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Biomedical subjects

O Lundgren

Publications and source records attributed to O Lundgren.

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

On the role of intramural nerves in the pathogenesis of cholera toxin-induced intestinal secretion.

Intestinal secretion was produced in anesthetized cats and rats by exposing isolated intestinal segments to cholera enterotoxin. Giving, for example, tetrodotoxin, a nerve-conduction-blocking agent, or adding lidocaine, a local anesthetic agent, to the solution in the intestinal segments markedly inhibited the rate of choleraic secretion, and in most experiments a net absorption of fluid was observed. The results suggest that intramural nervous mechanisms are involved in the pathogenesis of choleraic secretion.

Anesthetics, Local↗
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

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↗
PubMed1980

The effect of Apamin on nonadrenergic, noncholinergic nervous vasodilatations in the cat small intestine.

The intestinal vasodilation evoked by mechanical mucosal stimulation or by transmural electrical field stimulation was abolished by close i.a. injection of Apamin, a polypeptide originally isolated from bee venom. Apamin also blocked the vasodilatation induced by close i.a. infusion of vasoactive intestinal polypeptide (VIP). It is suggested that Apamin is a VIP receptor antagonist.

Animals↗
PubMed1980

Villous tissue osmolality, water and electrolyte transport in the cat small intestine at varying luminal osmolalities.

Villous tissue osmolality and net transport for water, sodium, potassium and chloride were determined in the feline small intestine when exposing the mucosa to solutions with different mannitol concentrations (0, 100, 315 and 600 mmol/l). Tissue osmolality at the villous tip varied with luminal osmolality. At the villous base, on the other hand, tissue osmolality remained around the plasma osmolality regardless of the osmolality of the luminal fluid. Transport rates for water were affected in the way predicted from the lumen to tissue osmolality difference. A net flux from tissue to lumen was always recorded for the studied electrolytes. The hydraulic conductivity (Lp) of the intestinal epithelium with dilated intercellular spaces was estimated from the present results to be around 30 x 10(-12) cm x s-1 x Pa-1. When the intercellular spaces were collapsed Lp was estimated to be 15 x 10(-12 cm x s-1 x Pa-1.

Animals↗
PubMed1980

Vasoactive intestinal polypeptide, 5-hydroxytryptamine and reflex hyperaemia in the small intestine of the cat.

1. The release of vasoactive intestinal polypeptide (VIP) into venous blood from the small intestine of the cat was studied when mechanically stimulating the intestinal mucosa and during close intra-arterial infusions of 5-hydroxytryptamine (5-HT) or isopropylnoradrenaline. The studies were performed on anaesthetized cats given atropine.2. Mechanical stimulation of the intestinal mucosa induced a vasodilatation and a release of VIP into the intestinal venous blood. Intra-arterial administration of tetrodotoxin was given in doses that blocked the vasoconstrictor effect of the regional sympathetic nerve fibres. This also abolished the vascular response and the release of VIP into blood upon mechanical stimulation.3. Close intra-arterial administration of 2-bromo-lysergic acid diethylamide reduced the VIP release and the intestinal vasodilatation upon mucosal stimulation to largely the same extent.4. Close intra-arterial infusions of 5-HT produced a marked release of VIP from the intestine and a moderate vasodilatation. Close intra-arterial infusions of isopropylnoradrenaline, which caused a pronounced intestinal vasodilatation, evoked only a small release of VIP.5. The results are compatible with the hypothesis that the vasodilatation in the gut, induced by mechanical mucosal stimulation, is mediated via an intramural nervous reflex containing a neurone capable of releasing VIP. It is proposed that the nervous reflex is activated by the release of 5-HT from the enterochromaffin cells evoked by mechanical stimulation of the mucosa.

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↗
PubMed1979

Effects of vasoactive intestinal polypeptide on blood flow, motility and fluid transport in the gastrointestinal tract of the cat.

The effect of close intraarterial infusions of vasoactive intestinal polypeptide (VIP) on gastric motility, intestinal fluid transport and colonic motility were studied in the cat. Regional blood flow was also followed in all experiments. In the stomach VIP produced a gastric relaxation and a blood flow increase. The motility response was similar to that observed when eliciting the vago-vagal reflex relaxation by distending the esophagus. In the small intestine a hyperemia and a decrease of net water uptake was observed. When infusing small amounts of VIP a decrease of net water uptake was seen without any change of intestinal blood flow. Large amounts of VIP produced a transient secretory state in the small intestine. In the colon a hyperemia was seen immediately upon starting the infusion of the drug. After 2-3 min of infusion a contraction of the colon was apparent. The administration of atropine to the animal did not significantly affect any of the responses produced by VIP. The results are discussed in relation to VIP as a possible neurotransmitter in the gastrointestinal tract.

Animals↗
PubMed1979

Vascular anatomy and tissue osmolality in the filiform and fungiform papillae of the cat's tongue.

The vascular anatomy of the filiform and fungiform papillae of the feline tongue was studied by i.a. injection of India ink. Vascular loops of various appearances were found in the types of papillae studied, i.e. the large and the small filiform papillae and the fungiform ones. Such hairpin loops may function as countercurrent exchangers and to test this hypothesis tissue osmolality was determined in the papillae, while exposing them to various isotonic electrolyte solutions. The large filiform papillae with a vascular arrangement similar to that of intestinal villi exhibited a marked osmolar gradient from tip to base when exposed to a solution containing both glucose and sodium. If sodium and/or glucose was excluded from the solution, tissue osmolality was significantly decreased. This was also the case when the chloride ions of the solution was substituted with sulphate. The small filiform papillae are only provided with one or a few capillary loops. They exhibited a less marked osmolar gradient than the large ones and one of the different electrolyte solutions decreased the gradient. In the fungiform papillae a tissue hyperosmolality at the tip was also demonstrated. It is proposed that the papillary epithelium is provided with active transport mechanism(s) and that the papillary vessels function as countercurrent multipliers. The functional importance of these mechanisms are tentatively discussed.

Animals↗
PubMed1979

The effect of vasodilatation and sympathetic nerve activation on net water absorption in the cat's small intestine.

The rate of net water uptake from the feline small intestine has been investigated during control conditions, during graded infusions of the vasodilator drug isopropylnoradrenaline, and during electrical stimulation of the regional sympathetic nerve fibres to the gut. Net water absorption rate was largely unaffected by intestinal vasodilatation. The fraction of the absorbate transported via the lymphatics remained also constrant at 20-40% of the total absorption regardless of blood flow rate. Stimulating the sympathetic nerve fibres to the small intestine increased, however, net water absorption rate. The increase was particularly pronounced when blood pressure was kept constant during the period of stimulation. The absorption rate was on an average almost doubled at a stimulation frequency of 8 Hz during constant pressure conditions. The mechanism(s) explaining this nervous control of water absorption are tentatively discussed.

Adrenergic Fibers↗
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

Importance of sodium and glucose for the establishment of a villous tissue hyperosmolality by the intestinal countercurrent multiplier.

The intestinal countercurrent multiplier has earlier been shown to create an increased tissue osmolality in the villi (Jodal et al. 1978). In the present paper the importance of varying the luminal contents on the creation of the villous hyperosmolality was investigated using the cryoscopic technique described by Jodal et al. (1978). The perfusion solutions used contained 0, 25 or 147 mmol Na/l and were either provided with mannitol or glucose (30 mmol/l). It was demonstrated that sodium was of particular importance for the establishment of the villous hyperosmolality while glucose only contributed significantly at low luminal sodium concentrations. It is therefore proposed that glucose only in the absence of sodium in the luminal perfusate may effectively participate in the generation of the villous tissue hyperosmolality via the countercurrent multiplication mechanism.

Animals↗
PubMed1979

Villous tissue osmolality and intestinal transport of water and electrolytes.

The villous tissue hyperosmolality created by the intestinal countercurrent multiplier has been proposed to be of importance for fluid transport across the intestinal epithelium in vivo. This study was performed to test this hypothesis. Net transport of fluid and electrolytes (sodium, potassium and chloride), as well as unidirectional fluxes of water and sodium were determined in the small intestine of the cat. The villous osmolality was altered by varying the composition of sodium and glucose in the isotonic solutions perfusing the intestinal lumen. Net transport of fluid was correlated to tissue osmolality mainly due to an increase of the unidirectional flux of water from lumen to tissue with augmented tissue osmolality. The results are thus consistent with the view that the intestinal countercurrent multiplier is of essential importance for net water transport. A correlation was found between net water and net sodium intestinal transport. A similar correlation was also demonstrated between net sodium and net chloride absorption rates in the jejunum while in the ileum net loss of sodium into the intestinal lumen was not accompanied by any corresponding loss of chloride ions. This observation suggests the presence of a sodium independent transport mechanism for chloride in the ilium but not in the jejunum.

Animals↗
PubMed1979

Effects of cholera toxin on villous tissue osmolality and fluid and electrolyte transport in the small intestine of the cat.

The effects of cholera toxin on tissue osmolality and on net transport rates of water, sodium, chloride and potassium as well as on unidirectional fluxes of water and sodium were studied in vivo. In all experiments the toxin caused a net secretion of water, sodium, chloride and potassium. The unidirectional sodium transport from tissue to lumen was increased while the flux in the opposite direction was reduced 180 min after cholera toxin instillation. Cholera toxin produced only a small reduction in the villous tissue hyperosmolality, created by the intestinal countercurrent exchanger. This reduction was far too small to explain the observed net secretion of fluid and solutes induced by the cholera toxin. Other mechanisms underlying the cholera secretion are discussed.

Animals↗
PubMed1979

Exchange of krypton-85 between the blood vessels of the human uterine adnexa.

A miniature Geiger-Müller probe was inserted into one ovary of 8 women undergoing hysterectomy. A control probe was inserted into the other ovary of 2 of the women. Krypton-85 in 0.15 M-NaCl was infused into the adjacent utero-ovarian vein and the radioactivity was registered for 5--14 min after the infusion. An increase of radioactivity was recorded in the ovary in 5 cases. In one of the women with 2 probes, no increase in radioactivity was observed in the control ovary. The results show a local transfer of gas from the ovarian branch of the uterine vein into the adjacent ovary, which may be due to a countercurrent exchange mechanism between the vessels of the human uterine adnexa.

Adult↗