Search PubMed⌕ Search

Biomedical subjects

U Haglund

Publications and source records attributed to U Haglund.

At least 199 records · Page 11Linked to original sources
PubMed1982

The effect of different anticholinergics on the gastric acid response to sham feeding in man.

Modified sham feeding by the chew and spit technique stimulates gastric acid secretion at a level about 50% of peak acid output. This response is vagal and can be totally blocked by vagotomy. The effect on the acid response to modified sham feeding produced by a quaternary amine, benzilonium bromide, and a presumably more selectively acting antimuscarinic drug, pirenzepine, was compared. The drugs were given 45 min and 10 min before the start of the sham feeding, respectively. Benzilonium bromide, 1 + 1 mg, blocked 73% of the acid response to sham feeding and pirenzepine, 10 + 10 mg, blocked 48% of the response. The difference was not statistically significant. The data confirm that a part, about one third, of the acid response to sham feeding is non-cholinergic, although it is vagal.

Adult↗
PubMed1982

Mucosal lesions in the feline small intestine in septic shock.

The incidence and possible pathogenic mechanisms in the development of small intestinal mucosal lesions in experimental septic shock were investigated in cats. Mucosal lesions were found in 50% of the animals following a standardized bacteremia, and 15% had pronounced mucosal damage. The development of these lesions was not correlated with intestinal vasoconstriction or to portal hypertension but with decreased systemic arterial blood pressure during the last hour of the experiments. The correlation between mucosal damage and arterial hypotension in septic shock supports the view that these lesions are caused by hypoxia secondary to an increased efficiency in the countercurrent exchange mechanisms of oxygen in the villi.

Animals↗
PubMed1982

An evaluation of the functional implications of the intestinal mucosal lesions in shock.

Small intestinal mucosal lesions are reported in clinical shock and are commonly found in experimental shock. Experimental series in which shock is induced by regional intestinal ischemia or IV infusion of live Escherichia coli in cats or by graded intestinal vascular occlusion in rats are described. In all series mucosal damage was related to pronounced hypotension or mortality. In the cat models myocardial dysfunction was demonstrated in vivo by IV volume load and recording of changes in left ventricular filling pressure as related to cardiac performance. Following intestinal ischemia in cats and intestinal vascular obstruction in rats the intestinal venous plasma was found to contain cardiotoxic factors when tested in vitro. It is proposed that the development of small intestinal mucosa lesions in shock tends to further aggravate hypotension by causing intestinal release of cardioinhibitory material.

Animals↗
PubMed1982

Acid secreting gastric heterotopia in the duodenum.

Heterotopic gastric mucosa was found in the duodenum of a female patient with duodenitis and acid hyposecretion. The heterotopic isolated fundic glands were shown to accumulate 14C-aminopyrine in basal state and on stimulation with histamine suggesting that the heterotopic mucosa secreted acid. The ectopic acid secretion in the duodenal bulb suppressed gastric acid secretion, and might have caused the duodenitis and at least partly the clinical symptoms. The heterotopic gastric mucosa could be removed surgically by local excision. This procedure, combined with a Nissen fundoplication for suspected reflux oesophagitis, was followed by total symptomatic relief and normalization of gastric acid secretion.

Choristoma↗
PubMed1981

Vascular and metabolic effects of methylprednisolone and phenoxybenzamine during controlled hypotension in the dog.

The relationship between central haemodynamics and vascular and metabolic parameters in skeletal muscle was studied in dogs subjected to controlled haemorrhagic hypotension and treated with cumulative doses of methylprednisolone (4-32 mg x kg-1), (or saline in the control group), followed by phenoxybenzamine. There were no significant haemodynamic or metabolic changes between the groups during the injections of steroid or saline. The alpha-adrenergic receptor blockade caused, as found earlier, a pronounced vasodilation in the steroid group, which was parallelled by an increase in muscle blood flow in the same order of magnitude. There was no clearcut relationship between metabolic and vascular effects in the groups. Despite the significant difference in blood flow between the groups after phenoxybenzamine, only small and insignificant differences were seen in muscle metabolites, with the exception of muscle lactate which showed higher values in the steroid group. The study provides further evidence in support of the hypothesis that the haemodynamic effects of the combination of methylprednisolone and phenoxybenzamine are of neurogenic origin.

Animals↗
PubMed1981

Graded intestinal vascular obstruction. IV. An analysis of the pathophysiology in the development of refractory shock.

Pathophysiological mechanisms of importance for mortality in shock were studied using different modes of treatment in a standardized intestinal vascular obstruction model. In an untreated series the degree of intestinal mucosal damage, but not the increase in hematocrit, correlated to mortality. The importance of hypovolemia, instability of membranes, and metabolic blockage were studied in several series by giving saline, dextran 40, dextran 70, albumin, methylprednisolone, glucose, and glucose-insulin-potassium. Dextran 70 was the only agent which significantly reduced mortality--from 88 to 58%. This effect was, however, not due to hemodilution nor to prevention of mucosal lesions. In an additional series the effects of dextran 70 on intestinal electrolyte concentration, on pulmonary trapping of platelets, and on cardioinhibitory effects in vitro of intestinal venous plasma were evaluated in comparison with untreated shock. Dextran 70 prevented the electrolyte changes and platelet trapping in the lung, and the cardioinhibitory effect of intestinal venous plasma was reduced. A combination of these mechanisms may be of importance in producing mortality in this shock model.

Animals↗
PubMed1981

Central hemodynamic responses to venous, aortal or portal infusion of live E. coli bacteria in the cat.

The central hemodynamic responses were studied in experimental sepsis in cats, following various routes of infusion of live E. coli bacteria. The aortic blood flow (ABF) was electromagnetically recorded. The pulmonary artery was cannulate for pressure recording. Platelet and white blood cell concentrations, PO2, PCO2, pH and oxygen saturation were measured at intervals. I.v. infusion of bacteria induced initially decreased ABF, systemic hypotension, pulmonary hypertension. Portal infusion evoked, on the other hand, increased ABF, but induced no significant change in systemic or pulmonary arterial blood pressures. Aortal infusion induced responses in between. The initial hemodynamic changes were followed by relative normalization after 5-10 min. Then, in all series, a progressive fall in ABF and systemic blood pressure were noticed. Within 5 min following bacterial infusion the platelet and white blood cell concentrations fell to 65 and 50%, respectively. In all series a moderate metabolic acidosis developed. Thus, the initial hemodynamic response following infusion of live E. coli was dependent on the route of infusion; intraportal infusion induced initially a more hyperdynamic state. The different initial central hemodynamic responses did not influence the subsequent development of a hypotensive shock state.

Animals↗
PubMed1981

Intestinal hemodynamic effects of varying the route of infusion of live E. coli bacteria in the cat.

The responses of the series-coupled vascular sections in the feline small intestine were studied in experimental sepsis induced following various routes of infusion of live E. coli bacteria. The intestinal hemodynamics were followed by means of plethysmography combined with direct recording of the intestinal venous outflow. After 2 hours of bacterial infusion the experiments were terminated. Infusion of E. coli in the inferior caval vein induced initially hypotension, decreased intestinal blood flow (Q) and increased intestinal vascular resistance (R). Portal venous infusion induced, on the other hand, an initial arterial blood pressure increase, an increase of Q and a decrease of R. Aortal infusion evoked only minor initial changes. The early response was in all series followed by a progressive hypotension during which Q decreased and R increased gradually. There were no changes in intestinal tissue volume, indicating that there was no pooling of blood or extravasation of fluid, during the experiments. Intestinal mucosal lesions were equally distributed in the three series. Thus, depending on the route of infusion live E. coli induced intestinal vasoconstriction or vasodilatation. Regardless the route, there was no intestinal pooling of blood or fluid. Hypotension developed in most cats after 120 min, regardless the site of infusion and the initial vascular response.

Animals↗
PubMed1981

Graded intestinal vascular obstruction. II. Effects of antibiotic pretreatment in the rat.

This study was performed to elucidate whether bacteria, or products of bacterial origin, could account for the circulatory collapse following a 1-hour intestinal vascular obstruction in the rat. Animals pretreated with clindamycin, in a way previously shown to induce characteristics otherwise found only in germ-free rats, were compared to controls pretreated with saline. Graded intestinal vascular obstruction was applied and four different pressure levels were used. Mortality increased with the applied pressure but there was no difference between the clindamycin-pretreated rats and controls. Hematocrit increased equally in all pressure levels and was not influenced by pretreatment. The amount of fluid lost from the serosal surface of the intestines was not correlated to the pretreatment used, the increase in hematocrit, or mortality. In the higher pressure levels, characteristic microscopic intestinal mucosal lesions were found in both series and the degree of mucosal damage correlated with increase mortality.

Animals↗
PubMed1981

Graded intestinal vascular obstruction. III. An analysis of pathogenic mechanisms.

A standardized model allowing graded obstruction of the intestine and its vascular supply was used in rats. Application of high pressures (100 and 120 cm of water) has previously been found to induce high mortality and intestinal mucosal lesions. This study was performed to elucidate the possible importance of nervous depressor reflexes and release of cardiotoxic material in the pathogenesis of the induced circulatory collapse. Denervation of the intestines made the blood pressure reduction during the period of obstruction less pronounced. Intestinal venous plasma obtained following one hour of obstruction with high pressure had a significant inhibitory effect when tested on isolated rabbit papillary muscles as compared to plasma obtained following obstruction with lower pressure. Pretreatment with clindamycin had no effect on this variable. It is suggested that the release of cardiotoxic factors is one pathogenetic factor in the development of the circulatory collapse following intestinal shock.

Animals↗
PubMed1981

Effects of regional vasopressin infusion of intestinal series-coupled vascular sections.

The effects induced by infusion of vasopressin into the superior mesenteric artery on the small intestinal series-coupled vascular sections were studied in cats and compared to those evoked by stimulation of the regional sympathetic nerves. The doses used were similar to those recommended for clinical purposes. Vasopressin induced an increase in intestinal resistance to blood flow, which at higher doses was biphasic with an initial pronounced effect followed after a few min by a less marked steady state response. Vasopressin induced no effect on the intestinal capillary filtration coefficient, did not change the isovolumetric equilibrium and evoked only a minor decrease in regional blood volume. When compared with sympathetic nerve stimulation the latter induced a less marked steady state increase in intestinal blood flow resistance but a more pronounced decrease in regional blood volume and a decrease in capillary filtration coefficient. The effects following vasopressin infusion were in the doses used not that pronounced that they could be considered potentially harmful for the small intestinal tissue.

Animals↗
PubMed1981

Vascular responses of small intestine and liver to regional infusion of vasopressin.

The vascular responses of the small intestine and liver to regional infusion of vasopressin were measured continuously and synchronously in anaesthetized cats. When infused into the superior mesenteric artery there was a marked initial blood flow reduction (peak response) followed by a sustained but moderately reduced flow (steady state). Corresponding to the peak response the portal pressure fell significantly. This reduction was only transient, however. Vasopressin infused into the hepatic artery caused if anything only a shortlasting decrease of hepatic flow. Concomitantly there was also a transient decrease of portal pressure. The findings indicate that continuous regional infusion of vasopressin causes a considerable reduction of intestinal blood flow without interfering with hepatic arterial circulation.

Animals↗
PubMed1980

Septic shock.

Explore the source record for details and available documents.

Animals↗
PubMed1980

Effects of adrenergic neuron and ganglion blockers on hemodynamics and plasma catecholamine levels after corticosteroids during hemorrhagic shock in the dog.

The involvement of adrenergic mechanisms in the ability of massive doses of methylprednisolone to potentiate the vasodilatory effects of phenoxybenzamine during controlled hemorrhagic shock was investigated. Dogs were subjected to ligation of the adrenals and, with the exception of the controls, were pretreated with either hexamethonium or bretylium. Despite careful surgery, the adrenal ligation, per se, failed to alter the concentration of plasma catecholamines. Hexamethonium and bretylium, on the other hand, both decreased the levels of plasma catecholamines: noradrenaline to a greater extent than adrenaline. Methylprednisolone was almost ineffective after ganglionic or adrenergic neuron blockade. Furthermore, the degree of vasodilation after methylprednisolone and phenoxybenzamine seemed to correlate better with plasma noradrenaline than with adrenaline. These findings indicate that the ability of methylprednisolone to induce vasodilation in the presence of adrenergic alpha-receptor blockade in hypovolemic shock in the dog relies on an intact release of noradrenaline from postganglionic adrenergic nerve terminals.

Adrenal Medulla↗
PubMed1980

Chromosome aberrations and sister chromatid exchanges in Swedish paint industry workers.

Workers in the Swedish paint industry exposed to a mixture of organic solvents, mainly containing xylene or toluene, were investigated for genotoxic effects. No difference in the frequency of sister chromatid exchanges (SCE), 0.192 and 0.193 per chromosome, respectively, was noted in the peripheral lymphocytes of the exposed group of 17 workers and their matched reference group. No correlation was found between xylene or toluene exposure and SCE frequency nor between total solvent exposure and SCE frequency. The frequency of chromosome aberrations was also investigated for the five most exposed workers and their matched referents, and no difference was found. There was no correlation between SCE and chromosome breaks.

Adult↗
PubMed1980

Management of massive gastroduodenal haemorrhage.

A special program for management of massive gastrointestinal bleeding was 1976 introduced in the surgical service of Sahlgren's Hospital in Göteborg. The main points in this program were: careful observation in an intensive care unit, standardized treatment, early diagnostic gastroduodenoscopy, strict indications for emergency operation and recommendation of type operation. This paper deals with 55 patients subjected to emergency operations in 1976 with the diagnosis erosive gastritis, gastric ulcer or duodenal ulcer. The results are compared to an earlier study in 1962-71 in the same hospital. It was found that the mortality was unchanged during the two periods, 25% during 1962-71 and 24% during 1976. At a first glance the new program might seem ineffective. However, the part of elderly patients was much higher during 1976 than during 1962-71. Thus, the patients during 1976 must be considered much more of a surgical challenge. As old patients often have coexisting severe diseases they are surgically most unfit. Probably a more conservative attitude is justified in this particular group of patients.

Adult↗