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This study was designed to determine the pH of the intestinal surface in the rat jejunum in an attempt to investigate the effect of potential damaging agents on the microclimate-pH. A significant pH gradient was observed between the mucosal surface and the bulk phase; however, the microclimate-pH usually ranged from 6.5 to 7.5, irrespective of the wide range in the bulk pH. When the bulk pH was either 7.3 or 4, the microclimate-pH was approximately 6.7, while the microclimate-pH was approximately 7.4 when the bulk pH was raised to 9. The distance of the pH gradient was found to be approximately 900-1300 microns. After treatment with ouabain (10 mM) or amiloride (8 mM), or replacement of Na+ with Li+, the microclimate-pH significantly increased compared with the control (buffer solution). Chlorpromazine (2 mM) and ouabain also significantly increased the microclimate-pH, but at the same time, chlorpromazine decreased the bulk pH so that a more marked pH gradient was observed. Both aspirin (10 mM) and acetazolamide (80 mg/kg, iv) significantly decreased the microclimate-pH under the condition of the acidic bulk phase pH. N-Acetyl-L-cysteine (5%) induced marked changes in microclimate-pH, the direction depending upon the bulk phase pH. Neither taurocholic acid (10 mM) nor glucose (10 mM) significantly changed the microclimate pH.
The effects of several phenothiazine derivatives (PTDs) and quinidine (QD) on the jejunal microclimate-pH in rats were studied using a microelectrode. Chlorpromazine, thioridazine, chlorpromazine sulfoxide (CPZSO), trifluoperazine, prochlorperazine, and QD at concentrations of 1 mM increased this microclimate-pH by 0.15-0.3 pH units, while 1 mM diethazine and 1 mM promethazine had little effect on it. The increases in the microclimate-pH caused by PTDs and QD were concentration dependent and reversible. We studied the effects of PTDs on the fluidity of intestinal brush border membranes and on the release of proteins from the intestinal tissue to the lumen. The PTD-induced changes in microclimate-pH could not be explained by either of these nonspecific effects on the membranes. Then, the effects of PTDs on Na+,K+-ATPase activity and Mg2+-ATPase activity were studied using the jejunal homogenate. Each PTD inhibited Na+,K+-ATPase and Mg2+-ATPase activity to some extent. The inhibitory effects on Na+,K+-ATPase and Mg2+-ATPase activity were compared with the PTD-induced increases in the microclimate-pH. No good correlation was obtained between the IC50 values of PTDs for Na+,K+-ATPase activity and the concentrations required to increase the microclimate-pH by 0.1 pH unit, while IC50 values of PTDs for Mg2+-ATPase activity showed a relatively good correlation, except for that of CPZSO. These findings suggest that the effects of PTDs on the microclimate-pH were not nonspecific, although the increases in the microclimate-pH caused by PTDs cannot be fully explained by the inhibitory effects of these compounds on either Na+,K+-ATPase activity or Mg2+-ATPase activity alone.
Segments of guinea pig jejunum, proximal and distal colon and of rat jejunum were superfused either in vivo or in vitro with different electrolyte solutions. The pH in the bulk phase solution and at the surface of the epithelium was measured with two different types of glass pH-microelectrodes, a pointed tip (Hinke-type) and a flat membrane electrode (Dubuisson-type); both types of electrodes gave the same results. The existence of a pH-microclimate at the surface of the mucosa was demonstrated under both in vivo and in vitro conditions. In vivo the pH-microclimate was stable and virtually independent of changes in the luminal bulk phase pH. When the bulk phase pH of the guinea pig colon was changed between pH 5 and pH 8.6, the mean pH in the microclimate was 7.08 +/- 0.15 (n = 163) in the proximal colon and 6.91 +/- 0.14 (n = 75) in the distal colon. In the guinea pig jejunum pH in the microclimate was 7.37 +/- 0.21 (n = 10) while the luminal pH was 7.27 +/- 0.10. Under in vitro conditions, the pH in the microclimate was more acidic (guinea pig jejunum delta pH 0.93, rat jejunum delta pH 0.40, guinea pig proximal colon delta pH 0.22). Addition of glucose (10 mM) or short-chain fatty acids (80-90 mM) to the luminal solution or replacement of sodium by lithium did not influence the pH in the microclimate significantly. Also the addition of acetazolamide, amiloride, SITS or sodium deoxycholate to the luminal solution, did not affect the pH in the microclimate in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)
Axenically cultivated Entamoeba histolytica, trophozoites, strains HM-1:IMSS and HM-38, were suspended in solutions of NaCl, 330 mOsm, of varying pH and ammonium concentrations. Short-term viability was inversely proportional to the ammonia concentration of the medium and was independent of the ammonium concentration and pH. The NH3-induced ameba killing was associated with a cellular alkalosis and cell swelling. While short-term trophozoite viability was unaffected by changes in the medium pH over the range 5.5-8.0, long-term viability was reduced by high pH, and of three pH values tested (6.27, 7.27, and 8.27), trophozoite growth was greatest at the lower value. Chemotaxis was observed in media over the pH range 5.5-8.0, and attenuated chemotaxis was observed in trophozoites in media containing NH3 (0.1 mM). The cecal content total ammonia concentration and pH and the in vivo mucosal microclimate pH were measured in young adult male rats, hamsters, and gerbils. Ceca of the three rodent species were also inoculated with HM-38 trophozoites and 7 days later the cecal contents were studied for signs of amebic infection. Infections were absent in the rat, the species with highest luminal total ammonia concentration and mucosal microclimate pH. All gerbils were infected. This species had the lowest mucosal microclimate pH. The hamster, with the intermediate microclimate pH, had a low infection rate (1 of 5). It is proposed that when ammonium diffuses from the large intestinal lumen into a more basic mucosal microclimate, it is converted to ammonia, and the combination of this ammonia and the high microclimate pH threatens Entamoeba trophozoite viability and reduces the probability of a given ameba penetrating the mucus blanket and invading the mucosal epithelium.
1. Single-barrelled pH-sensitive microelectrodes filled with liquid ion exchanger were used to study the layer of microclimate pH in the vicinity of the surface of rat jejunum in vitro. 2. During perfusion with a Na+-containing solution of pH 7.30, a layer having a pH gradient ranging from 7.30 (pH of the luminal bulk phase) to 6.05 +/- 0.03 (pH of the deepest region) was detected in eighteen different animals. The thickness of the layer was estimated to be 600-700 microns. No regional difference was seen along the height of the villus. 3. The addition of D-glucose to the perfusion solution significantly augmented the acidity of the deepest region without changing the thickness of the layer. On the other hand, the elimination of Na+ from the perfusion solution caused a significant reduction of the pH gradient. The lowest pH changed from a control value of 6.18 +/- 0.15 (n = 13 measurements from three animals) to 6.46 +/- 0.06 (n = 13). The gradient was sensitive to amiloride in the presence of Na+, K+, Ca2+ and Cl- had no significant effect on the microclimate pH. 4. Depletion of the surface mucus by treatment with dithiothreitol significantly raised the pH of the deepest region. 5. Glycylglycine and L-carnosine were found to reduce the microclimate pH gradient significantly, while glycine did not. 6. These results indicate that H+ secretion by the Na+-H+ antiport and the formation of mucus layer are important factors for maintaining the microclimate pH layer, and that H+-coupled co-transport, such as H+-dipeptide co-transport, causes a significant diminution of the microclimate pH gradient.
1. Micellar solubilization of lipolytic products is an important step in lipid absorption. However, micelles are not absorbed intact; dissociation of lipolytic products from bile salt micelles must occur. The dissociation of micelles has been postulated to occur in an acidic microclimate. 2. The effect of an acidic microclimate on the uptake of micellar fatty acid was examined in the rat intestine. We reported that the presence of a lower pH microclimate is associated with a higher fatty acid uptake, suggesting that a lower pH enhances fatty acid uptakes from the micelles. 3. Fatty acid uptake from solutions containing a constant amount of bile salt (10 mM) and varying amounts of fatty acid (3.3-26.4 mM) revealed a saturation phenomenon which reflects the fatty acid carrying capacity of a 10 mM-taurocholate solution. 4. There was a linear relationship between fatty acid uptake and fatty acid concentration when the micellar solutions contained a constant ratio of fatty acid and taurocholate (1.32). 5. Our results indicate that the fatty acid carrying capacity of the micelle and the number of micelles in the solution are both important determinants for the amount of fatty acids delivered to the microclimate. The amount of fatty acids derived from the dissociation of micelles within the microclimate determines fatty acid uptake by the intestine.
This study was designed to determine the effect of epidermal growth factor (EGF) in the lumen on the pH of the intestinal surface in the rat jejunum, which is referred to as "microclimate-pH". In the control experiment, a significant pH gradient was observed between the mucosal surface (approximately pH 6.8) and the bulk phase (approximately pH 7.3). The microclimate-pH was decreased by 0.2-0.6 pH units after addition of higher concentrations of EGF (3-100 nM) to the lumen. The microclimate-pH thus decreased recovers to the control value by replacing EGF with TES buffer, suggesting that the EGF effect is reversible. Considering that the Na+-H+ exchanger exists on the luminal membrane of the intestinal cells, the decrease in the microclimate-pH which was induced by EGF added to the luminal side may be due to the activation of Na+-H+ exchanger.
The main directions in the research and study of industrial microclimate are represented in the article. Evaluation of the microclimate based on thermophysiology, studies of correlation between the environmental temperature and the human functional status helped to establish the normal parameters, measures of the overheating and the overcooling prophylaxis. New data about the immediate and late effect of single microclimate parameters on the human functional status necessitate the creation of new methodic approaches to the evaluation and control of microclimate conditions.
K+ concentrations were measured with K+ sensitive liquid ion exchanger microelectrodes in situ and in vitro in the mucus layer at the luminal cell surface of the proximal and the distal colon in guinea pig. In a first series of experiments K+ concentrations were increased in the luminal solution from 0 to 70 mmol X l-1; the serosal K+ concentrations were kept in vitro at 5.4 mmol X l-1. In the proximal colon mean K+ concentration in the microclimate was in vitro 7.9 +/- 3.5 mmol X l-1, and independent from mucosal concentrations. In the distal colon in vitro, and in situ in the proximal as well as in the distal colon, K+ concentrations in the microclimate were increased slightly when K+ concentrations were elevated in the luminal solution up to 70 mmol X l-1. In a second series of in vitro studies K+ concentrations were also altered in the serosal fluid. In the proximal and in the distal colon K+ concentrations increased linearly with elevated K+ concentrations in the serosal solutions. A temporarily interrupted mucosal blood flow resulted in a significant increase in the K+ concentration in the microclimate. A paracellular shunt pathway and a high preepithelial diffusion barrier for K+ would explain the observed K+ concentrations in the microclimate at the luminal cell surface.
As a result of the proposed study it was established that a complex action of carbon oxide and toluene++ in 300 mg/m3 concentration in a combination with heating microclimate (leading to a maximum heat labour condition) results in an increased total biological effect. The coefficient to the complex action of carbon oxide and heating microclimate is equal to 2.5 and toluene++ and heating microclimate to 1.9. These coefficients should be taken into account in establishing hygienic norms for the chemical compounds.
It is shown in the paper that sensitivity of human organism to the toxic action of toluene is not changed under exposure to the microclimate, producing allowable thermal state, and is increased under exposure to the heating microclimate leading to the development of maximum thermal state. Under toluene exposure in the concentration 300 mg/m3 resistance to the heating microclimate under the conditions of joint exposure to these factors is reduced, which is manifest in an earlier onset of the maximum thermal state in people under observation.
Through the research performed it was established that man's sensitivity to the toxic properties of carbon oxide (CO) is not influenced by microclimates with permissible temperature characteristics, and the sensitivity increases under the influence of heating microclimates leading to the limit temperature conditions. With carbon oxide (CO) in concentration 300 mg/m3, the endurance of heating microclimate under a complex influence of these factors decreases what manifests itself in earlier limit temperature conditions of the examined persons.
A new approach to heat acclimatization has been shown to be feasible during laboratory experimentation. Wearing microclimate suits containing dry ice as the coolant, three groups of men were subjected to a moderate work rate in three different environments for 4 h/d for 8 d. Physiological responses on a subsequent heat tolerance test indicate that the group subjected to an environment of 32.0 degrees C W. B. and 33.5 degrees C D.B. were fully heat acclimatized. The 33/35 degrees C group were also well-acclimatized but developed dangerously high body temperatures during the first 2 d. Only partial acclimatization was achieved by the 31/33 degrees C group. The reason why the men acquire heat acclimatization while wearing the microclimate suits in a hot environment is probably that microclimate cooling does not prevent body temperature from rising--it only prevents it from rising excessively. It should be remembered that only one-third of the body is cooled while the rest shows the normal sweating response.
1. Short-chain fatty acid absorption in hen colon is protonated across the apical border coupled to an apical electrogenic proton pump. 2. The surface pH of the isolated colonic epithelium was 6.27 +/- 0.05, when incubated in Krebs-phosphate buffer pH 7.0. 3. Propionate 7 and 40 mmol/l in the incubation medium (pH 7.0) increased microclimate pH to 6.47 +/- 0.04 and 6.56 +/- 0.04. Inhibition of metabolic activity by potassium cyanide 1 mmol/l increased surface pH to 6.66 +/- 0.06. 4. The calculated concentration of propionic acid in the microclimate is near-linearly related to the propionate concentration. Thus, the acid microclimate is not responsible for the Michaelis-Menten like kinetics of propionate transport.
Microclimate is an important factor in modern intensive stockbreeding. At any rate, it ought to be judged in the context of other stress factors. Since microclimate is variable in the stable, it ought to be measured with the purpose of possibly effectuating a correction. The microclimate of a stable, which is also dependent on the outer climate situation, cannot always be improved solely by means of ventilation. However, the ventilation system should always be coordinated with the dung removal system of the stable.
The microclimate in fattening houses of the TEROZ TACHOV type was studied in two fattening seasons. One of the houses had the original ventilation based on negative pressure and the other was tested as to the function and effect of overpressure ventilation. Under the given conditions, the comparison of the two systems showed that the pressure ventilation drove more air through the zone where the animals were kept, and was connected with higher cooling. Dust nuisance was reduced by the pressure ventilation system, but the temperatures and humidites in the fattening houses were influenced, since it slightly increased the temperatures in the house as a result of the flow of hot air from outside in summer, and considerably cooled the microclimate in the house in winter. Nevertheless, the pressure ventilation system provided a better microclimate for the pigs: their gains were higher and the mortality was lower.
A study was performed to examine microclimate in 14 stables belonging to 10 horsemen's teams and clubs; five of these houses were new-built. In five race-horse stables housing 16 horses each, on an average, where the optimum air temperature ranged from 10 degrees C to 12 degrees C, measurements and examinations were performed in the winter period and the following results were obtained: space per 1 horse housed 42.9 plus or minus 8.7 m-3, relative air humidity 74.3 plus or minus 3.8%, CO2 concentration 0.175 plus or minus 0.027%, NH3 concentration 0.00135 plus or minus 0.00044%. A large majority of horse stables under our conditions lack suitable ventilating equipment for winter and for cold periods. Together with the present-day building technology and with excessive space of box-type houses, this implies that microclimate conditions are unsuitable and harmful to health; in particular, this is true of cold and wet conditions. In the existing stables this problem can be solved by additional heating, preferably with the hot-air system. It is necessary that horse stables should have good thermal-insulation characteristics, with plastered brick walls 45 cm in thickness and with thermally insulated loft. Floors must be solid, hard, and plane. Modern building technology and new materials must secure all the required parameters, with due respect to all factors constituting microclimate and to purposeful layout of race horse stables. It appears desirable to issue a state standard for the construction of horse stables.