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Biomedical subjects

O Lundgren

Publications and source records attributed to O Lundgren.

At least 109 records · Page 6Linked to original sources
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↗
PubMed1984

The involvement of the enteric nervous system in the intestinal secretion evoked by cyclic adenosine 3'5'-monophosphate.

Intestinal fluid secretion was evoked in vivo in rats and cats by introducing dibutyrylcyclic adenosine 3,5-monophosphate (db-cAMP) or theophylline, a phosphodiesterase inhibitor, in the intestinal lumen. The intestines were denervated periarterially. It was demonstrated that three compounds of varying chemical structure and with different modes of action on nerves (tetrodotoxin, lidocaine, hexamethonium) decreased the secretory response 60-70%. It is concluded that the secretion induced by increasing the intracellular cAMP concentrations is in part evoked via the enteric nervous system.

Animals↗
PubMed1984

Further evidence for a glucose-activated secretory mechanism in the jejunum of the cat.

The present study was undertaken to further test the hypothesis of a glucose-induced secretory mechanism in the jejunum of the cat (Sj ovall et al. 1983 b). The experimental design was based on the sodium dependence of active glucose uptake from the intestinal lumen. The rate of glucose uptake from a sodium-free and a sodium-containing perfusate was compared and we also investigated the effect of splanchnic nerve stimulation (SNS) on glucose absorption. The results revealed no difference in "resting" glucose uptake between the two groups. Glucose uptake from the sodium-free solution decreased on SNS whereas no such effect was seen in the sodium-containing segments. These findings can be explained by an SNS evoked inhibition of the glucose induced secretion of sodium from the crypts, which will be rate limiting for glucose uptake when no sodium is present in the perfusate. The findings are thus consistent with the concept of a glucose activated sodium secretion. Data are also presented which indicate that this secretory response is mediated by the enteric nervous system.

Animals↗
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 hemorrhage on intramural blood flow distribution, villous tissue osmolality and fluid and electrolyte transport in the cat small intestine.

The hemodynamic response in the parallel-coupled vascular sections of the cat small intestine were studied before, during and after a two hour period of hemorrhage (about 30 per cent of estimated blood volume). Fluid and electrolyte transport and villous tissue osmolality were also measured. Biopsies for histology were taken at the end of all experiments. The animals were divided in two groups, undamaged and damaged, according to the degree of mucosal damage observed. 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 flows. Total intestinal blood flow was lower in the damaged as compared to the undamaged group during hypovolemia. No difference in absorptive site blood flow was observed between the two groups during hypovolemia. Furthermore, no decrease of red blood cell flow in the "villi" was recorded in either group after hemorrhage. Consequently, mucosal lesions developed despite an unchanged oxygen transport capacity to the villi. The pathophysiology of the mucosal lesions is briefly discussed. Net fluid and sodium absorption was after hemorrhage increased in the undamaged group reflecting a decrease in the tissue to lumen transport of sodium. After retransfusion net fluid and sodium absorption returned to control. In the damaged group, however, net fluid and sodium absorption was decreased after hemorrhage. The increased rate of fluid and electrolyte transport observed in the undamaged small intestine after hemorrhage, is proposed to be an important mechanism for fluid replacement after hemorrhage.

Acid-Base Equilibrium↗
PubMed1984

Effect of cimetidine on augmented gastric blood flow in duodenal ulcer patients.

Blood flow in the human stomach was measured during operation with a 85Krypton washout method which made simultaneous determinations of total blood flow and intramural flow distribution possible. The antrum and the corpus of the stomach could be investigated separately. Eleven patients with duodenal ulcer disease were studied during pentagastrin infusion and after the addition of cimetidine, 3 mg/kg bw, to evaluate the effect of the drug on augmented gastric blood flow. Eight recordings were made over the corpus of the stomach and three recordings over the antrum. Cimetidine caused a 66 +/- 5% decrease (mean +/- SE; range 56-86) in acid secretion and a 62 +/- 5% decrease (range 44-91) in the corpus mucosal blood flow within 15 minutes. Changes were only seen in the acid secreting part of the stomach while the antral circulation remained unaltered. It is concluded that the decrease in pentagastrin induced vasodilatation in the stomach seen after giving cimetidine was secondary to an inhibition of acid secretion.

Animals↗
PubMed1984

Neurotransmitters involved in the colonic contraction and vasodilatation elicited by activation of the pelvic nerves in the cat.

Stimulation of the pelvic nerves causes a contraction of and an increased blood flow in the feline colon. This study was performed to analyze the possible neurotransmitters involved in this response. The colonic contraction and hyperemia caused by pelvic nerve stimulation (5 Hz, 5 ms, 5 V) were not affected by the substance P antagonist (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-substance P, by substance P tachyphylaxis, or by naloxone (0.2-0.3 mg/kg body wt, i.a.). However, after treatment with atropine (0.5 mg/kg body wt, i.v.), naloxone blocked the contraction evoked by pelvic nerve stimulation (p less than 0.01), whereas the vasodilator response was unchanged. Distension of the rectum with a water-filled balloon or mechanical stimulation of the anal wall with a glass rod elicits a pelvo-pelvic reflex with colonic contraction and hyperemia. The contraction elicited by rectal distension was completely abolished by atropine (0.5 mg/kg body wt, i.v.). However, in atropinized animals, mechanical stimulation of the anal wall caused a contraction of the distal colon that was blocked by naloxone (0.2-0.3 mg/kg body wt, i.a.). The hyperemia was not affected by atropine or by naloxone. The results indicate the existence of at least three motor-neuronal systems in the distal colon: one cholinergic and one enkephalinergic system mediating colonic contractions, and one system mediating vasodilatations with another transmitter.

Animals↗
PubMed1984

Effect of intravenous dopamine infusion on intramural blood flow distribution and fluid absorption in the feline small intestine.

The aim of the study was to investigate the effects of dopamine on the intestinal mucosal blood flow and transport function. Dopamine was infused intravenously at 20 micrograms X kg-1 X min-1 in anesthetized cats. Total and intramural blood flow in an isolated jejunal segment was measured by a combined drop-flow and 85Kr clearance technique. Net fluid transport was recorded by two independent perfusion methods. Unidirectional sodium transport was estimated from luminal 22Na disappearance. Dopamine induced a pronounced mucosal vasodilatation up to 400% of control values. Concomitantly, net fluid and sodium absorption increased by 50%. The effect on sodium transport was due to a pronounced decrease in tissue-to-lumen sodium flux, a pattern similar to the one seen on alpha-adrenergic stimulation. The effect of dopamine on blood flow was unaffected by phentolamine, 1 mg X kg-1, whereas the absorptive response was abolished. The findings indicate that dopamine induces a mucosal vasodilation via one mechanism (possibly dopaminergic) and enhances fluid transport via another mechanism, probably alpha-adrenergic.

Animals↗
PubMed1983

Vagal control of the motor functions of the lower esophageal sphincter and the stomach.

Vagal control of the motor functions of the lower esophageal sphincter and the stomach is briefly reviewed. The vagal influence is in principle the same in the two tissues. There exists one set of vagal fibers which evokes a contractile response. This response is mediated via cholinergic muscarinic receptors. Another set of fibers evokes a relaxation via a non-cholinergic, non-adrenergic mechanism. The neurotransmitter involved in this response is not established. Observations reported in the literature suggest that an interneuron releasing 5-hydroxytryptamine may be involved. At the effector cells vasoactive intestinal polypeptide and/or adenosine triphosphate may be the neurotransmitter(s).

Adenosine Triphosphate↗
PubMed1983

Intestinal water transport.

The current knowledge of the physiology of the transport of sodium and water across the intestinal epithelium is summarized. A brief review of its hormonal and nervous control is also given.

Animals↗
PubMed1983

The effect of vagal nerve stimulation on net fluid transport in the small intestine of the cat.

The effect of electrical vagal nerve stimulation on intestinal net fluid transport rate was studied in the small intestine of the cat. The splanchnic nerves were severed in all experiments. Absorption was quantified with a new gravimetric technique which made it possible to study fluid transport also during intestinal motility. The stimulation characteristics were varied to activate selectively low threshold fibres or low and high threshold fibres. The observations did not reveal any affects of low threshold stimulation on intestinal fluid transport whereas an inhibition was seen when also the high threshold fibres were stimulated. This inhibitory vagal mechanism could also be elicited after the administration of atropine. Atropine in itself increased "resting" net fluid absorption. The results speak against a role for vagal cholinergic mechanisms in the control of net fluid absorption. There seem, however, to be tonically active intramural cholinergic pathways and noncholinergic inhibitory vagal neurons of unknown physiological significance.

Acetylcholine↗
PubMed1983

The effect of splanchnic nerve stimulation on blood flow distribution, villous tissue osmolality and fluid and electrolyte transport in the small intestine of the cat.

The effect of splanchnic nerve activation on intestinal fluid transport and intramural blood flow distribution was examined in the cat. Previous reports from our laboratory have demonstrated that splanchnic nerve activation increases fluid absorption. The present study was performed to elucidate the mechanisms behind this effect. The results showed an increase in net sodium and chloride transport on splanchnic nerve activation whether intestinal blood flow decreased or not. The effect on sodium transport was due to a decrease in lumen to tissue flux. The effect could not be explained by a decrease in local blood flow, as it was present despite constant blood flow in both the villous and crypt regions. No change was seen in the villous osmolality gradient on splanchnic nerve activation. On the basis of these findings, it is proposed that the in vivo effect of splanchnic nerve activation is due to a decrease in fluid and electrolyte secretion, probably occurring in the intestinal crypts.

Animals↗
PubMed1983

The involvement of intramural nerves in cholera toxin induced intestinal secretion.

In previous reports we have suggested that nervous reflexes are involved in the pathophysiology of cholera secretion and that these nervous reflexes involve a cholinergic synapse and a neuron with vasoactive intestinal polypeptide (VIP) as neurotransmitter. These proposals were further analyzed in this study. Tetrodotoxin (TTX) and lidocaine applied on the serosal surface inhibited cholera secretion in segments of rat small intestine. Fluid absorption in control rats was not significantly changed. Hexamethonium given i.v. decreased cholera secretion in the cat. No additional inhibition of cholera secretion was observed after giving TTX close i.a. Furthermore, the intestinal secretion evoked by VIP was not influenced by hexamethonium given i.v. or TTX given close i.a. The present observations support the hypothesis of a role for nervous reflexes in cholera secretion. The results suggest that at least a major part of the proposed nervous reflex(es) in cholera have a cholinergic synapse. Furthermore, the VIP-ergic neuron is situated "distal" to the cholinergic neuron in the reflex(es) closer to the effector cells.

Animals↗
PubMed1983

Intramural blood flow distribution in the small intestine of the cat studied by carbon monoxide uptake and 85krypton elimination.

Carbon monoxide (CO) uptake from the feline small intestine was measured to investigate if it could be used to determine blood flow in the superficial parts of the intestinal mucosa. Several observations were made that substantiated this proposal: 1) Lowering PCO in the intestinal lumen from 100 to 70 kPa did not influence the rate of CO absorption during "resting" blood flow conditions, while the same reduction of lumen PCO resulted in a decreased rate of CO uptake during isoprenaline induced vasodilatation. These observations suggest that CO uptake was flow limited during "rest" and diffusion limited during vasodilation. 2) Lowering perfusion pressure or totally occluding the intestinal vascular supply markedly reduced the rate of CO uptake. 3) The diffusion distance for CO into the tissue was calculated to be 75-225 micron, i.e. CO mainly diffused into the villous tissue. 4) The flow values calculated from the CO measurements were of the same order of magnitude as earlier reported with other techniques (microspheres, indicator dilution method). It was concluded that CO absorption mainly reflected villous blood flow during "resting" and low intestinal blood flow. Total blood flow (venous drop recorder) and muscle layer blood flow (85Kr elimination) were measured simultaneously to CO uptake. From these determinations "resting" blood flow distribution in the small intestine was calculated.

Animals↗
PubMed1983

On the mode of action of the sympathetic fibres on intestinal fluid transport: evidence for the existence of a glucose-stimulated secretory nervous pathway in the intestinal wall.

The effect of sympathetic nerve stimulation or close i.a. infusion of noradrenaline on net fluid transport was investigated on anesthetized cats. In the presence of glucose in the solution perfusing the intestinal lumen the adrenergic mechanisms increased net fluid absorption in normal intestines. Substituting glucose with mannitol in the perfusate abolished this effect of adrenergic stimulation on the net fluid uptake. Furthermore, the effect of noradrenaline on net fluid transport in normal or choleraic intestines was abolished by tetrodotoxin (TTX), a nerve conductivity blocking agent. This suggests that the sympathetic influence is dependent on intraluminal glucose and that noradrenaline exerts its effect mainly via nerves. TTX significantly increased fluid uptake from normal intestines perfused with an isotonic electrolyte solution containing glucose while a considerably smaller effect was seen in intestinal segments perfused with a solution with mannitol. Based on these findings it is proposed that glucose in some way activates intramural nervous reflex(es) in the intestinal wall. According to this hypothesis the enhancement of fluid transport induced by adrenergic stimuli is explained by an inhibition of the glucose-activated nervous secretion.

Animals↗
PubMed1983

Effect of apamin on release of vasoactive intestinal polypeptide (VIP) from the cat intestines.

The effect of apamin, a polypeptide from bee venom, on the release of vasoactive intestinal polypeptide (VIP) during active neurogenic vasodilatation in the intestines was studied in vivo in anesthetized cats. Three non-adrenergic, non-cholinergic mechanisms were investigated, i.e. the vasodilatation seen upon transmural electrical field stimulation, pelvic nerve activation and stimulation of the intramural nerves with 5-hydroxytryptamine (5-HT) infused i.a. Apamin given close i.a. abolished the three vasodilator responses. Concomitantly, the increase of VIP release was also markedly diminished although apamin increased the rate of VIP release seen in the "resting" control period. The results are in agreement with the hypothesis that VIP is the neurotransmitter in the three investigated vasodilator mechanisms.

Animals↗
PubMed1983

The effect of apamin on non-adrenergic, non-cholinergic vasodilator mechanisms in the intestines of the cat.

The effects of apamin, a polypeptide isolated from bee venom, on different vasodilator mechanisms in the small and large intestines were studied in atropinized cats. In the large intestine vasodilatation in response to pelvic nerve stimulation was either abolished or markedly diminished by I.A. apamin. However, neither the contraction of colonic muscle which occurred under these conditions nor sympathetic vasoconstriction was significantly influenced by apamin, suggesting that the effect of the peptide was not a non-specific effect on nerves or vascular smooth muscle. In the small intestine it was observed that the nervous vasodilatation induced by transmural electrical field stimulation or mechanical mucosal stimulation was either diminished or abolished by apamin. Intestinal vasodilatation, caused by close I.A. infusions of 5-hydroxytryptamine (5-HT), was abolished by apamin. After giving apamin 5-HT infusions induced a vasoconstriction in five out of six experiments. Vasodilatation induced by vasoactive intestinal polypeptide (VIP) was not significantly affected by apamin. In a series of in vitro experiments on rat portal vein, dose-response curves of several putative intestinal neurotransmitters were determined in the presence and absence of apamin. The following substances were tested: VIP, substance P, bradykinin, 5-HT, ATP and adenosine. Apamin had no effect on the dose-response curves of any of these compounds. The results are discussed in relation to the possibility that apamin may act by blocking the release of a putative peptidergic transmitter from nerve terminals.

Adenosine Triphosphate↗