Analysis of the Buffering Systems in Dental Plaque

1988 ◽  
Vol 67 (2) ◽  
pp. 438-446 ◽  
Author(s):  
R.P. Shellis ◽  
G.H. Dibdin

A semi-micro method was used for investigation of the buffering properties of whole plaque, plaque fluid, and washed plaque bacteria. Artifacts associated with titration of samples containing live bacteria were noted and their effects estimated. All three sample types showed minimal buffering in the region of neutrality, with much stronger buffering in the regions pH 4-5.5 and pH 8-9. For the range pH 4-7, almost 90% of the total buffer capacity of plaque appeared to be accounted for by macromolecules of bacterial cell walls and plaque matrix. Extracellular buffers in plaque fluid removable by centrifugation contributed up to 11%. These buffers (probably soluble proteins, peptides, organic acids, and phosphate) are, potentially at least, capable of exchange with saliva. In vitro, bicarbonate (dissolved in the extracellular fluid) contributed only 2-5% of total buffering; there was no evidence of formation of carbamino compounds. However, in vivo, salivary bicarbonate may be important as a continually replenished source of additional buffering.

2008 ◽  
Vol 21 (4) ◽  
pp. 993-997 ◽  
Author(s):  
G. Pasquantonio ◽  
C. Greco ◽  
M. Prenna ◽  
C. Ripa ◽  
L.A. Vitali ◽  
...  

Streptococcus mutans is the major cause of dental plaque and is often associated with biofilm formation. The aim of this study is to evaluate the activity of a hydrosoluble derivative of chitosan against S. mutans biofilms in vitro and in vivo. Strains of S. mutans were isolated from the dental plaque of 84 patients enrolled in the study. The antibacterial activity of chitosan was determined by broth microdilutions. The effect of chitosan at different concentrations and exposure times on S. mutans biofilms at different phases of development was assessed by a clinical study using the classical “4-day plaque regrowth” experiment in adult volunteers. The MIC values of chitosan were between 0.5 and 2 g/L. Compared to distilled water, the chitosan solution significantly decreased the vitality of plaque microflora (p≤0.05). Chlorhexidine, used as a positive control, reduced vitality even further. The results showed that S. mutans in the adhesion phase (4 h) was completely inhibited by chitosan at any concentration (0.1, 0.2, 0.5XMIC) or exposure time investigated (1, 15, 30, 60 min), while S. mutans at successive stages of accumulation (12–24 h) was inhibited only by higher concentrations and longer exposure times. These data confirm the effective action of chitosan against S. mutans biofilms.


PEDIATRICS ◽  
1987 ◽  
Vol 79 (1) ◽  
pp. 38-46
Author(s):  
Machiko Ikegami ◽  
Yotaro Agata ◽  
Tarek Elkady ◽  
Mikko Hallman ◽  
David Berry ◽  
...  

Natural sheep surfactant, rabbit surfactant, human surfactant, and surfactant TA were compared for in vitro surface properties and for responses of preterm lambs to treatment. Equivalent amounts of sheep, rabbit, and human surfactants were needed to lower the surface tension to less than 10 dynes/cm, whereas four times less surfactant TA similarly lowered the surface tension. Surface-spreading rates were similar for the surfactants. The surface adsorption of the batch of human surfactant tested was much slower than was adsorption of the other surfactants. Ventilation was significantly improved in all surfactant-treated lambs relative to the control lambs, indicating the general efficacy of the surfactant treatments. Overall, surfactant TA had the best in vitro characteristics, yet the preterm lambs treated at birth with surfactant TA had lower Po2 values and higher ventilatory requirements than did the sheep surfactant-treated lambs. The in vivo responses to rabbit surfactant were intermediate between the responses to sheep surfactant and to surfactant TA. Human surfactant resulted in the least effective clinical response. More of the phosphatidylcholine associated with human surfactant and surfactant TA was lost from the alveoli and lung tissue after four hours of ventilation than was lost from sheep or rabbit surfactant-treated lambs. More intravascular radiolabeled albumin leaked into the alveoli of the surfactant TA-treated lambs than sheep or rabbit surfactant-treated. lambs. The four surfactants also had different sensitivities to the effects on minimum surface tensions of the soluble proteins present in alveolar washes. The study demonstrates that the range of clinical responses was not predictable based on the in vitro surface properties that we measured. The surfactants behaved differently with respect to loss from the lungs and sensitivity to soluble proteins. Factors other than surface properties are important for the in vivo responses to surfactant treatments.


1984 ◽  
Vol 57 (3) ◽  
pp. 907-912
Author(s):  
S. Javaheri ◽  
A. De Hemptinne ◽  
I. Leusen

The purpose of this study is to systematically describe the construction of pH-sensitive double-barreled microelectrodes for extracellular use. The most important advantages of these microelectrodes are as follows: the reference and the pH barrels are next to each other, and therefore the measured pH is not affected by asymmetric or slowly spreading direct current potential. The diameter of the tip of the microelectrodes is between 7 and 35 micron. These pH-sensitive microelectrodes are generally stable and Nernstian. They can be used repeatedly both in vivo and in vitro to measure tissue extracellular fluid pH. Some applications are described.


1981 ◽  
Vol 241 (5) ◽  
pp. H700-H707 ◽  
Author(s):  
D. W. Snyder ◽  
W. A. Crafford ◽  
J. L. Glashow ◽  
D. Rankin ◽  
B. E. Sobel ◽  
...  

Lysophosphoglycerides accumulate in ischemic myocardium. To determine whether lysophosphatidylcholine (LPC) concentrations increase in extracellular fluid and may be arrhythmogenic, the anterior descending coronary artery of the open-chest cat (n = 12) was perfused with a Krebs-albumin solution after 10 min of ischemia and the effluent assayed for LPC. A twofold increase in LPC (0.097 +/- 0.02 to 0.170 +/- 0.03 mM) was observed. Microelectrode intracellular recordings from from normal feline endocardium at pH 7.4 in vitro revealed little change in action potentials when superfused with feline plasma despite augmented LPC to twice normal levels (0.74 mM). However, at pH 6.7, marked changes were elicited by LPC-enriched plasma including diminished resting membrane potential (-96 +/- 1 to -35 +/- 7 mV), amplitude (102 +/- 3 to 36 +/- 8 mV), maximum rate of rise (Vmax) of phase 0 (178 +/- 24 to 26 +/- 11 V/s), and conduction velocity with fractionation of the action potential. Acidified control plasma decreased only Vmax (from 161 to 57 V/s). Thus LPC increases twofold in effluents from cat myocardium in vivo after 10 min of ischemia and, coupled with ischemia-induced acidosis, is sufficient to induce marked electrophysiological derangements in vitro.


1985 ◽  
Vol 248 (3) ◽  
pp. G261-G271 ◽  
Author(s):  
K. A. Hubel

The effects of extrinsic and intrinsic nerves on ion and water transport by the intestine are considered and discussed in terms of their possible physiological function. Adrenergic nerves enter the small intestine via mesenteric nerves. Adrenergic tone is usually absent in tissues in vitro but is present in vivo. The nerves increase absorption in response to homeostatic changes associated with acute depletion of extracellular fluid. Cholinergic tone that reduces fluid absorption or causes secretion has been detected in the small intestine of humans, dogs, and cats and in the colon of humans. Extrinsic cholinergic fibers generally do not affect ion transport in small intestine but probably do so in colon. Whether peptides liberated in the mucosa affect enterocytes directly is not clear. Studies on humans and rabbits suggest that the role of substance P is minor. The physiological roles of vasoactive intestinal polypeptide (VIP) and somatostatin remain to be defined. Intraluminal factors also affect ion and water transport. Mucosal rubbing, distension, and cholera toxin cause fluid secretion; acid solutions in the duodenum cause alkaline secretion; these stimuli and hypertonic glucose liberate serotonin into the lumen, the mesenteric venous blood, or both. It has been proposed that the enterochromaffin cell is an epithelial sensory cell that responds to noxious stimuli within the lumen by liberating serotonin. The serotonin initiates a neural reflex through a nicotinic ganglion to liberate a secretagogue that acts on the enterocyte. The function of VIP in this proposed reflex is unclear. The variety of intraluminal stimuli that influence epithelial function implies that there is more than one type of epithelial sensory cell (or sensory mechanism). Prostaglandins may mediate the alkaline secretion caused by acid in the duodenum. There may be other effective substances. Although it has been known for years that intraluminal stimuli affect the coordination of smooth muscle functions, it is not known whether similar stimuli also influence salt and water transport as a meal traverses the alimentary canal.


1992 ◽  
Vol 38 (2) ◽  
pp. 85-91 ◽  
Author(s):  
Anthony J. Clarke ◽  
Claude Dupont

Bacterial cell walls and their structural units, particularly peptidoglycan, induce a vast variety of biological effects in host organisms. The pathobiological effects of peptidoglycan are greatly enhanced by various modifications and substitutions to its basic composition and structure. One such modification is the presence of acetyl moieties at theC-6 hydroxyl group of N-acetylmuramyl residues, and to date, 11 species of eubacteria, including some important human pathogens, such as Neisseria gonorrhoeae, Proteus mirabilis, and Staphylococcus aureus, are known to possess O-acetylated peptidoglycan. This review addresses the influence of O-acetylation of peptidoglycan on its resistance to degradation both in vitro and in vivo, the clinical importance of the modification, and the currently held views on the pathway for its biosynthesis. Key words: peptidoglycan, murein, O-acetylation, lysozyme, arthritis.


2015 ◽  
Vol 309 (8) ◽  
pp. C541-C550 ◽  
Author(s):  
Carla P. Carneiro de Morais ◽  
Juliano Z. Polidoro ◽  
Donna L. Ralph ◽  
Thaissa D. Pessoa ◽  
Maria Oliveira-Souza ◽  
...  

Physiological concentrations of angiotensin II (ANG II) upregulate the activity of Na+/H+ exchanger isoform 3 (NHE3) in the renal proximal tubule through activation of the ANG II type I (AT1) receptor/G protein-coupled signaling. This effect is key for maintenance of extracellular fluid volume homeostasis and blood pressure. Recent findings have shown that selective activation of the beta-arrestin-biased AT1 receptor signaling pathway induces diuresis and natriuresis independent of G protein-mediated signaling. This study tested the hypothesis that activation of this AT1 receptor/beta-arrestin signaling inhibits NHE3 activity in proximal tubule. To this end, we determined the effects of the compound TRV120023, which binds to the AT1R, blocks G-protein coupling, and stimulates beta-arrestin signaling on NHE3 function in vivo and in vitro. NHE3 activity was measured in both native proximal tubules, by stationary microperfusion, and in opossum proximal tubule (OKP) cells, by Na+-dependent intracellular pH recovery. We found that 10−7 M TRV120023 remarkably inhibited proximal tubule NHE3 activity both in vivo and in vitro. Additionally, stimulation of NHE3 by ANG II was completely suppressed by TRV120023 both in vivo as well as in vitro. Inhibition of NHE3 activity by TRV120023 was associated with a decrease in NHE3 surface expression in OKP cells and with a redistribution from the body to the base of the microvilli in the rat proximal tubule. These findings indicate that biased signaling of the beta-arrestin pathway through the AT1 receptor inhibits NHE3 activity in the proximal tubule at least in part due to changes in NHE3 subcellular localization.


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