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Biomedical subjects

U Haglund

Publications and source records attributed to U Haglund.

At least 217 records · Page 12Linked to original sources
PubMed1980

Intestinal vascular and central hemodynamic responses in the cat following i.v. infusion of live E coli bacteria.

Septic shock was induced in cats by i.v. infusion of live E. coli bacteria. The reactions of the series-coupled sections of the small intestinal vascular bed were followed continuously by a plethysmographic technique. Intestinal venous outflow was recorded using a drop counting technique. Intestinal venous outflow was recorded using a drop counting technique. The chest was opened and blood flow in the ascending aorta was followed electromagnetically. Pulmonary arterial blood pressure was recorded after direct cannulation. Following infusion of washed E. coli bacteria suspended in saline, a rapid early response was evident. This was characterized by arterial hypotension, unchanged aortic blood flow, pulmonary hypertension, and intestinal vasoconstriction. After 5-10 min a period of relative normalization followed. After 30-60 min a second phase, characterized by general circulatory deterioration, developed. The induced septic shock was initially characterized by a slight intestinal vasoconstriction. There was no accumulation of blood or fluid in the intestinal vascular bed; an isovolumetric state was thereby maintained in intestinal tissue throughout the experiments.

Animals↗
PubMed1980

Pulmonary vascular reactions in experimental septicemia, A preliminary report.

Septicemia was induced in cats by infusion of live E. coli bacteria into the inferior vena cava, the portal vein or the aortic arch. Systemic arterial blood pressure, aortic blood flow, pulmonary arterial blood pressure, intestinal blood flow and portal venous pressure were recorded continuously and arterial platelet and white blood cell counts and acid-base balance measured at intervals. Infusion of E.coli into the inferior vena cava induced an initial response characterized by systemic pressure reduction, unchanged or increased aortic blood flow and pulmonary hypertension. Intestinal blood flow decreased moderately, while portal pressure remained unchanged. The arterial infusion evoked a similar response. After portal infusion there was a more pronounced increase of aortic blood flow, a significantly less elevation of the pulmonary artery pressure, and the intestinal blood flow was maintained. The changes induced in arterial acid-base balance or in platelet and white cell counts were not influenced by the route of administration. It is concluded that the route of administration of bacteria is of importance when considering the relevance of experimental data to clinical septic states.

Animals↗
PubMed1980

Hemodynamic effects of systemic or portal IV infusion of live E coli bacteria in the cat. A preliminary report.

The reactions in the series-coupled vascular sections of the small intestine and the changes in aortic blood flow, systemic arterial, and pulmonary arterial blood pressure were followed continuously in cats made septic by IV infusion of live E coli bacteria for 2 hours. Peripheral venous infusion initially induced systemic hypotension, pulmonary hypertension, and increased aortic blood flow, but decreased intestinal blood flow. These changes were normalized within 5-10 minutes. During the next 110 minutes systemic arterial blood pressure, aortic blood flow, and intestinal blood flow decreased continuously while intestinal blood flow resistance remained in the control range. Portal venous infusion induced a significantly less pronounced initial pulmonary arterial blood pressure increase. No initial intestinal vasoconstriction was noticed and intestinal blood flow resistance decreased during the bacterial infusion. In both series only small and insignificant changes of intestinal tissue volume were seen. The data suggest that the route of infusion is important to the response in experimentally-induced sepsis. The constant intestinal tissue volume argues against intestinal pooling as being of importance to the development of low blood pressure in septic shock.

Animals↗
PubMed1980

Graded intestinal vascular obstruction: I. Description of an experimental shock model in the rat.

The aim of this study was to standardize a model allowing studies of mechanisms of importance for developing irreversible shock. The model should also be suitable for studying the effects of different modes of treatment. Graded obstruction of the intestine and its vascular supply in rats was induced with a hydrostatic pressure cuff. Three levels of obstruction pressure were used: 50, 100, and 120 cm water. Mortality increased from 0% in control groups to 75% in the highest pressure group. Increases in hematocrit occurred in all groups. Mucosal lesions, including total destruction of villi, were more severe in the two highest pressure groups, and the degree of mucosal lesion correlated with mortality. This shock model was developed to allow studies of factors of importance for survival. One such factor is the degree of mucosal lesion.

Animals↗
PubMed1980

Sister chromatid exchanges and chromosome aberrations in children after treatment for malignant lymphoma.

Sister chromatid exchanges and chromosomal aberrations were investigated in lymphocytes from 11 children with malignant lymphoma after cessation of treatment. Chemotherapy combined with radiation was administered, terminating between 4 months and 13 years before chromosome analyses were performed. The frequency of sister chromatid exchanges per chromosome was the same, 0.20, in the patients and a matched control group, although there was a significant heterogeneity between individuals. The number of cells with chromosome abnormalities increased from 2.9% in control children to 4.8% in treated patients, a nonsignificant increase. Only translocations showed a significant increase.

Adolescent↗
PubMed1979

Simultaneous staining of sister chromatid exchanges and Q-bands in human chromosomes after treatment with methyl methane sulphonate, quinacrine mustard, and quinacrine.

Human peripheral lymphocyte chromosomes were stained simultaneously for sister chromatid exchanges (SCEs) and Q-banding. No effect of treatment with MMS, QM, and Q on the distribution of SCEs in chromosomes was found compared with controls. The SCEs were distributed between chromosomes roughly according to metaphase length, with the shorter chromosomes underrepresented. The majority of SCEs were located to pale bands, while a few occurred in bright bands and at interfaces between pale and bright bands. A greater frequency than expected of SCEs had occurred at identical sites in homologous chromosomes. This frequency was significantly increased after treatment with MMS.

Chromosome Banding↗
PubMed1979

Intramural blood flows and flow distribution in the feline small intestine during arterial hypotension.

The vascular reactions of the parallel-coupled vascular sections of the small intestine were studied during hypotension at two different levels of intestinal arterial inflow pressure, using a 85Kr elimination technique. The regional hypotension was accomplished by partially occluding the superior mesenteric artery with a clamp and maintained for 2 h. At the higher level (50-55 mmHg) total intestinal blood flow decreased but not to the same relative extent as blood pressure due to the autoregulatory capacity of the intestinal vascular bed. The flow autoregulation was also reflected in a decreased blood flow resistance. The distribution of blood to the muscularis and mucosa-submucosa layer, respectively, did not change significantly during or after hypotension as compared to the prehypotensive level, since the relative flow decrease was the same in the mucosa-submucosa and in themuscularis. At the lower arterial pressure level (30-35 mmHg) a more marked decrease of intestinal blood flow and flow resistance was observed as compared to the experiments performed at the 50-55 mmHg pressure level. Moreover, muscularis blood flow was relatively more decreased than blood flow in the mucosa-submucosa implying the fraction of total blood flow diverted to the muscularis was significantly decreased. Despite this redistribution of blood flow, a histological damage was apparent only in the mucosa, particularly at the villous tips.

Animals↗
PubMed1979

On the protective role of the liver in the hypotensive state following intestinal ischemia.

Regional intestinal hypotension (arterial inflow pressure about 30 mmHg) was induced in cats by partially occluding the superior mesenteric artery with an adjustable clamp. The superior mesenteric vein was cannulated and the intestinal venous outflow recorded by a drop counter. The intestinal venous blood bypassed in one series the liver and was returned to the animal via the jugular vein. In two other series it was returned via the portal vein and in one of these also the hepatic arterial pressure was kept at 30 mmHg. Following two hours of regional intestinal shock a general cardiovascular derangement was evident in all series. This was not influenced by directing the intestinal venous blood flow through a normotensive or hypotensive liver. Characteristic intestinal mucosal lesions were found in all series. It is concluded that bypassing or directing the intestinal venous blood through a normotensive or hypotensive liver did not affect the local and general cardiovascular effects of regional intestinal hypotension.

Animals↗
PubMed1978

Cardiac and pulmonary function in regional intestinal shock.

After a two-hour period of regional intestinal shock (arterial inflow pressure 30 to 35 mm Hg; electrical stimulation of regional vasoconstrictor fibers at 6 Hz) a pronounced cardiovascular derangement is observed as reflected in a rapid fall in arterial blood pressure. In this study, central hemodynamics and lung function were investigated to elucidate if functional changes in the thoracic organs might explain the cardiovascular collapse. No alteration of pulmonary function was observed. A negative inotropic influence on the heart was, however, noted as judged by a decreased left ventricular stroke volume and left ventricular maximal pressure change in the face of an increased left ventricular end diastolic pressure. Based on earlier observations with the same shock model, it is proposed that the cardiac effects were caused by cardiotoxic material released from the hypoxic gut.

Animals↗
PubMed1978

On the chemical nature of the blood borne cardiotoxic material released from the feline small bowel in regional shock.

The cardiotoxic material released into blood from the feline small intestine during a 2 or 3 h regional shock period (inflow pressure to the small intestine 30--35 mmHg during a continuous activation of the regional sympathetic vasoconstrictor fibres at 6 Hz) has been analyzed with regard to three properties: 1. molecular mass determined by molecular filtrations; 2. solubility in a nonpolar solvent (ether); 3. heat stability by heating plasma to 80 degrees C for 30 min. The results obtained suggest that the cardiotoxic material consists of at least two heat stable fractions. One is water soluble with a molecular mass between 500 and 1 000 d and the other is lipid soluble with an unknown molecular mass.

Adrenergic Fibers↗
PubMed1978

Nervous release of vasoactive intestinal polypeptide in the gastrointestinal tract of cats: possible physiological implications.

1. The release of vasoactive intestinal polypeptide (VIP) into blood from the gastrointestinal tract was studied when eliciting autonomic nervous effects known to be mediated via non-adrenergic, non-cholinergic nerve fibres. All studies were performed on animals given atropine. 2. Electrical stimulation of the low threshold vagal fibres to the stomach did not significantly change gastric volume or VIP concentration in the venous effluent from the stomach. Stimulating the high threshold fibres, on the other hand, produced a gastric relaxation concomitant with a significant increase of venous plasma VIP concentrations. When eliciting a similar vagal relaxation of the stomach by distending a balloon the oesophagus a significant increase of venous plasma VIP concentration was also recorded. 3. Mechanical stimulation of the mucosa of the small bowel increased intestinal blood flow and a significant increase of venous plasma VIP concentration was observed. 4. Stimulation of the pelvic nerves to the colon produced a transient vasodilation and a significant increase of VIP in the venous effluent from the large bowel. A maintained vasodilation in the colon was induced by mechanically stimulating the rectal mucosa. This vascular response was accompanied by a significant raise of venous plasma VIP concentration. 5. The results demonstrate that all the studied nervous effects known to be mediated via non-adrenergic, non-cholinergic nerve fibres were accompanied by significant increases of the VIP concentration in the venous effluent. The possible physiological implications of these findings are discussed and it is proposed that VIP may be a neurotransmitter in the gastrointestinal tract.

Adrenergic Fibers↗
PubMed1978

Intestinal ischemia and shock factors.

Perfusion pressure reduction to the small intestinal vascular bed for 2 hours to followed by characteristic villous damage and a general cardiovascular derangement. In an extensive series of experiments on cats it was demonstrated that the cardiovascular derangement could not be ascribed to any pooling of blood and/or fluid in the small intestine. Cardiotoxic material has been demonstrated in the cat intestinal venous blood in in vivo and in vitro experiments using working rat hearts and isolated rabbit papillary muscles. A relationship between the extent of the villous damage and the appearance of cardiotoxic material in the intestinal venous blood has been found. The cardiotoxic material seems to consist of at least two heat stable fractions. One is water soluble with a molecular mass between 500 and 1,000 daltons and the other is lipid soluble with an unknown molecular mass.

Animals↗
PubMed1977

The significance of sympathetic nervous activity for the development of the intestinal mucosal lesions in shock.

A 2-hour period of regional hypotension at 30-35 mmHg in the feline small bowel was produced by partial occlusion of the superior mesenteric artery. In one series of animals the sympathetic fibres in the splanchnic nerves were stimulated bilaterally at 6 Hz throughout the hypotension. In another group of animals no such stimulation was performed on the denervated intestinal segments. A mucosal damage was observed in both series and it was graded histologically according to Chiu et al. (1970). The two groups were also compared as regards the magnitude of the blood pressure fall occurring during the first hour after the period of intestinal hypotension. No statistically significant difference could be demonstrated between the two series of experiments with regard to mucosal damage or blood pressure fall. It is hence concluded that sympathetic nervous activity does not contribute to any measurable extent to the development of mucosal damage and cardiovascular deterioration observed in connection with regional intestinal hypotension. The explanation for this is discussed.

Animals↗