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Biomedical subjects

H Mustonen

Publications and source records attributed to H Mustonen.

31 records · Page 2Linked to original sources
PubMed1995

Milk and egg phospholipids act as protective surfactants against luminal acid in Necturus gastric mucosa.

BACKGROUND: Our previous studies indicate that milk phospholipids have anti-ulcer properties in rats and humans, possibly by forming a hydrophobic surfactant layer at the epithelial surface. In the present study we measured intracellular pH and parameters of membrane resistances in gastric epithelium exposed to luminal acid using a microelectrode technique. METHODS: Chambered isolated Necturus maculosus antral mucosa was exposed to pH 2.3, with or without 20-25 min pre-treatment with milk or egg phospholipids. The pH in surface epithelial cells was measured with double-barrelled liquid sensor pH/PD-microelectrodes. RESULTS: Pre-treatment with phospholipids (2500-5000 micrograms P/mL) significantly (P < 0.01, n = 14) opposed intracellular acidification. Phospholipids significantly (P < 0.05, n = 14) increased the ratio of apical and basal membrane resistances, suggesting that they primarily affect the apical cell membrane. In contrast, there was no significant change in transmucosal resistance suggesting lack of effect on paracellular shunts in the 'leaky' epithelium. CONCLUSIONS: Exogenous phospholipids of dietary origin may be used to form a protective layer in the gastric mucosa against irritants.

Animals↗
PubMed1993

Preepithelial mucus-HCO-3 layer protects against intracellular acidosis in acid-exposed gastric mucosa.

The role of the preepithelial mucus-HCO-3 layer in protection against intracellular acidosis was investigated in isolated Necturus gastric antral mucosa exposed to luminal acid by simultaneous measurement of intracellular pH (pH(i)) and extracellular surface pH (pHs) in surface epithelium with microelectrode technique. Acidification of the luminal perfusate to pH 2.5 acidified pH(i) in surface epithelial cells from 7.33 +/- 0.02 to 7.20 +/- 0.04, whereas pHs fell from 6.75 +/- 0.21 to 5.20 +/- 0.25 (P < 0.01; n = 9), followed by a steady state for at least 2 h. Inhibition of epithelial HCO-3 secretion and transport by removal of serosal HCO-3 and CO2 (HEPES and O2 substitution) during acid exposure provoked a progressive acidification of pHs from 5.60 +/- 0.41 to 2.74 +/- 0.14 in 30 min (P < 0.01; n = 9), which was accompanied, after a 5- to 10-min delay, by acidification of pH(i) from 7.21 +/- 0.03 to 5.68 +/- 0.26 (P < 0.01). Digestion of the surface mucus gel by pepsin (5% wt/vol) at pH 2.5 caused a slow acidification of pHs from 5.22 +/- 0.59 to 3.60 +/- 0.46 within 2 h. This was followed by a more rapid acidification to 2.53 +/- 0.38 (P < 0.01; n = 7), with concomitant acidification of pH(i) from 7.19 +/- 0.05 to 6.03 +/- 0.33 (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcysteine↗
PubMed1992

Intracellular pH in isolated Necturus duodenal mucosa exposed to luminal acid.

Regulation of intracellular pH (pHi) and its maintenance within physiological ranges during exposure to luminal acid was studied in isolated Necturus duodenal mucosa using liquid sensor microelectrodes. Exposure of the mucosa to luminal pH 2.7 caused significant intraepithelial acidification. Subsequent removal of HCO3-/CO2 (HEPES/O2 substitution) from the serosal perfusate caused a further decrease of pHi. Blocking of HCO3- transport across the basolateral cell membrane by addition of 4-acetamido-4,isothiosyanostilbene-2,2-disulfonic acid (SITS) to serosal perfusate also caused a slight but significant decrease of pHi. Removal of Na+ (choline substitution) from the serosal perfusate during acid exposure likewise caused a significant decrease in pHi, as did serosal addition of an inhibitor of Na+/H+ antiport, 1 mmol/L amiloride. When Na+ was removed from the serosal perfusate after HCO3- removal, pHi first rapidly acidified; this was followed after an initial 5-minute steady state by an uncontrolled progressive acidification at a rate of 0.33 pH unit/15 min without any further steady state. A similar but weaker effect could also be shown with amiloride addition. The epithelial surface pH was 7.13 +/- 0.08 at the apex of mucosal villus and 7.42 +/- 0.11 (n = 5) in the cryptal area between the villi, i.e., greater than 1 pH unit higher than that of the luminal bulk solution (pH 6), thus suggesting active alkalization of the epithelial surface. Removal of serosal HCO3-/CO2 decreased surface pH significantly both at the villus apex and at the cryptal area, suggesting that the surface alkalization is mediated by transport of serosal HCO3- to the epithelial surface. The data suggest that pHi in acid-exposed duodenal mucosa is primarily maintained within physiological range by an HCO3(-)-dependent mechanism, which, at least in part, exerts its action extracellularly by forming an alkaline buffer layer at the epithelial surface. If adequate serosal (or systemic) HCO3- is not available, a second-line Na(+)-dependent and amiloride-sensitive pHi-regulatory mechanism, presumably an Na+/H+ antiport, becomes the main regulator of pHi.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1991

Exogenous surface-active phospholipid protects Necturus gastric mucosa against luminal acid and barrier-breaking agents.

The nature of the protective action of exogenous surface-active phospholipid on gastric mucosa was studied in isolated Necturus antral mucosa by measuring intracellular pH and intraepithelial potentials and resistances with a microelectrode technique. Exposure of the antral mucosa to luminal pH 2 acidified intracellular pH in surface epithelial cells by 0.6-0.3 pH units. A 20-minute pretreatment with exogenous (pulmonary) surfactanlike phospholipid completely abolished this effect. Obviously, phospholipid protected the mucosa against intracellular acidosis by decreasing the apical cell membrane conductance to H+ (and other ions), because it increased apical cell membrane resistance by +108% and total transcellular resistance by +86% but had no significant effects on paracellular or total transepithelial resistances. In mucosas exposed to three barrier-breaking agents, 10 mmol/L acetylsalicylic acid, 20% (vol/vol) ethanol, and 10 mmol/L taurocholate, at acid luminal perfusate (pH 2.0-2.5), a profound intracellular acidification of 0.9-1.3 pH units/15 min occurred. Pretreatment of the tissue with phospholipid significantly opposed intracellular acidification, but the modulatory influences on the changes in intraepithelial potentials or resistances were less conspicuous and mostly insignificant.

Animals↗
PubMed1991

Registration of arthroplasties in Finland. A nationwide prospective project.

Data on hip and knee arthroplasties have been compiled on a nationwide basis in Finland since 1980. Forty-five major departments contribute to the study providing data on the type of operation, the implant used, the diagnosis, and the 1-year clinical results. In the case of revision, new data are sent to the register, enabling survivorship analysis. Between 1980 and 1988, 25,966 operations were reported. Fifty-six percent had been made for primary osteoarthrosis, 22 percent for rheumatoid arthritis, 6.3 percent for secondary arthrosis, and 0.5 percent for CDH. In 1988, the total number of arthroplasties was 4,628: about two thirds hip and one third knee replacements. The annual incidence of primary total hip arthroplasties in 1988 was 58 per 100,000 inhabitants and that for the knees 25 per 100,000 inhabitants. More than 40 percent of the patients were under 65 years of age. In the whole series, primary thromboembolic complications occurred in 1.4 percent, luxations in 1.4 percent, infection in 0.9 percent, and evacuated hematoma in 0.6 percent. The annual frequency of re-arthroplasty increased between 1980 and 1988 from 9.8 to 13.6 percent, indicating an increasing orthopedic work load in the future.

Aged↗
PubMed1990

Tolerance of rat duodenum to luminal acid.

The tolerance of the duodenal mucosa to luminal acid was investigated by measuring with a liquid sensor pH microelectrode technique the epithelial surface pH (pHs) and subepithelial tissue pH (pHt) in rat proximal (duodenal bulb, Brunner gland area) and distal duodenum exposed to luminal acid. Under basal conditions, pHs was roughly equal in both parts of the duodenum; proximal duodenum, 7.40 +/- 0.14 (mean +/- SEM) at the villus tip and 7.54 +/- 0.16 at the depth of crypt; distal duodenum, 7.46 +/- 0.19 and 7.55 +/- 0.09, respectively. Yet, exposure of the mucosa to luminal acid (10 mM HCl) provoked a significantly lesser decrease of pHs (0.25 +/- 0.13 vs 0.42 +/- 0.12 pH units) in the proximal duodenum, suggesting that the response of epithelial HCO3 secretion to luminal acid is stronger in that part of the duodenum. Further, the initial acidification of pHs was followed in the proximal duodenum by a secondary alkalinization of pHs, leading to normalization of pHs, which may suggest activation of compensatory protective mechanisms. pHt at the villus tip was likewise roughly equal in both parts of duodenum (7.29 +/- 0.05 vs 7.17 +/- 0.04), but, again, acidification of the luminal perfusate progressively from 10 to 100 mM HCl induced a much earlier and significantly more profound acidification in the distal than in the proximal duodenum. The possible contribution of Brunner glands to the greater mucosal tolerance to acid in the proximal duodenum was assessed by investigating whether stimulation or inhibition of Brunner gland secretion modulates the response of the duodenal mucosa to acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1990

Intracellular pH in isolated Necturus antral mucosa exposed to luminal acid.

Regulation of intracellular pH in gastric epithelial surface cells exposed to luminal acid was investigated in isolated Necturus antral mucosa using microelectrode technique. Exposure of the mucosa to luminal pH 2 acidified intracellular pH from 7.21 +/- 0.01 to 6.95 +/- 0.04 (N = 50). Removal of Na+ from the perfusates or addition of amiloride (1 mM) to serosal perfusate (containing HCO3-) had no influence on intracellular pH during exposure to pH 2 (N = 6), but removal of HCO3-/CO2 from or addition of 4, acetamido-4-isothiocyanatostilbene-2,2-disulfonic acid (0.5 mM) to the serosal perfusate (containing Na+) acidified intracellular pH from 7.02 +/- 0.03 to 6.45 +/- 0.15 (p less than 0.01, N = 10) and from 6.97 +/- 0.06 to 6.58 +/- 0.26 (p less than 0.01, N = 6), respectively, in 15 min. In tissues exposed to mucosal pH 6, epithelial surface pH was about 1.3 pH units higher than pH of the mucosal bulk solution. Removal of Cl-/HCO3- from the serosal perfusate acidified epithelial surface pH by about 0.5 pH units (p less than 0.01, N = 6), suggesting that serosal HCO3- sustains intracellular pH, at least in part, by generating an alkaline buffer layer at the epithelial surface. In the absence of HCO3-/CO2, a stable intracellular pH was obtained when the tissue was exposed to mucosal pH 2.7, but in this situation intracellular pH was sensitive to Na+ removal or amiloride addition, intracellular pH decreasing from 7.00 +/- 0.07 to 6.48 +/- 0.10 (p less than 0.01, N = 6) and from 6.86 +/- 0.06 to 6.32 +/- 0.01 (p less than 0.01, N = 7), respectively, in 15 min. The data suggest that in gastric epithelium exposed to luminal acid, physiological intracellular pH is primarily maintained by the buffer action of serosal HCO3- transported to the epithelial surface to impede the entry of luminal H+ into mucosal tissue. Removal of the sheltering HCO3- unmasks a second line, Na(+)-dependent and amiloride-sensitive intracellular pH regulatory mechanism, presumably a Na+/H+ antiport.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1990

Alcohol use and its control in Finnish and Soviet marriages.

The paper reports the results of a comparative study conducted in Finland and in Estonia. A representative sample of young couples were interviewed in both countries. Husbands in both countries usually drink more often than their wives and are less dependent on their spouses' drinking company. Wives are more likely to attempt to control their spouses' drinking. Drinking and its control are associated with the emotional relationship between the spouses, and the attempts to control are logically associated with the controlled person's frequency of drinking. The wife's attempts to control the husband's drinking are more a blue collar than a white collar phenomenon. Finnish women and men drink more often than their Estonian counterparts. Maybe as a result of the greater frequency of drinking, drinking in Finland is more family-oriented than in Estonia. The Estonian culture seems more prone to informal control of the family members' drinking. These differences may be at least partly caused by differing alcohol policy climate in the two countries.

Adult↗
PubMed1990

Gastric mucosal acid-base balance.

Acute gastric ulceration induced by haemorrhagic shock is associated with profound intramucosal acidification due to diffusion of luminal H+ into the mucosa. High-HCO3- metabolic alkalosis protects the mucosa against this ulceration, whereas low-HCO3- respiratory alkalosis does not, suggesting that lack of systemic and intramucosal HCO3-, rather than tissue acidosis per se, renders the mucosa susceptible to ulceration. In normal mucosa, disruption of the mucosal barrier by taurocholate, ethanol or acetylsalicylic acid leads to efflux of alkali (HCO3-) from the mucosa, with generation of an alkaline buffer layer at the epithelial surface to protect the mucosa from further damage. In ischaemic mucosa no such protective alkaline layer is formed, and exposure to luminal acid leads to severe acidification of and damage to the mucosa. The efflux of alkali may be driven by capillary hydrostatic pressure, since no such protective alkaline efflux occurs in vitro, but rather exposure to luminal acid and barrier-breaking agents results in intracellular acidification. The potential pathogenetic role of a disrupted intramucosal acid-base balance, as well as the protective effect of systemic and intramucosal HCO3- in acute gastric stress ulceration is further substantiated by the in vitro findings that perfusion conditions simulating in vivo ulcerogenic conditions provoke intracellular acidosis, and serosal HCO3- significantly contributes to the maintenance of normal intracellular pH in surface epithelial cells exposed to luminal acid.

Acid-Base Imbalance↗
PubMed1989

Effect of barrier-breaking agents on intracellular pH and epithelial membrane resistances: studies in isolated Necturus antral mucosa exposed to luminal acid.

Features of "H+ back-diffusion" after disruption of the gastric mucosal barrier were investigated by assessing, with a microelectrode technique, the influence of three barrier-breaking agents, taurocholate (10 mM), ethanol (20% vol/vol), and acetylsalicylic acid (10 mM) on intracellular pH and epithelial membrane potentials and resistances in isolated Necturus antral mucosa exposed to luminal acid (pH 3). Exposure of the mucosa to each of the three agents induced intracellular acidification of surface epithelial cells, but the pattern of pHi behavior was different for each agent: taurocholate induced immediate acidification of pHi, ethanol acidified pHi after a delay of 4-6 min, whereas acetylsalicylic acid initially alkalinized pHi, whereafter a rapid acidification of pHi occurred. Assessment of intraepithelial membrane resistances indicated that taurocholate primarily increases cellular conductance, decreasing in particular Ra. In contrast, ethanol mainly increased paracellular conductance, but also decreased cellular resistance, in particular Ra. Acetylsalicylic acid initially increased cell membrane resistances and Ra/Rb, whereafter a rapid decrease of Ra/Rb and Rt occurred. In each instance, the decrease of Ra/Rb preceded acidification of pHi. The data suggest that all three agents induce intracellular acidification by increasing the conductance of the apical cell membrane to H+, but in ethanol-treated tissues paracellular conductance primarily contributes to H+ back-diffusion.

Animals↗
PubMed1988

Evaluation of genetic counselling: recall of information, post-counselling reproduction, and attitude of the counsellees.

Of the families who had received genetic counselling between 1972 and 1981, 791 replied to a questionnaire which covered recall of information, post-counselling reproduction and attitudes towards counselling and prenatal diagnosis. Eighty percent had adequate knowledge of mode of inheritance and 74% of recurrence risk. Knowledge of mode of inheritance was poorest in multifactorial transmission (63%) and knowledge of recurrence risk in X-chromosomal disorders (61%). Forty-five per cent of the families had started a pregnancy after the counselling. 25%). Early lethality of the disorder and feasibility of a prenatal study contributed to positive reproductive decisions. Nine per cent of the children born after the counselling were affected by the disorder in question. The observed risks tended to match well with the expected ones. Sixty-two per cent of the respondents felt that the counselling had had a great or moderate impact on their reproductive plans. Forty-two per cent expressed a wish to hear the counsellor's opinion in addition to the facts. This was more common when the disorder was severe. Although most couples (53%) wished to have a prenatal study, if feasible, and abort an affected foetus, 16% were against abortion in such a case and 31% wished to have the study but were ambiguous about an abortion.

Evaluation Studies as Topic↗
PubMedDate not supplied

Brief intervention for male heavy drinkers in routine general practice: a three-year randomized controlled study.

The aim of this research was to evaluate the effectiveness of long-term brief intervention in routine general practice. In five primary care out-patient clinics in a Finnish town, 296 male early-phase heavy drinkers consulting a general practitioner (GP) for various reasons were identified. Control group C (n = 88) was informed of the risks of drinking after the screening and were advised at the subsequent feedback about 2 weeks later to reduce their drinking. Groups A (n = 109) and B (n = 99) were offered in addition seven and three brief intervention sessions, respectively. All GPs took part, whether or not they indicated a special interest. The main outcome measures were differences between beginning and end-point at 3 years in self-reported alcohol consumption, mean corpuscular volume (MCV), and serum carbohydrate-deficient transferrin, aspartate aminotransferase, alanine aminotransferase and gamma-glutamyltransferase. There were no statistically significant differences between study groups A, B and C in mean changes in outcome measures. Within all the groups, MCV decreased. Depending on the outcome measure used and the study group analysed, clinically significant reduction of drinking was found in 25-53% of the subjects. In routine general practice, giving additional sessions of brief intervention may not be as effective as in special research conditions. Factors reducing the effectiveness of brief intervention programmes should be investigated, so that primary health care staff can be better supported in their efforts.

Adult↗