[The greater the crowd, the greater the risk of accidents. How good is our disaster planning and who is to finance it?].
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Accidents↗
Biomedical subjects
E Fellenius
Publications and source records attributed to E Fellenius.
Fatty acids suppress recovery of heart function after hypothermic perfusion.
Working rat hearts were perfused for 15 minutes at 37 degrees C before switching to a Langendorff perfusion (60 mm Hg aortic pressure) at 10 degrees C for 40 minutes of hypothermic arrest. Ventricular function was allowed to recover for 15 minutes at 37 degrees C by reestablishing the prehypothermic conditions. The perfusate was Krebs-Henseleit bicarbonate buffer containing 3% bovine serum albumin and either glucose (11 mmol/L) or glucose (11 mmol/L) plus palmitate (1.2 mmol/L) and gassed with 95% O2 and 5% CO2. In hearts receiving glucose alone as substrate, coronary flow was maintained constant during the 40 minutes of hypothermic arrest and returned to prehypothermic rates with rewarming. Ventricular function, as estimated by peak systolic pressure and heart rate, recovered to the prehypothermic level. When palmitate was added, coronary flow decreased continuously throughout the hypothermic perfusion (22% decrease by 40 minutes), and ventricular pressure development was lower throughout the rewarming perfusion. Tissue levels of adenosine triphosphate and creatine phosphate were well maintained and long-chain acyl coenzyme A and acyl carnitine decreased during hypothermia regardless of the substrate provided. With rewarming, tissue levels of adenosine triphosphate and creatine phosphate decreased in those hearts receiving palmitate. Omission of fatty acid either during hypothermia or during the first 5 minutes of rewarming improved recovery of function. Addition of oxfenicine to inhibit fatty acid oxidation, or inhibition of Ca2+ overload by verapamil and low perfusate Ca2+, prevented the effects of palmitate on ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)
Acyl Coenzyme A↗
Coxarthrosis and physical work load.
A case-referent study was performed on the possible relationship between physical work loads and an increased risk of developing coxarthrosis. The cases were 239 male recipients of a hip prosthesis as a result of severe idiopathic coxarthrosis; the referents were 302 men randomly selected from the general population. The work load was assessed through an interview and a self-administered questionnaire on the men's specific work periods. Men highly exposed to dynamic or static work loads had an increased relative risk of 2.42 (95% confidence interval 1.45-4.04) for developing coxarthrosis when compared with men with low exposure. Men with high exposure to heavy lifting between the ages of 30 and 49 years had the highest relative risk, 3.31 (95% confidence interval 1.97-5.57). Long-time exposure to physical work loads seems to be a risk factor for severe coxarthrosis among men.
Adult↗
Hyaluronan improves the healing of experimental tympanic membrane perforations. A comparison of preparations with different rheologic properties.
Preparations of hyaluronan at various concentrations and molecular weights were topically applied to experimental tympanic membrane (TM), perforations in the rat and their ability to improve the healing pattern was elucidated. The perforation occupied the upper posterior quadrant of the TM. Alterations in healing rate and quality of the healed TM were examined by otomicroscopy and in histologic sections. Hyaluronan enhanced the healing rate and resulted in less opacity and structural alteration of the scar area. Closure time for the TM perforation was correlated to the concentration of hyaluronan but not to its molecular weight or viscosity. Improved scar quality was obtained in the presence of hyaluronan irrespective of its rheologic properties. Hyaluronan improved the restoration of the fibrous connective tissue layer. Treatment of TM perforation in man with hyaluronan at high concentrations should be considered as an alternative to myringoplasty.
Administration, Topical↗
Histamine H2-receptor of human and rabbit parietal cells.
The histamine H2-receptor on the human parietal cell has been characterized by using dose-response curves and the negative logarithm of the molar concentration of an antagonist (pA2) analyses of cimetidine antagonism of betazole, histamine, and impromidine stimulation in isolated human and rabbit gastric glands. To evaluate the in vitro results, betazole-stimulated gastric acid secretion with and without cimetidine was also studied in healthy subjects. In the in vivo model, individual dose-response curves were shifted to the right with increasing cimetidine concentrations, but this was counteracted by increasing betazole doses, indicating competitive, reversible antagonism. The pA2 values ranged from 6.1 to 6.3. In isolated human gastric glands, impromidine was shown to be eight times more potent than histamine, indicating higher receptor affinity, but the maximally stimulated aminopyrine accumulation was the same as for histamine, and the pA2 values for cimetidine antagonism did not differ significantly, i.e., 5.7 (histamine) and 6.1 (impromidine). In isolated rabbit gastric glands, cimetidine inhibited the histamine- and impromidine-stimulated response with pA2 values of 6.0 and 7.3, respectively. Impromidine was shown to be approximately 100 times more potent than in human gastric glands, whereas histamine had the same potency. This confirms the role of the histamine H2-receptor and suggests a difference between the species concerning receptor affinity.
Adult↗
Possible causes of increased lung cancer incidence among butchers and slaughterhouse workers.
An excess of lung cancer among butchers and slaughterhouse workers has been reported in several record-linkage studies. In this case-referent investigation on the possibility of occupational exposures being related to the lung cancer excess, cases and referents were selected from butchers and slaughterhouse workers registered in the Swedish national census of 1960. The case group comprised all men in the study population dying from lung cancer between 1971 and 1982. Two reference groups were formed, ie, all individuals dying from other cancers and a random sample of all dead men in the study population during the same time period. The history of occupations, occupational exposures, and smoking habits was obtained from the next-of-kin by questionnaire. None of the occupational exposures that were studied (work with live animal care, in the bleeding area, on the killing floor, or with meat cutting, processing, curing, smoking, chilling and packaging) were associated with an increased lung cancer rate. Tobacco smoking habits may have contributed to the overall excess of lung cancer found previously for this occupational group.
Abattoirs↗
Inhibitory action of omeprazole on acid formation in gastric glands and on H+,K+-ATPase isolated from human gastric mucosa.
The inhibitory effect of omeprazole on acid formation has been studied in vitro in gastric glands and partly purified H+,K+-ATPase, prepared from mucosa obtained either from healthy subjects by gastroscopic biopsy or from gastric ulcer patients during antrectomy. The effect of omeprazole was compared with the inhibitory pattern of the H2-antagonist cimetidine. Acid production in the glands was determined by measuring the accumulation of 14C-aminopyrine. In glands isolated from patients, omeprazole inhibited acid production maximally stimulated by histamine, db-cAMP, and potassium in a dose-dependent manner, with an IC50 value of about 50 nM irrespective of the agonist used. In contrast, cimetidine inhibited only histamine-induced aminopyrine accumulation, with an IC50 of about 30 micron. The inhibitory effect of omeprazole in db-cAMP-stimulated glands from healthy volunteers was of the same magnitude as seen in glands from gastric ulcer patients. Basal aminopyrine accumulation in glands from both patients and healthy volunteers was almost totally inhibited by omeprazole, whereas cimetidine was without effect. Omeprazole also concentration-dependently inhibited the H+,K+-ATPase activity in isolated gastric membrane vesicles. The estimated IC50 value was 4 micron.
Adenosine Triphosphatases↗
Metabolic rates in normal and infarcted myocardium.
The effects of myocardial infarction in rat hearts on the utilization of fatty acids and glucose by the surviving, non-infarcted tissue were studied. Hearts were removed from the animals one-week post-infarcted and perfused in the isolated working heart preparation. Oxygen consumption and oxidation of palmitate and glucose were determined at two levels of cardiac work. Rates of substrate oxidation were estimated by 14CO2 production from [14C]-labeled substrates. This approach to measuring metabolic rates may seriously under-estimate the true oxidative rate particularly when measuring oxidation of long-chain fatty acids. Because of the large endogenous stores of fatty acids in tissue lipids, the [14C]-specific activity of the intracellular metabolites involved in the free fatty acids oxidation pathway do not equilibrate with the specific activity of the perfusate fatty acids oxidation pathway do not equilibrate with the specific activity of the perfusate fatty acid even when 14CO2 production has reached an apparent steady state. When comparing an experimental condition to the normal heart, a lower rate of 14CO2 production may not necessarily indicate a lower rate of oxidation of free fatty acids, but a difference in the rate of turnover of endogenous sources of unlabeled fatty acid such that the specific activity of intracellular metabolites equilibrate with extracellular labeled substrate to a lesser extent than in the normal heart. At physiological concentrations of fatty acids, a shift from fatty acid to carbohydrate oxidation occurred in the hypertrophied, surviving tissue following myocardial infarction in the rat.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Chronic infarction decreases maximum cardiac work and sensitivity of heart to extracellular calcium.
Rat hearts were infarcted in vivo by ligation of the left ventricular coronary artery to cause an initial 40% loss of viable tissue by weight. Due to compensatory hypertrophy of the surviving myocardium and progression of the infarct to scar tissue, the infarct represented approximately 25% by weight of the whole heart after 1 wk. After 1 or 3 wk, these infarcted hearts were removed and perfused in vitro by the working hearts technique. Ventricular pressure development and positive dP/dt were lower in infarcted hearts compared with sham-operated ones. O2 consumption and glucose utilization by viable tissue per unit pressure development was the same in normal and infarcted hearts. Levels of creatine phosphate and free creatine were decreased, but ATP and total adenine nucleotides were well maintained. The inotropic response to decreases in extracellular [Ca2+] was much greater in infarcted hearts than in sham controls. Prenalterol increased ventricular function proportionally more in infarcted than in the sham-operated hearts, suggesting that down regulation of beta receptors was not a problem. The infarcted hearts were much more sensitive to verapamil than control hearts. It is concluded that the depressed function of the noninfarcted tissue of chronically infarcted hearts is due in part to loss of functioning tissue mass and in part to decreased sensitivity to extracellular Ca2+.
Adenosine Triphosphate↗
Acid secretion in isolated gastric glands from healthy subjects and ulcer patients.
Isolated human gastric glands provide an in vitro model that can yield significant information about the mechanisms regulating gastric acid secretion at the parietal cell level. Aminopyrine, a weak base that accumulates in acid compartments, has been used as an indirect probe of H+ secretion. By means of a microscale technique it was possible to isolate oxyntic glands from gastroscopic biopsy specimens and thereby enable studies of healthy subjects and non-operated ulcer patients. Histamine (5.4 X 10(-5) M) and db-cAMP (10(-3) M) both induced a pronounced response, whereas the response to carbachol (4.5 X 10(-6) M), although still statistically significant, was less potent. The response to stimuli was twice as high in duodenal ulcer patients as in normal individuals. In contrast, the response in patients with a gastric ulcer located either in the prepyloric region or at the minor curvature on the antrum-corpus border was of the same magnitude as in healthy subjects. Pentagastrin did not induce any response in isolated gastric glands from normal individuals. Gastric acid secretion in vitro, measured as aminopyrine accumulation, did not decrease with increasing age of the individuals.
Adult↗
Effects of proximal gastric vagotomy and antrectomy on parietal cell function in humans.
Both proximal gastric vagotomy and antrectomy reduce maximal gastric acid secretion in vivo by about 60%. The combination of vagotomy and antrectomy reduces the maximal acid secretion by about 80%. This additive effect indicates that these surgical procedures differ in their mode of action. The function of isolated human oxyntic glands was studied before and after vagotomy and antrectomy, respectively, using radioactively labeled aminopyrine as a marker of parietal cell response. The basal accumulation increased after vagotomy, suggesting a vagally controlled inhibitory component. The carbachol response disappeared and the maximal response induced by histamine or dibutyryl-cyclic adenosine monophosphate was reduced by 60% (p less than 0.01) after vagotomy. This reduction could not be overcome by increasing the dose of dibutyryl-cyclic adenosine monophosphate. This indicates an intracellular effect of vagotomy peripheral to dibutyryl-cyclic adenosine monophosphate point of action. Antrectomy did not induce any statistically significant change at the glandular level, indicating that the reduced gastric acid secretion in vivo may be caused by a reduction in the number of oxyntic glands due to a removal of a trophic effect of antral gastrin.
Adult↗
Inhibition of gastric (H+ + K+)-ATPase by the substituted benzimidazole, picoprazole.
The substituted benzimidazole, picoprazole, inhibited the gastric (H+ + K+)-ATPase in a concentration-and time-dependent manner. Half-maximal inhibition of the (H+ + K+)-ATPase activity was obtained at about 2 . 10(-6)M under standard conditions. In addition to the inhibition of ATPase activity, parallel inhibition of phosphoenzyme formation and the proton transport activity were achieved. Radiolabelled picoprazole was found to bind to 100 kDa peptide; this peptide was shown by phosphorylation experiments to contain the catalytic centre of the (H+ + K+)-ATPase. Studies on the (Na+ + K+)-ATPase indicated that this enzyme was unaffected by picoprazole. From the data presented and from other pharmacological studies, it is proposed that this compound inhibits acid secretion at the level of the parietal cell by its ability to inhibit the gastric proton pump, the (H+ + K+)-ATPase.
2-Pyridinylmethylsulfinylbenzimidazoles↗
A micro-method for the study of acid secretory function in isolated human oxyntic glands from gastroscopic biopsies.
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Aminopyrine↗
Muscle fatigue and beta-blockers--a review.
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Adaptation, Physiological↗
Differentiation among inhibitory actions of omeprazole, cimetidine, and SCN- on gastric acid secretion.
The action of the substituted benzimidazole omeprazole (H 168/68) was studied in three different in vitro preparations: the isolated guinea pig gastric mucosa, isolated intact and permeable rabbit gastric glands, and hog fundic microsomal membrane vesicles containing H+-K+-ATPase. The effects of omeprazole were compared with those of cimetidine and thiocyanate (SCN-). Under all the conditions studied, cimetidine only counteracted histamine-induced acid secretion, consonant with its H2-receptor antagonism. In contrast, omeprazole and SCN- were found not only to inhibit histamine-induced secretion but also basal acid formation and acid formation induced by dibutyryl cAMP and a high cell medium concentration of K+. Moreover, acid production induced by ATP in permeable gastric glands was antagonized by omeprazole and SCN-, whereas cimetidine was without effect. The interaction pattern of omeprazole and SCN- was differentiated by studies using the weak base antipyrine in the isolated mucosal preparation, where it was found that antipyrine could reverse the inhibition induced by SCN- but not that of omeprazole. Furthermore, omeprazole was found to inhibit the isolated H+-K+-ATPase, whereas cimetidine or SCN- was without effect. In the isolated mucosal preparation omeprazole caused an increase in K+ secretion rates in parallel with the inhibition of acid formation. This was in contrast to what was observed for cimetidine and SCN-, which exhibited no such increased K+ secretion. The results obtained from intact mucosa and isolated glands are in agreement with the ability of omeprazole to inhibit the isolated H+-K+-ATPase and thus provide evidence of a novel mechanism of action for this inhibitor.
Adenosine Triphosphatases↗
Cardiostimulatory effects of prenalterol, a beta-1 adrenoceptor partial agonist, in vivo and in vitro. Correlation between physiological effects and adenylate cyclase activity.
The cardiostimulatory effects of prenalterol, a beta-1-adrenoceptor partial agonist, were studied in vivo and in vitro and compared to those evoked by isoprenaline, a full agonist, and to those of other partial agonists. In the anaesthetized rat, prenalterol and terbutaline were found not to elevate the myocardial cyclic AMP content; this was in sharp contrast to isoprenaline. Both partial agonists did, however, produce significant effects on heart rate. In the anaesthetized cat, prenalterol exhibited chronotropic and inotropic intrinsic activities of 88 and 76% respectively in relation to isoprenaline. No statistically significant increase in myocardial cyclic AMP content could however be detected. Prenalterol did not stimulate adenylate cyclase significantly in the cat myocardial homogenate. This was also true of the beta-2-adrenoceptor selective partial agonist procaterol. In this preparation, isoprenaline, noradrenaline and adrenaline acted as full agonists. Furthermore, prenalterol produced a concentration-dependent inhibition of isoprenaline-activated adenylate cyclase. Our data indicate that maximal cardiac stimulation occurs at a low level of adenylate cyclase activation and low myocardial cyclic AMP concentration when provoked by a full beta-adrenoceptor agonist. The maximal physiological effects of a partial agonist such as prenalterol may consequently be achieved at a marginal activation of the adenylate cyclase. The present data may thus support the hypothesis of a large beta-adrenoceptor reserve for full agonists in the heart.
Adenylyl Cyclases↗
Inhibition of acid secretion in isolated gastric glands by substituted benzimidazoles.
A new class of gastric acid inhibitors, substituted benzimidazoles (H 83/69 and H 149/94), have been tested in an isolated rabbit gastric gland preparation. Acid formation in the glands was stimulated by histamine, dibutyryl cAMP (DBcAMP), and high extracellular K+ concentrations, and the glandular secretory response was measured by changes in oxygen consumption and in accumulation of the weak base [14C]aminopyrine (AP). The substituted benzimidazoles inhibited AP accumulation induced by all stimulants in a dose-dependent noncompetitive manner. In contrast, cimetidine only inhibited histamine-induced AP accumulation. Basal AP accumulation, not affected by cimetidine, was also inhibited by the substituted benzimidazoles, as was the increase in glandular oxygen consumption produced by the addition of histamine and DBcAMP. Basal oxygen consumption was inhibited by about 15%. The substituted benzimidazoles, like AP, are weak bases and were also found to accumulate in the glands. Semiquantitative morphological studies of glands stimulated by histamine plus theophylline did not show any change in the enlarged secretory surface area after stimulation in the presence of inhibitory concentrations of H 149/94 (10(-4) M). The results suggest that substituted benzimidazoles have a mechanism of action different from that of H2-receptor antagonists and indicate a very distal site of action in the events leading to acid formation.
Aminopyrine↗
The effects of secretagogues of isolated human gastric glands.
The function of isolated human gastric glands has been studied in vitro by measuring the 14C-aminopyrine accumulation (RAP) in basal, unstimulated, conditions and after stimulation with different secretagogues. A microscale technique was used which enabled determinations of RAP in tissue obtained as gastroscopic biopsies. In addition, oxyntic-gland-containing mucosa was obtained at gastric resections for gastric or prepyloric ulcer disease. Histamine and cAMP derivative both induced maximal stimulation; RAP was approximately three times larger than in basal states. Carbachol induced a smaller but still significant stimulation. Pentagastrin did not increase RAP above the unstimulated level. Combinations of histamine and carbachol or pentagastrin did not induce a larger response than carbachol alone. The peak acid response to pentagastrin or betazole in vivo did not correlate with the maximum RAP in vitro.
1-Methyl-3-isobutylxanthine↗