprenaline infusion (2.4 nmol min-1) increased salivary amylase activity, [protein]; [HCO3]; [PO4] and [Ca], and amylase/Ca and protein/Ca ratios; reduced [Cl]; [K] and osmolality; but did not alter H+ activity; [urea]; [Na]; [Mg]; amylase/protein or saliva/plasma urea ratios. These data are consistent with isoprenaline stimulating acinar secretion of protein, Ca and PO4 but not the ion transport necessary for primary fluid formation at the endpieces and modifying transport of monovalent ions in the excurrent ducts. Consequently, the possum parotid has beta-adrenergic receptors in both the endpieces and excurrent ducts. Phenylephrine infusions at 2.4 and 24 nmol min-1 were without effect whereas phenylephrine at 240 nmol min-1 caused changes in salivary composition which paralleled those for isoprenaline administration but were generally of lesser magnitude. Thus, the possum parotid has few or no alpha-adrenergic receptors and the salivary response elicited was the result of cross-reaction of phenylephrine with beta-adrenergic receptors.

Adrenergic Agonists↗
PubMed1988

Mechanisms of terbutaline-induced inhibition of exocrine pancreatic secretion in humans.

Terbutaline, a selective beta 2-adrenoreceptor agonist, has recently been advocated as a potential agent for treating patients with pancreatic fistulae. In the present study, we attempted to quantify the presumed effects of terbutaline on exocrine pancreatic secretion in humans and to characterize possible mechanisms of action. In six healthy volunteers, the pancreas was stimulated by infusion of graded doses of secretin (15.5-250 ng/kg/h) or by infusion of secretin (15.5 ng/kg/h) plus graded doses of caerulein (3.3-30 ng/kg/h). The experiments were repeated in each subject without and with administration of terbutaline. Pancreatic secretion was assessed by a marker perfusion technique and plasma somatostatin and pancreatic polypeptide (PP) levels by radioimmunoassay. Terbutaline had no significant effect on secretin-stimulated pancreatic secretion, but significantly inhibited caerulein-stimulated pancreatic fluid secretion and trypsin output. Plasma somatostatin and PP levels were not affected by terbutaline. The inhibitory effect required the administration of pharmacologically large doses of terbutaline. We conclude that the weak inhibitory effect of terbutaline on exocrine pancreatic secretion is not mediated via somatostatin nor PP and that our data do not support a major role for beta-adrenergic mechanism as regulator of pancreatic secretion.

Adult↗
PubMed1978

Polymorphonuclear leukocytes as secretory organs of inflammation.

Polymorphonuclear (PMN) leukocytes mediate that phase of inflammation at which vascular responses become translated into tissue injury. After phagocytosis, the PMN leukocyte generates derivatives of molecular oxygen (O2-.,OH., and H2O2) that stimulate a metabolic burst and assist in the killing of microorganisms. They also release oxidation products of membrane fatty acids (e.g., arachidonate), which are detected as thromboxanes and protaglandins. After interaction of phagocytic ligands (immune complexes and C3b-opsonized particles), the PMN leukocyte secretes lysosomal enzymes from open phagocytic vacuoles, and, especially when phagocytosis is blocked by cytochalasin B, secretes them directly into the cell's surrounding fluids. Secretion is enhanced by agents that elevate intracellular levels of cyclic GMP, and inhibited by agents that raise cyclic AMP. These reciprocal changes are associated with assembly and disassembly (respectively) of cytoplasmic microtubules. These cytoskeletal structures, together with contractile elements, regulate in part the secretory events of inflammation in which lysosomal constituents (e.g., elastase, collagenase, and cathepsin G) are diverted from their intracellular depots to an inappropriate assault on the tissues of the host.

Blood Bactericidal Activity↗
PubMed1990

Meibomian gland dysfunction: some clinical, biochemical and physical observations.

Dysfunction of the meibomian glands resulting from contact lens wear has recently been recognized. This study shows that 30% of lens wearers develop some degree of meibomian gland dysfunction after 6 months of wear whereas only 20% of non-lens wearers have similar problem. Thirty-three per cent of the male wearers have dysfunctioning glands compared with 28% of female wearers. The incidence does not depend on the type of lenses worn. There was no detectable differences between the composition of the abnormal fluid secreted by the dysfunctioning glands and the clear fluid coming out of the normal unblocked glands, as shown by thin layer chromatography. On studying the melting point of the lipids, we found that material from abnormal glands melted at approximately 3 degrees C higher than the normal fluid.

Chromatography, Thin Layer↗
PubMed1991

Interaction between antisecretory opioid and sympathetic mechanisms in the rat small intestine.

UNLABELLED: The putative existence of an endogenous opioid antisecretory mechanism in the small intestine was tested in anaesthetized Sprague-Dawley rats. Cholera secretion was elicited with cholera toxin and net fluid secretion was measured in vivo using a gravimetric technique allowing on line registrations. Opioid blockade with naloxone (10 mg kg-1 i.v.) increased the cholera secretion significantly but had no effect on control absorption. Pretreatment with phentolamine (2 mg kg-1 i.v.) eliminated the effect of opioid blockade indicating an interaction between the opioid and the adrenergic mechanisms. The effect of naloxone on cholera secretion was unchanged after acute division of the sympathetic nerves to the intestine and removal of the adrenals. Chronic sympathetic denervation of the small intestine, on the other hand, abolished the effect of opiate blockade on the secretion. The antisecretory effect of sympathetic nerve stimulation was unchanged by opiate blockade. CONCLUSION: An intrinsic antisecretory opioid mechanism has been demonstrated in the small intestine of the rat. This endogenous opioid mechanism seems to decrease secretion indirectly via peripheral activation of the sympathetic antisecretory system.

Animals↗
PubMed1996

Ability of adenovirus vectors containing different CFTR transcriptional cassettes to correct ion transport defects in CF cells.

Cystic fibrosis (CF) airway epithelial cells exhibit defective adenosine 3',5'-cyclic monophosphate (cAMP)-mediated chloride (Cl) secretion, abnormal hyperabsorption of sodium (Na+), and aberrant fluid transport. Adenovirus-mediated transduction of cystic fibrosis transmembrane conductance regulator (CFTR) corrects these ion and fluid transport abnormalities in CF cells. However, several challenges remain pertaining to the use of adenovirus vectors for gene delivery, including the efficiency of gene transfer and the host response to the vector. To improve the efficacy of adenovirus-mediated gene transfer, we have constructed a series of recombinant adenoviruses containing different CFTR transcriptional units, and we have evaluated their relative ability to correct electrolyte and fluid transport in polarized CF airway epithelial cells. The ability of the vectors to correct the CF Cl- transport defects was greatest when the human cytomegalovirus promoter was used. The E1a and phosphoglycerate kinase promoters resulted in the greatest persistence of functional CFTR expression. Efficacy of gene expression by recombinant adenoviruses improved as the cells were treated with increasing multiplicities of infection, as the duration of viral contact with the target cells was lengthened, and when the virus concentration was increased. Transduction of functional CFTR Cl- channel activity reversed the abnormal Na+ hyperabsorption observed in CF cells in a dose-dependent manner, suggesting that Na+ channel activity is downregulated by CFTR. Although efficient correction of both cAMP-mediated Cl- transport and fluid secretion could be achieved readily with these vectors, normalization of the Na+ absorption required vector administration at high multiplicities of infection.

Adenoviruses, Human↗
PubMed2005

Aquaporins in development -- a review.

Water homeostasis during fetal development is of crucial physiologic importance. It depends upon maternal fetal fluid exchange at the placenta and fetal membranes, and some exchange between fetus and amniotic fluid can occur across the skin before full keratinization. Lungs only grow and develop normally with fluid secretion, and there is evidence that cerebral spinal fluid formation is important in normal brain development. The aquaporins are a growing family of molecular water channels, the ontogeny of which is starting to be explored. One question that is of particular importance is how well does the rodent (mouse, rat) fetus serve as a model for long-gestation mammals such as sheep and human? This is particularly important for organs such as the lung and the kidney, whose development before birth is very much less in rodents than in the long-gestation species.

Animals↗
PubMed1991

Establishment and characterization of a cholangiocarcinoma cell line from a Thai patient with intrahepatic bile duct cancer.

A new human cholangiocarcinoma cell line (HuCCA-1) was established from cholangiocarcinoma (CCA) tissue fragments surgically removed from a Thai patient with intrahepatic bile duct cancer. The growth medium used for the primary cell culture was Ham's F12 supplemented with 10% fetal bovine serum (FBS) and 10 ng/ml epithelial growth factor (EGF). Approximately one month later, the cells were subcultured in Ham's F12 supplemented with only 10% FBS. The population doubling time was approximately 55 hr. Staining of the cells for cytokeratin and mucin confirmed that the cells were mucin-secreting tumor of epithelial cell origin. The supernatant fluid secreted a number of non-specific tumor markers including CA125 and traces of MCA and AFP. The ability of the HuCCA-1 cell line to synthesize specific marker that may have potential in the diagnosis of cholangiocarcinoma is now being investigated.

Adenoma, Bile Duct↗
PubMed1975

The secretion of hyperosmotic fluid by the rectum of a saline-water mosquito larva, Aedes taeniorhynchus.

1. Fourth-instar larvae of the mosquito A. taeniorhynchus (Wiedemann), when living in sea water, drink at a rate of 100 nl h(-1) larva(-1) and maintain ionic and osmotic levels in the haemolymph at about one-third those of the external medium. 2. Hyperosmotic urine is produced in the rectum by secretion of fluid having an osmotic concentration and ionic composition similar to that of sea water, with the exception that potassium levels are elevated 18-fold in the secretion. The average rate of fluid secretion observed was 19 nl h-1) larva(-1) with a maximum of 92 nl h(-1) larva(-1). 3. The concentration and volume of rectal secretion may be too low to account completely for osmotic balance. The possible role of anal papillae is discussed in this regard.

Aedes↗
PubMed2003

Possible functional implications of aquaporin water channels in reproductive physiology and medically assisted procreation.

Spermatogenesis, the maturation of spermatozoa and their concentration and storage in the seminiferous vessels are associated with considerable fluid secretion or absorption in the male reproductive tract. These fluid movements are in total agreement with the presence of multiple aquaporin (AQP) water channel proteins in germ cells and other tissues within the male reproductive tract. A series of functions of prime importance have already been hypothesized for aquaporins in the physiology of male reproduction. Aquaporins could be involved in the early stages of spermatogenesis, in the secretion of tubular liquid and in the concentration and storage of spermatozoa in the epididymis. In the male reproductive tract, alterations in the expression and functionality and/or regulation of aquaporins have already been demonstrated to be at the basis of forms of male infertility. Indeed, rats with reduced reabsorption of seminiferous fluid in the efferent ducts have been shown to be sub-fertile or infertile. Functions have also been suggested in the fertilization process, where aquaporins may play a role in maintaining osmotic homeostasis in gametes during fertilization. Aquaporins have also been suggested to mediate water movement into antral follicles and to be the pathway for transtrophectodermal water movement during cavitation. Aquaporins are the subject of considerable technological interest for cryopreservation used in medically assisted procreation, as they could be the molecular pathway by which water and/or solutes move across the plasma membrane during the process of freezing/thawing gametes and embryos. Indeed, artificial expression ofAQP3 has been showed to improve the survival of mouse oocytes after cryopreservation.

Aquaporins↗
PubMed1990

Reversal and inhibition of cholera toxin-induced secretion in isolated rabbit ileum.

1. Cholera toxin (1 microgram/ml) abolished net fluid absorption by everted sacs of rabbit ileum, leading to net fluid secretion. This action occurred via the toxin-catalysed ADP ribosylation of the stimulatory GTP-binding protein Gs which is linked to adenylate cyclase. Nicotinamide (10 mM), a reaction product of ADP ribosylation, reversed cholera toxin-induced secretion, restoring absorption. Lower concentrations of nicotinamide induced partial reversal. 2. Nicotinamide (1 mM) blocked the secretory action of cholera toxin applied to ileal sacs. This inhibitory action was more effective in the presence of methionine (1 mM). 3. Other inhibitors of ADP ribosylation, benzamide and adenine, blocked the secretory action of cholera toxin. Hypoxanthine, an analogue and metabolite of adenine, was similarly effective. 4. Nicotinamide was not, however, effective in blocking or reversing the secretory action of theophylline (10 mM) or of heat-stable E. coli enterotoxin STa. This indicates that nicotinamide has a highly specific action against ADP ribosylating toxins. 5. It is proposed that nicotinamide reverses the secretory action of cholera toxin by reversing ADP ribosylation, simply by the law of mass action. This counters the established idea that the effects of cholera and other ADP-ribosylating toxins are irreversible under physiological conditions.

Adenine↗
PubMed2006

Transporters involved in regulation of intracellular pH in primary cultured rat brain endothelial cells.

Fluid secretion across the blood-brain barrier, critical for maintaining the correct fluid balance in the brain, entails net secretion of HCO(3)(-), which is brought about by the combined activities of ion transporters situated in brain microvessels. These same transporters will concomitantly influence intracellular pH (pH(i)). To analyse the transporters that may be involved in the maintenance of pH(i) and hence secretion of HCO(3)(-), we have loaded primary cultured endothelial cells derived from rat brain microvessels with the pH indicator BCECF and suspended them in standard NaCl solutions buffered with Hepes or Hepes plus 5% CO(2)/HCO(3)(-). pH(i) in the standard solutions showed a slow acidification over at least 30 min, the rate being less in the presence of HCO(3)(-) than in its absence. However, after accounting for the difference in buffering, the net rates of acid loading with and without HCO(3)(-) were similar. In the nominal absence of HCO(3)(-) the rate of acid loading was increased equally by removal of external Na(+) or by inhibition of Na(+)/H(+) exchange by ethylisopropylamiloride (EIPA). By contrast, in the presence of HCO(3)(-) the increase in the rate of acid loading when Na(+) was removed was much larger and the rate was then also significantly greater than the rate observed in the absence of both Na(+) and HCO(3)(-). Removal of Cl(-) in the presence of HCO(3)(-) produced an alkalinization followed by a resumption of the slow acid gain. Removal of Na(+) following removal of Cl(-) increased the rate of acid gain. In the presence of HCO(3)(-) and initial presence of Na(+) and Cl(-), DIDS inhibited the changes in pH(i) produced by removal of either Na(+) or Cl(-). These are the expected results if these cells possess an AE-like Cl(-)/HCO(3)(-) exchanger, a 'channel-like' permeability allowing slow influx of acid (or efflux of HCO(3)(-)), a NBC-like Cl(-)-independent Na(+)-HCO(3)(-) cotransporter, and a NHE-like Na(+)/H(+) exchanger. The in vitro rates of HCO(3)(-) loading via the Na(+)-HCO(3)(-) cotransporter could, if the transporter is located on the apical, blood-facing side of the cells, account for the net secretion of HCO(3)(-) into the brain.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1977

Epithelial cell extrusion during fluid transport in canine small intestine.

Epithelial cell extrusion during fluid transport was studied under both in vitro and in vivo conditions. The rate of cell extrusion from the villus tips in vitro increased by about onefold in the villi with obstruction of lymph flow associated with the increase of lymph and tissue fluid pressure. When lymph pressure in the jejunal and ileal villi was increased to 6.4 +/- .2 and 12.3 +/- .5 mmHg, respectively, by injection of Ringer solution into the central lacteals, fluid leaked out of the villi and a shedding of epithelium occurred. Vigorous villus spasmodic contraction induced by cocaine or atropine also caused a shedding of epithelium. Cells always appeared in the lumen of intestine in vivo either during fluid absorption or secretion. A copious secretion of fluid, increase of cell loss, and congestion of blood in the villi occurred by the action of cholera toxin, MgSO4, and choline chloride. The rate of cell loss was highest during fluid secretion induced by an elevation of tissue fluid pressure such as at high venous pressure or during intra-arterial histamine infusion. It is thus concluded that elevated tissue fluid pressure is involved in epithelial cell extrusion during fluid transport.

Animals↗
PubMed1992

Secretion of lung fluid by the developing fetal rat alveolar epithelium in organ culture.

We studied lung explants in submersion organ culture to examine the role of the developing fetal alveolar epithelium in the production of lung fluid. Fourteen-day-gestation fetal rat lungs were grown in a collagen gel matrix supplemented with F-12 media and 10% fetal calf serum. In this model, the lung continues to grow, secrete fluid, and become progressively cystic in morphology. There is gradual thinning of the distal epithelial layer, which is lined by alveolar type II cells and their precursors. After 6 to 8 days in culture, we impaled the cyst walls with a microelectrode and continuously recorded the transepithelial potential (psi t). Stable, baseline transepithelial potentials of -1.1 to -6.2 mV (mean +/- SEM = -3.3 +/- 0.11 mV, lumen negative, n = 34) were measured in bicarbonate-buffered Ringer's solution, suggesting active electrolyte transport. When bumetanide, an inhibitor of chloride secretion in other systems, was added to the bathing solution, psi t decreased from a baseline of -3.5 +/- 0.07 mV (mean +/- SEM) to a value of -2.2 +/- 0.07 mV, suggesting chloride transport contributes to the voltage (n = 18, P less than 0.0005). Isoproterenol hyperpolarized psi t from a baseline of -4.3 +/- 1.0 mV to -6.5 +/- 1.0 mV (n = 7, P less than 0.005). 8-(4-Chlorophenylthio) adenosine 3':5'cyclic monophosphate (CPT-cAMP) plus isobutylmethylxanthine (IBMX) similarly hyperpolarized psi t from a baseline of -4.6 +/- 0.4 mV to -7.3 +/- 0.7 mV (n = 11, P less than 0.005). Addition of bumetanide after stimulation with isoproterenol or CPT-cAMP/IBMX depolarized psi t.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Actin redistribution in mosquito malpighian tubules after a blood meal and cyclic AMP stimulation.

Fluid secretion by mosquito Malpighian tubules is critical to maintaining fluid and electrolyte balance after a blood meal. Endogenous cAMP levels increase in Malpighian tubules after a blood meal. Here, we determined if corresponding changes in intracellular actin distribution occur after a blood meal or dibutyryl-cAMP (db-cAMP) stimulation and whether altering actin turnover inhibits secretion. In untreated Malpighian tubules, beta-actin immunostaining was more intense in the apical region of adult Malpighian tubules than in the cytoplasm. Stimulation by a blood meal or db-cAMP significantly decreased beta-actin immunostaining in the non-apical region of the cell. Db-cAMP had similar effects in larvae and pupae Malpighian tubules. In contrast, no detectable shift in F-actin distribution was detected; however, F-actin bundles within the cytoplasm increased in size after treatment with db-cAMP. Pretreatment of Malpighian tubules with agents perturbing actin fiber assembly and disassembly decreased basal secretion rates and inhibited the stimulatory effects of db-cAMP. Our results show (1) beta-actin redistributes toward the apical membrane after a blood meal and this correlates temporally with increase urine flow rate and intracellular cAMP levels, (2) Malpighian tubules from all developmental stages exhibit this same response to db-cAMP-stimulation, and (3) dynamic assembly and disassembly of beta-actin is required for db-cAMP-stimulated secretion.

Actins↗
PubMed2004

Interferon-gamma regulates ClC-2 chloride channel in lung epithelial cells.

Epithelial Cl(-) channels mediate Cl(-) and fluid secretion in the lung. In cystic fibrosis, aberrant Cl(-) secretion is one of the major causes for lung fluid imbalance. Regulation of Cl(-) channels is therefore an important issue in the lung. IFN-gamma regulates Na(+) and Cl(-) channels and fluid transport in the lung, but the mechanisms involved in these regulations are not clear. In expression studies, we found that IFN-gamma increased ClC-2 transcripts in Calu-3 cells. Studies of the promoter identified a minimal promoter which interacts with transcription factors Sp1 and Sp3. However, reporter gene assays showed that IFN-gamma did not activate the promoter. Instead, IFN-gamma significantly increased ClC-2 transcript stability. Using Ussing chamber experiments, we demonstrate that IFN-gamma activates a pH-regulated and Cd(2+)-sensitive short circuit current, characteristic properties of the ClC-2 Cl(-) channel. These data suggest that IFN-gamma activates ClC-2 channel activity in lung epithelial cells via mRNA stabilization.

Animals↗