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Biomedical subjects

U Haglund

Publications and source records attributed to U Haglund.

At least 163 records · Page 9Linked to original sources
PubMed1985

Suture technique and early breaking strength of intestinal anastomoses and laparotomy wounds.

The influence of different suture techniques on early fascial and intestinal breaking strength was studied in rats subjected to either colonic anastomosis or median laparotomy only. Interrupted sutures were used throughout. The sutures were inserted either 3 mm or 1.5 mm from the wound edges. The breaking strength with the sutures in situ, i.e. the suture holding capacity, was measured either immediately or 48 hours after their insertion. The breaking strength of the sutured fascia, but not that of the colon, was higher when sutures were inserted at the longer distance from the wound edges. Postoperative decrease of suture holding capacity occurred in both colon and fascia, but only when the sutures had been placed near the incision.

Animals↗
PubMed1985

Beneficial effect of proteinase inhibitors on early breaking strength of intestinal anastomoses.

Rats were subjected to end-to-end anastomosis of the small intestine. The breaking strength was measured in different groups immediately after suture and after 24, 72 and 120 h. Tiopronin (Thiola), soya-bean trypsin inhibitor (STI), or saline solution, was given by continuous intravenous infusion during the test periods. In the saline groups there was a marked decrease in breaking strength at 24 and 72 h. Most of the strength was restored at 120 h. The metalloproteinase inhibitor tiopronin, which in a previous study had diminished the decrease in breaking strength at 24 h, was without effect at 72 h. Rats given STI, which is a group-specific serine proteinase inhibitor, had substantially higher values of breaking strength than saline-treated controls at 24 and 72 h. At 120 h no difference was found. Since the postoperative decrease in breaking strength could be attenuated by proteinase inhibitors, it seems to be due to proteinase activities. STI-treatment did not impair subsequent gain in mechanical strength during the fibroplasia period.

Amino Acids, Sulfur↗
PubMed1985

Postoperative decrease in suture holding capacity in laparotomy wounds and anastomoses.

Rats were subjected to oesophageal, gastroduodenal, small intestinal or colonic anastomosis or to a median laparotomy only. Interrupted sutures were used throughout. The breaking strength with the sutures in place, i.e. the suture holding capacity, was measured in different groups immediately after suture and after 48 hours. During the first 48 hours there was significant decrease in breaking strength, by 37% in oesophagus, 64% in the gastroduodenostomy, 70% (measured at 24 hours) in the small intestine, 72% in colon and 47% in the laparotomy wound. A reduction of suture holding capacity seems to be a generally valid reaction following tissue trauma induced by surgery.

Animals↗
PubMed1985

Role of free oxygen radicals in the development of gastrointestinal mucosal damage in Escherichia coli sepsis.

Live Escherichia coli were infused into anesthetized cats given 0.6 ml bile/kg and 80 mM HCl into the stomach. Systemic and pulmonary arterial blood pressures, cardiac output, and gastric blood flow were monitored. Gastrointestinal total wall and mucosal blood flow were measured by microspheres. The microscopic mucosal damage was graded 0-4 (stomach) or 0-5 (intestine). One group of cats (N = 8) received 5 mg yeast CuZn superoxide dismutase (SOD) as a bolus before bacteria followed by infusion 50 mg/3 hr. Four of these cats were also given catalase in the same dose. Controls (N = 8) had no treatment. After 3 hr gastric ulceration (grades 2-4) was found in controls but only in 50% of treated cats (P less than 0.1). About 50% and 25% of the cats in both groups developed significant small intestinal and colonic mucosal damage, respectively. SOD or SOD/catalase had no effect on late systemic hypotension, decrease in cardiac output, or transient increase in pulmonary pressure. Total gastric blood flow did not change, while at late sepsis gastric mucosal flow was decreased in the treated group. Small intestinal mucosal flow decreased in both series. It is concluded that free oxygen radicals may be of partial importance in the development of sepsis-induced gastric, but not intestinal, mucosal damage.

Animals↗
PubMed1985

Endoscopic diagnosis of gastric ulcer. Evaluation of the benefits of endoscopic follow-up observation for malignancy.

Examinations at an endoscopy unit in 1976 gave diagnoses of gastric cancer in 31 patients, malignant lymphoma in 3 and new benign gastric ulcer in 223 patients. Correctness of diagnosis was judged to be verified following surgery, autopsy, clinical follow-up or five-year survival. All the malignant lesions were macroscopically and/or microscopically recognized at the first examination, except for one that was then considered to be a submucosal or extragastric tumour, but was correctly diagnosed at surgery prompted by the endoscopic findings. Of the 223 benign ulcers, 219 received a correct diagnosis at the first examination. In the other four cases malignancy was macroscopically or microscopically suspected, but was excluded following surgical excision or repeat examination. Based on these data, the authors suggest that routine endoscopic follow-up of gastric ulcer to exclude malignancy is unnecessary if the primary examination has been performed by an experienced endoscopist, and if both the macroscopic and the microscopic (biopsy) judgement unreservedly are that the lesion is benign.

Adult↗
PubMed1985

Mucosal lesions of the small intestine after intestinal vascular obstruction in the rat.

Small intestinal mucosal lesions, characteristically restricted to the villous tissue, have been described in shock states of different types. We have found this type of mucosal lesion in a standardized intestinal ischemia shock in rat. The pathophysiology of the mucosal lesion has been debated. In earlier work we noted a tenfold increase of platelets in the ischemic intestine. The importance of reperfusion and local platelet accumulation for the development of ischemic lesions in the intestinal mucosa was studied. Biopsy specimens taken immediately before and after reperfusion of the ischemic small intestine showed the same degree of mucosal lesion, i.e. total disintegration of the lamina propria. In thrombocytopenic rats subjected to intestinal ischemia, the severity of mucosal lesion was the same as in normothrombocytic rats. The results indirectly support the hypothesis of local villous oxygen deficit as the pathophysiologic mechanism leading to lesions of the small intestinal mucosa in shock.

Animals↗
PubMed1985

Small intestinal mucosal lesions in feline septic shock: a study on the pathogenesis.

The pathogenesis of small intestinal mucosal damage in septic shock was explored in experiments on 15 cats given live E coli i.v. Villous (absorptive site) blood flow was studied by the carbon monoxide uptake technique using isolated small intestinal segments. In eight of the cats, segments were perfused intraluminally with oxygenated or nitrogenated saline. The main part of the small intestine was unperfused and served as control. Nine cats (60%) developed mucosal damage. They had significantly lower arterial blood pressure at the end of septicemia (56 +/- 6) than cats without mucosal damage (76 +/- 3 mmHg). Total intestinal blood flow was similar before or during septicemia. Villous blood flow before septicemia was 3.7 +/- 0.5 ml/min X 100 g intestine and 5.1 +/- 1.0 (n.s.) in the two groups, respectively, and remained unchanged. Intraluminal perfusion with oxygenated but not with nitrogenated saline prevented the development of mucosal damage. It was concluded that the small intestinal mucosal damage is due to hypoxia in spite of unchanged villous blood supply.

Acid-Base Equilibrium↗
PubMed1984

Oxidative tissue damage following regional intestinal ischemia and reperfusion in the cat.

Regional intestinal ischemia in cats resulted in an accumulation of hypoxanthine within 2 h, the concentration of which rose from 0.062 to 1.131 nmol/mg protein. A similar rise in AMP content (from 0.5 to 3.2 nmol/mg protein) was observed, but not in the ADP level. In parallel, ATP content decreased from 7.5 to 2.8 nmol/mg protein. Reperfusion of the ischemic tissue was followed by rapid metabolism of the purine metabolites; after 1 h of reperfusion the tissue level of hypoxanthine was 0.186 nmol/mg protein, of AMP 0.7 nmol/mg protein, and of ATP 4.3 nmol/mg protein. The oxidation of hypoxanthine, mediated by xanthine oxidase, is accompanied by the release of superoxide ions. Consequently, the concentration of oxidized glutathione was doubled upon reperfusion, while marked lipid peroxidation took place, as evidenced by the rise in conjugated diene content from 2.8 mumol/g tissue before reperfusion to 5.6 mumol/g tissue after 10 min of reoxygenation. In line with these findings is the fact that histologically observable damage occurred mainly in the presence of oxygen. These data indicate that, at least in our model, rapid reoxygenation is a major cause of "ischemic" tissue damage.

Adenine Nucleotides↗
PubMed1984

Beta-endorphin administered into the lateral ventricle of the brain causes pulmonary platelet trapping in rabbits.

Human beta-endorphin was injected into the cerebrospinal fluid in rabbits by means of a needle inserted into the lateral ventricle of the brain. Control rabbits received an equal amount of saline. beta-Endorphin induced a significant pulmonary platelet trapping compared to control. beta-Endorphin had no effect on arterial blood pressure, heart rate, platelet aggregability ex vivo or fibrinolytic activity (fibrinolytic plates). The plasma activity of antithrombin III, kallikrein-like activity and kallikrein inhibitor determined by means of chromogenic substrates was not influenced by beta-endorphin.

Adenosine Diphosphate↗
PubMed1984

Blood flow distribution, villous tissue osmolality and fluid and electrolyte transport in the cat small intestine during regional hypotension.

The hemodynamic reactions of the parallel coupled vascular circuits in the cat small intestine were studied before, during and after a two-hour period of intestinal hypotension induced by lowering the intestinal arterial inflow pressure by partially occluding the superior mesenteric artery during a continuous stimulation of the postganglionic nerves to the small intestine. Furthermore, fluid and electrolyte transport and villous tissue osmolality were measured. A histological examination of biopsies taken during and after the hypotensive period was also carried out. The animals were divided into two groups (undamaged and damaged) according to the histological appearance of the intestinal mucosa. The hemodynamic reactions were investigated with a method that made it possible to study total intestinal, absorptive site ("villous"), nonabsorptive site ("crypt") and muscle layer blood flow. Total intestinal blood flow was lower in the damaged group than in the undamaged group during the arterial hypotension. However, absorptive site blood flow was similar in the two groups. Consequently, a significantly larger fraction of blood flow was distributed to the "villi" in the damaged group. Moreover, absorptive site red blood cell flow was only slightly reduced despite the development of mucosal ulcerations. These findings are discussed in relation to the pathophysiology of the mucosal lesions. Net fluid, net sodium and net chloride absorption was unchanged in the undamaged group whereas in the damaged group a marked decrease was observed after lowering the perfusion pressure. The decrease in net sodium absorption was due to a decrease in the lumen to tissue transport of sodium. Thus, the capacity of the small intestine to absorb fluid and electrolytes is unchanged even during a marked arterial hypotension with a pronounced decrease of intestinal blood flow as long as no mucosal damage has developed.

Animals↗
PubMed1984

Effects of dihydroergotamine on the feline cardiovascular response to intravenous infusion of live Escherichia coli bacteria.

A septic shock state was induced in cats by intravenous infusion of live Escherichia coli bacteria. Cats pretreated with an unspecific 5-HT blocker, dihydroergotamine (DHE), or with a specific 5-HT blocker, ketanserin, were compared with a series receiving bacteria without pretreatment. DHE pretreatment prevented the reduction in systemic arterial blood pressure found in the other series during the 2-hour period of septic shock. Pretreatment could not influence the increased vascular resistance in the pulmonary vascular bed or the early increase in pulmonary arterial blood pressure. Peripheral blood flow distribution was studied using radioactive labelled microspheres. Compared to bacteremia without pretreatment, the 5-HT blockers increased CNS blood flow and ketanserin also prevented the reduction in pancreatic blood flow. Gastric blood flow and gastric mucosal blood flow remained unchanged in all series as did the small intestinal total blood flow. Small intestinal mucosal blood flow, however, was reduced after 2 h of bacteremia. Microscopy revealed no gastric epithelial damage while the jejunal mucosa was characteristically damaged. There was no correlation between the changes in the small intestinal blood flow and the degree of mucosal damage, however, supporting the countercurrent theory for the pathogenesis of these lesions.

Animals↗
PubMed1984

Radiology in primary gastric lymphoma.

Upper gastro-intestinal radiographic studies in 19 patients with primary gastric lymphoma (PGL) were reviewed and compared with studies in matched patients with adenocarcinoma. The very large infiltrating tumour (n = 10) was significantly more often found in patients with PGL, whereas the ulcerative lesion was the predominating feature in patients with adenocarcinoma (n = 15). Furthermore a coarse, irregular mucosal pattern and shallow ulcerations were frequently associated with PGL (n = 18). There was no difference in survival time between the two groups of patients. PGL is a rare disease, with two new cases annually in a population of 230 000, and therefore easily misjudged.

Adenocarcinoma↗
PubMed1984

Acute gastric mucosal ulceration in septic shock. An experimental study on pathogenic mechanisms.

Intravenous infusion of live. E. coli bacteria in cats did not induce microscopic damage to the gastric mucosa within 3 hours. However, if the cats before the induction of bacteremia were given 80 mM HCl and 0.6 ml gallbladder bile/kg b.w. microscopic mucosal damage developed regularly in the corpus-fundus area of the stomach. The gastric mucosal damage was not associated with significant decrease of total gastric blood flow as measured continuously electromagnetically or decreased gastric mucosal blood flow measured early and late during sepsis using radioactively labelled microspheres. Neither was the development of gastric mucosal damage associated with reduced gastric wall collagen concentration nor in RNA, DNA concentrations or RNA/DNA ratio in the gastric mucosa.

Acute Disease↗
PubMed1984

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↗
PubMed1984

Posthypotensive generation of superoxide free radicals--possible role in the pathogenesis of the intestinal mucosal damage.

Graded small intestinal ischemia was induced in cats by partial occlusion of the superior mesenteric artery. Specimens from the small intestine were studied at the end of the hypotensive period, 10 min and 60 min posthypotensively . Specimens obtained late during hypotension revealed characteristic mucosal damage in all cases. However, the intestinal mucosal damage was more pronounced in the specimens taken posthypotensively . This aggravation was prevented if the cats were given superoxide dismutase (SOD) during the hypotensive period. Further, the intestinal tissue concentration of total glutathione was reduced posthypotensively . It is suggested that the posthypotensive aggravation of the intestinal mucosal damage is caused by generation of cytotoxic oxygen free radicals. Data favouring the suggestion that the glutathione-glutathione peroxidase system is an important generator of free radicals in intestinal ischemia is presented.

Animals↗