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Biomedical subjects

E Kivilaakso

Publications and source records attributed to E Kivilaakso.

At least 91 records · Page 5Linked to original sources
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

Failure of long limb Roux-en-Y reconstruction to prevent alkaline reflux esophagitis after total gastrectomy.

Postoperative reflux esophagitis is usually not seen in connection with Roux-en-Y reconstruction after total or subtotal gastrectomy. An isoperistaltic jejunal limb of adequate length (over 40 cm) is considered to prevent reflux of duodenal contents into the esophagus with consequent injury of the esophageal mucosa that otherwise may ensue. The present paper describes four patients who developed postoperative reflux esophagitis as a complication after total gastrectomy, despite a well-functioning Roux-en-Y reconstruction. It is possible that the intraabdominal generalization of cancer which was concomitantly observed in three of our four patients, may have had a contributory influence on the development of the condition by decreasing esophageal mucosal resistance, thus rendering the mucosa vulnerable to even minimal amounts of intra-esophageal regurgitation of duodenal contents, and that alkaline reflux esophagitis appearing after an interval in a patient who had an adequate Roux-en-Y reconstruction after total gastrectomy, may be the first sign of intraabdominal tumor recurrence despite negative x-ray examinations.

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↗
PubMed1990

Decreased risk of gastric stump carcinoma after partial gastrectomy supplemented with bile diversion.

The exact incidence of gastric stump cancer is not known. The reported incidence figures vary greatly, even in studies using similar methods. The aim of this study was to re-evaluate the risk of gastric stump cancer after gastric surgery for peptic ulcer in the Finnish population. A total of 285 patients (252 men and 33 women) operated on for benign peptic ulcer between 1948 and 1954 were followed-up till the end of 1984 (mean for men = 19.4 years, for women = 22.9 years). At the end of 1984 58 patients (20%) were still alive with no verified gastric cancer. One patient developed gastric cancer within five years after the operation and was excluded from the series. Nine patients (3%) were lost to follow-up. Six patients (four men and two women) of the total 285 had developed gastric cancer 6, 7, 8, 21, 25 and 27 years after operation. The risk of getting gastric cancer in a control population (no operation) of equal size and age during a similar follow-up period was 6.71 cases for men and 0.86 cases for women (total = 7.57). The observed number (6 patients) does not differ significantly (P greater than 0.5) from the expected number (7.57). According to this study the risk of gastric cancer is not significantly increased by partial gastrectomy for benign peptic ulcer.

Adult↗
PubMed1990

Decreased risk of gastric stump carcinoma after partial gastrectomy supplemented with bile diversion.

The exact incidence of gastric stump cancer is not known. The reported incidence varies greatly, even in studies using similar methods. The aim of this study was to re-evaluate the risk of gastric stump cancer after gastric surgery for peptic ulcer in the Finnish population. A total of 285 patients (252 men and 33 women) operated on for benign peptic ulcer between 1948 and 1954 were followed-up till the end of 1984 (mean follow-up for men = 19.4 years, for women = 22.9 years). At the end of 1984, 58 patients (20%) were still alive without verified gastric cancer. One patient developed gastric cancer within five years after the operation and was excluded from the series. Nine patients (3%) were lost to follow-up. Six patients (four men and two women) of the total 285 developed gastric cancer 6, 7, 8, 21, 25 and 27 years after the operation. The risk of contracting gastric cancer in a control population (no operation) of equal size and age during a similar follow-up period was 6.71 cases for men and 0.86 cases for women (total = 7.57). The observed number (6 patients) does not differ significantly (P less than 0.5) from the expected number (7.57). This study shows that the risk of gastric cancer does not significantly increase after partial gastrectomy for benign peptic ulcer.

Female↗
PubMed1989

Pseudocysts in chronic pancreatitis. Surgical results in 102 consecutive patients.

Preoperative symptoms, diagnoses, and postoperative outcomes in 102 consecutive patients with pancreatic pseudocysts were analyzed. Upper epigastric pain, loss of weight, obstructive jaundice, and sudden arterial bleeding from the pseudocyst were the most common preoperative symptoms. Ultrasonography, computed tomography, and endoscopic retrograde cholangiopancreatography were the most useful diagnostic tools in the evaluation of the presence, size, location, and possible pancreatic ductal communications of the pseudocyst. In a single thick-walled pseudocyst, the best long-term results were achieved by internal drainage. Pancreatic resection is justified if the patient already has diabetes or multiple pseudocysts or if the pseudocyst is not amenable to internal drainage. The most fatal preoperative complication was a sudden arterial bleeding from a pseudocyst. In treating this complication, hemostasis with transcystic arterial ligation and external drainage of the pseudocyst gave the best results.

Adult↗
PubMed1989

Prostaglandin protection against hemorrhage-induced gastric stress ulceration in the rat.

The present study investigates whether prostaglandins "cytoprotect" the gastric mucosa against hemorrhage-induced stress ulceration by assessing the influence of 16,16-dimethyl prostaglandin E2 (16,16-dm PGE2) on gross and microscopic lesion formation, intramucosal tissue pH, H+ back-diffusion, and mucosal blood flow in rat gastric mucosa exposed to luminal acid (100 mM HCl) during hemorrhagic shock (13 ml/kg for 20 min). Intramucosal tissue pH was measured using pH-sensitive antimony microelectrodes, and mucosal blood flow was measured by the radiolabeled microsphere technique. 16,16-dm PGE2 (5 micrograms/ml topically) significantly protected the gastric mucosa against gross (lesion index 2.25 +/- 0.34 vs 0.87 +/- 0.21) and microscopic (lesion index 2.12 +/- 0.20 vs 0.87 +/- 0.09) damage during the shock. This protection was associated with a significantly lesser acidification of the mucosa during the shock (intramural tissue pH 6.67 +/- 0.08 vs 6.03 +/- 0.17). In order to elucidate whether the lesser intramucosal acidification was due to diminished entry of H+ (H+ back diffusion) into or better disposal of H+ from the mucosa, the influences of 16,16-dm PGE2 on transmucosal H+ fluxes and mucosal blood flow were determined. It appeared that 16,16-dm PGE2 had no influence on the rate of H+ back-diffusion, but it significantly enhanced mucosal blood flow both in the corpus (0.23 +/- 0.04 vs 0.14 +/- 0.03 ml/min/g) and in the antrum (0.24 +/- 0.03 vs. 0.14 +/- 0.03 ml/min/g) during the shock.(ABSTRACT TRUNCATED AT 250 WORDS)

16,16-Dimethylprostaglandin E2↗
PubMed1989

Adenocarcinoma arising in Barrett's esophagus.

The main goal of this study was to evaluate the development of adenocarcinoma in patients with Barrett's esophagus. During the period from January 1975 to December 1985, a total of 134 patients had endoscopically severe esophagitis and/or Barrett's esophagus. In these patients, 32 (24%) met the macroscopic and histologic criteria for the diagnosis of Barrett's esophagus. A check-up study of these patients was performed in 1987. Adenocarcinoma developed in three patients during the follow-up period of 166.1 patient-years. Dysplasia in the columnar epithelium was found in two of these patients six and 15 months before the diagnosis of adenocarcinoma. The third patient with adenocarcinoma was detected in endoscopic follow-up in 1987. In addition, the endoscopic examination showed unchanged Barrett's epithelium in all but three patients despite the operative and/or medical treatment 3-12 years (mean 6.7 years) earlier. We conclude that Barrett's esophagus is a potential premalignant condition and careful endoscopic surveillance for dysplasia in the columnar epithelium of the distal esophagus is mandatory in patients with Barrett's esophagus.

Adenocarcinoma↗
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↗
PubMed1989

Acute gastric mucosal lesions, haemodynamic and microcirculatory changes in the thermally injured rat.

Early postburn changes in central haemodynamics, organ blood flow distribution and morphology of the gastric mucosa were studied using a standarized thermal skin injury model. Organ blood flow and cardiac output were determined using radioactive microspheres. In the control animals no marked changes in cardiac output or organ blood flow were observed, and the gastric mucosa remained essentially undamaged. After burn injury and no fluid resuscitation, cardiac output decreased by 78 per cent, and blood flow to the stomach, pancreas, spleen, muscle, skin and kidneys also decreased markedly and to about the same degree as the cardiac output, however the adrenal flow remained roughly unchanged at the baseline level. Gross and microscopic lesions developed in the stomach, especially in the corpus. In animals given fluid resuscitation after burn injury cardiac output decreased by 38 per cent during the experiment, but blood flow in the stomach, brain, kidneys and spleen remained fairly constant, while pancreatic and muscle blood flow decreased and adrenal blood flow increased markedly. The gastric mucosa showed only minor microscopic, but no macroscopic lesions at the end of the experiment. The results indicate that acute thermal skin injury induces profound changes in central haemodynamics and organ blood flow which can, however, largely be overcome by adequate fluid resuscitation. The data also suggest that, as in other examples of 'stress ulceration', impaired mucosal blood flow may underlie the stress ulceration which complicates severe burns.

Acute Disease↗
PubMed1989

Treatment of pancreatic fistulas with somatostatin and total parenteral nutrition.

Nineteen pancreatic fistulas were treated with somatostatin (ST) and total parenteral nutrition (TPN). Five of the fistulas developed in an uninflamed pancreas, whereas 14 fistulas developed secondary to a necrotizing or chronic pancreatitis. Fistular output varied between 20 and 800 ml/day (median, 160 ml) during TPN before ST treatment; amylase concentration was 10,500-800,000 UI/l. Twelve of 16 (75%) fistulas were contaminated with bacteria. Thirteen of 19 (68%) fistulas closed after a median treatment of 7 (range, 2-14) days. Seven of eight fistulas with open drainage to the bowel healed, whereas only one of six with obstructed drainage closed. All of the uninfected fistulas and half of the infected fistulas closed. The findings suggest that somatostatin treatment speeds up the closure of pancreatic fistulas with open drainage to the bowel but is not beneficial when the intestinal drainage of the fistular region to the bowel is obstructed.

Adult↗
PubMed1988

Subepithelial tissue pH of rat gastric mucosa exposed to luminal acid, barrier breaking agents, and hemorrhagic shock.

Tissue pH in the immediate subepithelial layer of rat gastric mucosa was measured using H+-selective microelectrodes. Exposure of the mucosa to luminal acid (50-150 mM) caused a significant acidification of the subepithelial tissue. Contrary to expectation, disruption of the mucosal barrier with taurocholate (10 mM), acetylsalicylic acid (10 mM), or ethanol (20% vol/vol) during acid (100 mM HCl) perfusion promoted no further acidification of the subepithelial tissue but rather caused an alkalinization of the primarily acidified subepithelial tissue. When hemorrhagic shock was induced during acid perfusion, a profound acidification of the subepithelial tissue occurred even though a much lower luminal acidity (10 mM HCl) was used. Also, taurocholate had no alkalinizing influence on subepithelial pH during hemorrhagic shock, but caused a rapidly progressing and irreversible drop of the subepithelial tissue pH. The findings suggest that in normal stomach with intact "mucosal barrier," H+ back-diffusion occurs during exposure to acid. However, disruption of the mucosal barrier seems to lead to alkali (HCO3-) efflux from the mucosa, which neutralizes the influxing H+, thus "masking" H+ back-diffusion and protecting the mucosa. Yet, when adequate supply of HCO3- to the mucosa is blocked during exposure to a barrier-breaking agent and acid, increased H+ back-diffusion becomes again "unmasked," leading to extensive acidification and ulceration of the mucosa.

Animals↗
PubMed1988

Intracellular pH in isolated Necturus antral mucosa in simulated ulcerogenic conditions.

Intracellular pH (pHi) was measured with proton-sensitive liquid sensor microelectrodes in isolated Necturus antral mucosa, paying special attention to arranging experimental conditions to simulate conditions frequently associated with in vivo "stress ulceration." Intracellular pH in mucosas perfused under standard conditions (Ringer's solution containing HCO3-/CO2) was 7.22 + 0.02 (n = 27). Removal of Na+ and HCO3- or addition of amiloride or 4-acetamido-4-isothiocyanostillbene-2,2-disulfonic acid (blockers of Na+/H+ and Cl-/HCO3-exchangers) had no influence on steady-state pHi, suggesting that these ion exchangers do not significantly contribute to the maintenance of pHi in the presence of normal external pH. Acidification of mucosal (luminal) perfusate to pH 3 (mimicking the presence of gastric acid) had no influence on pHi, but mucosal pH 2 (10 mM HCl) acidified pHi to 6.93 +/- 0.07. Acidification of serosal (nutrient) perfusate to pH 6 (mimicking intramucosal acidosis caused by back-diffusion of luminal H+) acidified pHi to 6.72 +/- 0.10. Removal of Na+ from and addition of amiloride to the serosal perfusate during exposure to serosal pH 6.0 induced further acidification of pHi, suggesting that in this acidotic situation (with very low ambient HCO3- concentration) a Na+/H+ exchanger does contribute to the maintenance of steady-state pHi. Increased PCO2 (10% vol/vol in the gas) in a slightly acidic milieu (mimicking mucosal ischemia) likewise acidified pHi to 6.73 +/- 0.05. A combination of mucosal acid (pH 3), high PCO2 (10% CO2), and low serosal pH (pH 6) (mimicking conditions that prevail, for example, during hemorrhagic shock) acidified pHi and ultimately resulted in cell death. These derangements of intracellular acid-base balance may have pathogenetic importance also in in vivo stress ulceration.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1987

Analysis of 58 patients surviving more than ten years after operative treatment of gastric cancer.

We evaluated 58 patients who were still alive more than ten years after operative treatment of gastric cancer. We reexamined their histologic specimens and compared them with those of matched paired controls of the same sex and age who had died of gastric cancer. Forty-two patients consented to a follow-up study. The age of the patients did not affect survival. For patients with gastric cancer, those with distal cancer or an ulcer simulating cancer had had a better prognosis. Forty percent of the patients had had an early gastric cancer. Only two patients had had lymph node metastases in regional lymph nodes, and macroscopic tumor growth through the serosa had been recorded in only four cases. In 23 cases, a distal resection had proved successful. No significant correlation between intestinal or diffuse types of cancer and prognosis was observed. One recurrence after ten years was found; in one case, there was a new cancer in the gastric remnant. In addition, biopsy specimens from two patients showed grave dysplasia. We suggest that throughout their lives annual follow-up examinations be performed in patients who have undergone radical operations for gastric cancer.

Adult↗
PubMed1987

Role of lipase in the pathogenesis of experimental esophagitis in the rabbit.

The role of lipase in the pathogenesis of reflux esophagitis was investigated in an experimental model in which an in situ isolated segment of rabbit esophagus was perfused (at pH 7) with a solution containing lipase in concentrations of 2 and 10 mg/ml. The severity of mucosal damage was assessed using the following indicators of mucosal integrity: transmucosal potential difference, net flux of sodium, and mucosal permeability to erythritol labeled with carbon 14, a neutral molecule with a greatest molecular diameter of 8.2 nm. Furthermore, the morphologic characteristics of esophageal damage were studied by light and scanning electron microscopy. The results suggest that lipase significantly decreased transmucosal potential difference and increased mucosal permeability to sodium and erythritol labeled with carbon 14. Morphologically, lipase induced cytoplasmatic vesiculation and widening of intercellular spaces within the basal cell layer. The epithelial cell layers were also often seen to be sloughed off with consequent exposure of the subepithelial connective tissue at the mucosal surface. The findings suggest that lipase has an adverse effect on the esophageal mucosa that may have pathogenetic significance in clinical reflux esophagitis.

Animals↗
PubMed1987

Total and near-total gastrectomy for gastric cancer in patients over 70 years of age.

A total or near-total gastrectomy was performed in 52 patients over 70 years of age in our hospital from 1975 through 1982. The hospital mortality rate was 9.6 percent. The operation was palliative in nine patients. In these patients, the operation was performed because of an obstructing cancer. At last follow-up, 11 patients had survived more than 5 years and 6 patients were alive and free of disease more than 3 years after the operation. Total and near-total gastrectomies seem to be justified in elderly patients in good overall physical condition.

Age Factors↗
PubMed1987

Morphology of lysolecithin-induced damage on esophageal mucosa. An experimental light and scanning electron microscopical study.

The morphology of the esophageal mucosal damage induced by lysolecithin was investigated in an experimental model, where an isolated segment of rabbit esophagus was purfused in situ with lysolecithin, alone or in combination with HCl. The results indicate that lysolecithin alone causes no morphological damage to the esophageal mucosa. However, when combined with HCl, lysolecithin causes widening of intercellular spaces and detachment of superficial cells leading ultimately to disclosure of denuded submucosal collagen bundles. This suggests that, in clinical situations lysolecithin refluxed from the duodenum into the stomach and further to esophagus may have importance in the pathogenesis of reflux esophagitis when gastric acid is present, too. In contrast, under unacidic conditions (i.e., in the pathogenesis of alkaline reflux esophagitis) lysolecithin seems to be of minor importance.

Animals↗