Search PubMed⌕ Search

Biomedical subjects

E Kivilaakso

Publications and source records attributed to E Kivilaakso.

At least 145 records · Page 8Linked to original sources
PubMed1981

The role of mucosal carbonic anhydrase in the protection of gastric mucosa against luminal H+.

Carbonic anhydrase is exceptionally abundantly present in the gastric mucosa, including the epithelia surface cells. Inhibition of carbonic anhydrase activity with acetazolamide enhances the susceptibility to ulceration in rabbit antrum. It also abolishes the protection against ulceration afforded by intravenous HCO3- in rats. Acetazolamide likewise abolishes the protection against ulceration afforded by the presence of HCO3- in the incubation medium for isolated frog gastric sacs. These findings suggest a protective function for carbonic anhydrase in gastric mucosa.

Acetazolamide↗
PubMed1981

Disturbances in gastric motility during hypovolaemic shock.

In piglets hypovolaemic shock causes motorical disturbances and gastroduodenal dysrhythmia which both lead to increased duodenogastric reflux and to elevated concentrations of lysolecithine in the stomach. During a long lasting and severe shock gastric movements and electrical control activity waves totally cease. These changes can be observed as well endoscopically as using myoelectrogrammes. Exposition of the gastric mucosa to duodenal juice together with ischemia causes intramucosal haemorrhages and superficial erosions resembling human stress ulcers.

Animals↗
PubMed1981

Effect of bile salts and related compounds on esophageal mucosa.

Several potentially harmful agents present in the gastric juice or duodenal contents were assessed in terms of their ability to cause damage to the esophageal mucosa using an in vitro technique. In the presence of luminal acid (pH 3.5), taurocholate and pepsin and, to a lesser degree, lysolecithin adversely affected the mucosa causing increased diffusion of luminal H+ into the mucosa, a mechanism which may play a significant role in the pathogenesis of acidic reflux esophagitis. In the absence of luminal acid (pH 7.4) trypsin and the deconjugated bile salts cholate, chenodeoxycholate and deoxycholate affected the mucosa and possibly play a more important role in the pathogenesis of alkaline reflux esophagitis.

Animals↗
PubMed1981

Resection of the pancreas for acute fulminant pancreatitis.

The records of 30 consecutive patients treated by pancreatic resection for acute hemorrhagic or necrotizing pancreatitis from 1974 to 1978 were reviewed. Formal subtotal or near to total resection of the pancreas was undertaken whenever vigorous nonoperative therapeutic measures did not bring rapid improvement of the condition of the patient. The rationale was that removal of the diseased pancreatic tissue would prohibit the progress of inflammation and abolish the development of complications directly associated to the inflammatory process itself. There was no intraoperative mortality, but 11 patients died after the operation. Of the 19 survivors, eight had an uncomplicated postoperative course, whereas 11 patients recovered only after severe complications, usually requiring multiple reoperations. Among the most important complications were intra-abdominal sepsis, septicemia, upper gastrointestinal tract bleeding, respiratory insufficiency, renal insufficiency and perforations of the gastrointestinal tract. After a follow-up period of one to five years, five patients have remained completely free of symptoms. In 12 patients, diabetes has developed, and four patients had recurrent mild attacks of pancreatitis. All but two patients have resumed their previous work or other activities of living.

Acute Disease↗
PubMed1980

The gastric mucosal barrier and ulceration.

The gastric mucosal barrier is that property which defends against acid and which impedes diffusion of acid from the lumen into the mucosa. The disappearance of luminal H+ is linearly related to luminal (H+) both in the normal stomach and in stomachs exposed to barrier breakers. The latter invaribaly produce anatomic evidence of surface cellular injury. Strong direct evidence for back diffusion of luminal H+ derives from the recent demonstration of a highly significant correlation between the disappearance of luminal H+ and the pH of the lamina propria measured by an implanted microelectrode. The permeabilities of the antrum and fundus to H+ differ from each other in the same species and in different species. Gastric ulceration does not occur in the absence of luminal acid and is not dependent upon the absolute loss of H+ from the luminal solution. Mucosal ischemia induced by hemorrhage reduces tolerance against ulceration as does inhibition of acid secretion, acidification of the tissue caused by absence of nutrient bicarbonate, inhibition of carbonic anhydrase, and blockade of anion exchange by SITS. A tentative schema is proposed by which defense against luminal acid is accomplished in gastric mucosa.

Acid-Base Equilibrium↗
PubMed1980

Serum phospholipase A2 in human acute pancreatitis.

The main problem in the diagnosis of acute pancreatitis is the early detection of the fulminant forms. So far, there is no single laboratory test that affords an unequivocal measure of the severity of the disease. We have studied the serum phospholipase A2 concentrations of 66 consecutive patients with acute or chronic relapsing pancreatitis. Fifty-two patients had a mild spontaneously healing form of the disease, whereas eight patients developed a pseudocyst or an abscess. Six patients had operatively established haemorrhagic pancreatitis. The serum phospholipase A2 concentrations were significantly higher in the patients with haemorrhagic pancreatitis than in those with a spontaneously healing disease. Moreover, in the patients with a milder form of the disease the serum phospholipase A2 concentrations correlated with prognostic signs suggested by others. The results suggest that the assaying of serum phospholipase A2 might be a valuable tool in the diagnosis and follow-up study of patients with acute pancreatitis.

Acute Disease↗
PubMed1980

Effect of bile salts and related compounds on isolated esophageal mucosa.

The effect of several potentially harmful agents in gastric juice and duodenal contents on esophageal mucosa was investigated in the presence or absence of luminal H+ using an in vitro technique. Isolated rabbit esophageal mucosae were incubated in an Ussing chamber, and during exposure to the test agents mucosal integrity was assessed by measurement of mucosal potential difference (PD), tissue electrical resistance (R), and when luminal acid was present, the tissue permeability to H+. At pH 3.5 taurocholate caused a marked decrease in the PD and R and a substantial increase in the rate of luminal H+ loss. This effect was dependent on the presence of luminal H+, since no changes were observed with taurocholate at pH 7.4. In contrast, two of the three deconjugated bile salts tested at pH 7.4, deoxycholate and chenodeoxycholate, caused a profound reduction in the PD and R, similar to that observed with taurocholate in the presence of H+. Pepsin in the presence of H+, lysolecithin to a lesser degree, and trypsin in the absence of H+ also adversely affected isolated esophageal mucosa, but the effects were less pronounced than those caused by bile salts. Our data suggest that different mechanisms are operative in the pathogenesis of acidic and alkaline reflux esophagitis. In the presence of gastric H+, pepsin, and conjugated bile salts are the substances responsible for the greatest injury. In contrast, when acid is absent, trypsin and especially deconjugated bile salts are more crucial pathogenetic factors.

Animals↗
PubMed1980

Effect of 16-16-dimethyl-prostaglandin E2 on ulceration of isolated amphibian gastric mucosa.

In order to investigate the cytoprotective action of 16-16-dimethyl-prostaglandin E2 (16-16D), we studied its effect on sacs of isolated amphibian gastric mucosa known to ulcerate with high frequency in the absence of nutrient HCO3-. The actions of 16-16D, 2.85 X 10(-6) M, were also studied in an in vitro chamber. The incidence of ulceration in HCO3- -free nutrient media containing 10(-4) M histamine was significantly reduced by 16-16D. When artificial gastric juice (AGJ) was instilled into the lumen of the sac, protection occurred only after a pretreatment period of 60 min. Cytoprotection was not observed when active secretion of H+ was inhibited with 10(-3) M metiamide, and AGJ was placed in the lumen of the sac. In open sheets of fundus stimulated with 10(-4) M histamine, 16-16D did not influence H+ secretion. Isc was significantly higher than in control tissues. We conclude that 16-16D is cytoprotective in amphibian gastric mucosa by an action independent of changes in acid secretion or in blood flow. In addition, our studies suggest that 16-16D may increase the availability to the surface cells of nutrient HCO3- produced by actively secreting oxyntic cells.

16,16-Dimethylprostaglandin E2↗
PubMed1978

Effect of the acid secretory state on intramural pH of rabbit gastric mucosa.

Intramural pH of the gastric mucosa was measured using a microelectrode technique in rabbit gastric pouches under different secretory conditions and luminal acidity. Exposure of spontaneously secreting or metiamide-treated fundic pouches to a relatively high concentration of luminal acid. HCl 120 mM, for 60 min, led to a marked net loss of luminal H+ which was associated with a significant decrease in the intramural pH (7.28 +/- 0.09 to 6.88 +/- 0.10 and 7.23 +/- 0.07 to 6.99 +/- 0.09, respectively). A linear relationship was observed between the rates of net disappearance of luminal acid and the intramural pH. All 10 spontaneously secreting and five metiamide-treated pouches had superficial mucosal erosions. In contrast, when fundic pouches were exposed to luminal acid in histamine-treated animals, the net loss of luminal H+ was negligible and the intramural pH remained at its base-line level (7.25 +/- 0.07). Histamine stimulation without acid in the lumen caused a small but insignificant increase in the intramural pH (7.27 +/- 0.03 to 7.39 +/- 0.05). Only three of the eight histamine-treated fundic pouches had lesions. In the antral pouches the intramural pH changes in response to exposure to luminal acid were smaller and histamine treatment did not influence the intramural pH. None of the antral pouches had lesions. The results suggest that acidification of the tissue by the diffusion of luminal acid may be an important factor in the pathogenesis of acute gastric ulceration. The acid secretory state of the gastric mucosa can significantly influence the acid-base balance in the mucosa and thus modify its response to acid diffusing from the lumen. Histamine stimulation protected the gastric mucosa by improving its buffering capacity and/or otherwise decreasing the diffusion of H+ from the lumen into the mucosa.

Animals↗
PubMed1978

Treatment of idiopathic thrombocytopenic purpura in adults. Long-term results in a series of 41 patients.

The results of treatment of idiopathic thrombocytopenic purpura (ITP) were analysed in a series of 41 patients 2 to 10 years (median 4 years) after initial treatment. There was one spontaneous remission. A good or fair long-term result was obtained in 11 patients after prednisone treatment, in 20 of 24 patients after splenectomy, and in 3 of 4 patients after immunosuppressive treatment. Short duration of symptoms and rapid response to prednisone had some value in predicting a good long-term result of prednisone treatment. Young age, a good response to prednisone and splenic sequestration of platelets were associated with good results after splenectomy, as was rapid postoperative normalization of platelet counts. These factors were unable to disclose with certainty a refractoriness to splenectomy. Nevertheless splenectomy was regarded to be the treatment of choice in all patients not adequately controlled with corticosteroids.

Adult↗
PubMed1978

Effects of lysolecithin on isolated gastric mucosa.

The effects of lysolecithin, a normal constituent of duodenal juice, on gastric mucosa were measured under isolated conditions. In a relatively low concentration (0.5 mg/ml), lysolecithin, added to the luminal side, caused liberation of organic acids without altering the spontaneous rate of mineral (i.e., HCl) acid secretion by fundic mucosa. The low concentration of lysolecithin also did not appear to affect other active ion transport processes or permeability of either fundic or antral mucosa. However, at a higher concentration (1 mg/ml) lysolecithin inhibited spontaneous mineral acid secretion by fundus, altered active transport of other ions, and increased mucosal permeability of both fundic and antral mucosa. The results suggest that intraluminal lysolecithin in concentrations found in vivo may contribute to gastric mucosal damage.

Animals↗