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Biomedical subjects

O Lundgren

Publications and source records attributed to O Lundgren.

At least 91 records · Page 5Linked to original sources
PubMed1987

Mechanisms underlying the small intestinal fluid secretion caused by arachidonic acid, prostaglandin E1 and prostaglandin E2 in the rat in vivo.

Prostanoids were given intraluminally (PGE2) or infused close intra-arterially (PGE1 and PGE2) or arachidonic acid was administered intraluminally to denervated jejunal segments of the rat in vivo. These experimental manoeuvres caused a net fluid secretion, although a 1,000-fold higher concentration of the prostanoids was needed from the luminal than from the vascular side. I.v. hexamethonium or serosally applied lidocaine diminished the induced fluid secretion suggesting that the prostanoids act mainly by eliciting local secretory reflexes in the enteric nervous system. This nerve-mediated secretion is not accompanied by any increase in tissue cAMP. However, at higher i.a. concentrations of PGE2 there seems to be a non-neurogenic effect on the enterocytes associated with an increase in tissue cAMP.

Alprostadil↗
PubMed1987

Tissue penetration and measuring depth of laser Doppler flowmetry in the gastrointestinal application.

Tissue penetration of laser light and measuring depth (depth sensitivity) for laser Doppler flowmetry in the gastrointestinal application were studied in the feline and human bowel and stomach with a wall thickness of from 2.1 to 7.0 mm. Mucosal and serosal recordings from corresponding sites in the gastrointestinal tract were comparable and in the intestine correlated to total blood flow. Laser light was reflected by a mirror placed on the opposite side of the bowel wall, and hyperemic reactions were similarly recorded from both sides of the bowel with wall thickness up to 6 mm. Placing layers of unperfused feline small intestine (average thickness, 2.1 mm) between the probe and the perfused feline gastric wall attenuated the laser Doppler signal in an exponential manner. We conclude that with this instrument, the tissue penetration and measuring depth of laser Doppler flowmetry are at least 6 mm in the gastrointestinal application.

Animals↗
PubMed1987

Intestinal vascular obstruction shock in the rat. Effect of 2 dextran solutions on blood and plasma volumes, cardioinhibitory activity in blood and pulmonary platelet trapping.

Pathophysiologic mechanisms involved in the dextran effect on mortality in intestinal shock in rats were studied, using a standardized model for intestinal vascular obstruction. Both dextran 70 and dextran 40 (respective mean molecular weights 70 X 10(3) and 40 X 10(3) d) given to shocked rats reduced but did not prevent the cardioinhibitory action of intestinal venous plasma in vitro. Both dextrans prevented platelet trapping in the lungs. Reduction in blood and plasma volumes was found in shocked rats given saline or dextran 40, but not following dextran 70. These differences were found after 120 min, but not after 240 min, when all shocked groups had lower blood and plasma volumes than in non-shocked controls. The results indicate that several mechanisms influence the effect of dextran 70 on mortality of rats in intestinal shock. Previously observed difference in mortality rates after infusion of dextran 70 and dextran 40 could not be explained by mechanisms studied in this series of experiments.

Animals↗
PubMed1986

Intestinal vascular obstruction in the cat. Right heart function in a shock model.

Cardiovascular function was studied in a model of intestinal vascular obstruction in cats. To measure right ventricular end diastolic pressure and maximal dP/dt, a tip transducer catheter was placed into the right ventricle. The intestinal vascular obstruction resulted in shock with decreases of blood pressure, cardiac output, and external cardiac work. Small intestinal mucosal lesions were found in all shocked cats. At an increased preload to the heart, right ventricular function was depressed in shocked cats. The model corresponds to one used earlier in the rat, where cardioinhibitory activity in venous blood was found in vitro. In this corresponding model of intestinal shock in the cat a depressed function of the right ventricle of the heart was found in vivo.

Animals↗
PubMed1986

The adrenergic nervous control of fluid transport in the small intestine of normotensive and spontaneously hypertensive rats.

Intestinal net fluid transport in normotensive Wistar Kyoto rats (WKR) and spontaneously hypertensive rats of the Okamoto strain (SHR) were studied during 'rest', during electrical stimulation of the regional sympathetic fibres as well as after acute denervation and alpha-adrenergic receptor blockade (phentolamine). During 'rest' no statistically significant difference in fluid transport rate could be demonstrated between WKR and SHR. Cutting the left splanchnic nerve, severing the periarterial nerves or giving phentolamine turned net fluid absorption to net fluid secretion in most SHR, whereas fluid absorption was little influenced in WKR by these procedures. Stimulating the left splanchnic nerve (2, 4, 8 Hz) markedly increased net fluid uptake or decreased net fluid secretion in SHR in a frequency-dependent manner. A small effect was seen in WKR at a stimulation rate of 4 Hz. The 'spontaneous' fluid secretion in denervated intestinal segments of SHR was accompanied by a net chloride secretion. Giving hexamethonium i.v. turned net fluid and chloride secretion into water and ion absorption, suggesting that the secretion was evoked by secretory nervous pathways in the enteric nervous system. It is concluded that the 'spontaneous' fluid and electrolyte secretion seen in denervated intestines of SHR is normally 'concealed' by an augmented rate of firing in the regional adrenergic nerve fibres controlling fluid and electrolyte transport. The possible importance of the 'spontaneous' intestinal secretion in SHR in the pathophysiology of arterial hypertension is tentatively discussed.

Adrenergic Fibers↗
PubMed1986

The net fluid secretion caused by cyclic 3'5'-guanosine monophosphate in the rat jejunum in vivo is mediated by a local nervous reflex.

The tissue concentration of cyclic 3'5'-guanosine monophosphate (cGMP) has been shown to increase in the small intestine when net fluid secretion is evoked by the heat-stable enterotoxine of Escherichia coli. Lipophilic cGMP analogues are also known to elicit intestinal fluid secretion. It is therefore believed that an increase in intracellular cGMP concentration in enterocytes mediates this secretion. The present study reports that the fluid secretion, elicited by placing two different cGMP analogues, dibutyryl-cGMP and 8-Br-cGMP, in the intestinal lumen of anaesthetized rats in vivo, is significantly inhibited by atropine, hexamethonium and lidocaine. It is proposed that cGMP activates a reflex in the enteric nervous system which, in part, explains the observed fluid secretion.

Acetylcholine↗
PubMed1986

Blood flow distribution, lymph flow, villus tissue osmolality and fluid and electrolyte transport after exposing the cat small intestine to sodium deoxycholate.

The effect of luminal perfusion of a dihydroxy bile salt (sodium deoxycholate) on net fluid transport, intestinal haemodynamics, lymph flow, electrolyte transport and villus tissue osmolality was studied in cat jejunum. Furthermore, the effects of hexamethonium and tetrodotoxin, two drugs influencing nervous activity, were investigated. Concomitant to net fluid secretion, the bile salt increased mucosal blood flow whereas capillary filtration coefficient and lymph flow remained unchanged. Net sodium and chloride transport changed from absorption to secretion. The change of sodium transport was due to both an increased flux from tissue to lumen and a reduced flux in the opposite direction. Villus tissue hyperosmolality was reduced. None of the effects on intestinal haemodynamics correlated with the change in net fluid transport. Furthermore, hexamethonium and tetrodotoxin inhibited the secretion of fluid and electrolytes without influencing the induced changes in intestinal haemodynamics. It is concluded that the bile salt induces intestinal fluid secretion by stimulating an active secretory process in the crypts via enteric nerves. A minor part of the total change in net fluid transport may be due to a reduced uptake in the villi.

Animals↗
PubMed1986

Intestinal fluid and electrolyte transport in man during reduced circulating blood volume.

The effect on intestinal net transport of fluid and electrolytes of a reduced circulating blood volume was studied in the human jejunum with the triple lumen perfusion technique. The blood volume was reduced by changing the lower extremities from an elevated to a dependent position combined with a venous stasis. The tilting manoeuvre, probably resembling a bleeding of about 600-800 ml, significantly increased net absorption of fluid, sodium and chloride while glucose transport was unaffected. Concomitantly the blood flow decreased and vascular resistance increased in the forearm vascular bed. The results are consistent with the hypothesis that activity in the sympathetic nervous system initiated from unloading of the cardiopulmonary volume receptors enhances intestinal absorption of fluid and electrolytes. The results also indicate that the human intestines are an important target organ in the compensatory mechanisms activated during hypovolaemia due to - for example, haemorrhage.

Adult↗
PubMed1986

Involvement of the enteric nervous system in the intestinal secretion induced by sodium deoxycholate and sodium ricinoleate.

Rat small intestine was continuously perfused for up to 3 h with two different concentrations of sodium deoxycholate (4 and 8 mM) or with sodium ricinoleate (6 mM). The 4-mM bile salt solution produced a secretion that developed to a maximal rate within 3 h, whereas the maximal rate was reached within 1 h with the 8-mM bile salt solution. Hexamethonium, a ganglionic blocker, and lidocaine, a local anesthetic, always reduced the net fluid secretion to approximately zero irrespective of the rate of bile-salt-induced secretion, the concentration of the bile salt, or the perfusion time. Fluid secretion induced by sodium ricinoleate was, like the bile-salt-induced secretion, markedly inhibited by hexamethonium and lidocaine but not by atropine. It is concluded that the rate of secretion induced by the bile salt is related to the monomer concentration of free bile salt molecules in close proximity to or within the intestinal epithelium. The intestinal fluid secretion is mainly due to stimulation of an active secretory process via an activation of enteric nerves. Sodium ricinoleate evokes secretion via similar nervous reflex mechanisms.

Animals↗
PubMed1986

Assessment of blood flow in the small intestine with laser Doppler flowmetry.

Blood flow in the small intestine was assessed in 48 patients by laser Doppler flowmetry. Mucosal and serosal flowmeter signals were compared during 'resting' conditions, vascular occlusion, and reactive hyperemia. Serosal flowmeter recordings were compared with the total blood flow of a bowel segment as measured by venous collection. The magnitudes of the mucosal (n = 49) and serosal (n = 49) flowmeter signals were comparable throughout the whole range of flowmeter signals (r = 0.97; p less than 0.001). A correlation coefficient of 0.95 (n = 51; p less than 0.001) was obtained between serosal flowmeter signals and total blood flow during 'resting' and reduced blood flows. During vasodilatation after a vascular occlusion, blood flow was underestimated by the flowmeter. A calibration curve could be constructed for approximate interpretation of the flowmeter signals in absolute flow units. The present study underlines the potential of laser Doppler flowmetry in the assessment of blood flow in the human small intestine.

Adolescent↗
PubMed1986

Measurement of colonic blood flow with laser Doppler flowmetry.

Colonic blood flow was measured with laser Doppler flowmetry during operation in 62 patients and during coloscopy in 15 patients. In 18 subjects mucosal and serosal laser Doppler signals were compared during 'resting' conditions, vascular occlusion, and reactive hyperemia. The mucosal (n = 36) and serosal (n = 36) flowmeter signals were of the same order of magnitude throughout the whole range of flowmeter signals (r = 0.96; p less than 0.001). In eight subjects total venous outflow from a colonic segment was measured simultaneously with flowmeter recordings from the serosal side. A correlation coefficient of 0.95 (n = 46; p less than 0.001) was obtained between total intestinal blood flow and serosal flowmeter signal during 'resting' and reduced blood flows. In this flow range a calibration curve was constructed for interpretation of the flowmeter signals in absolute flow units. The wall thickness of the bowel determined the quantitative relationship between flowmeter signal and total intestinal blood flow. It is concluded that laser Doppler flowmetry represents a potentially very interesting non-invasive, continuous method for the quantitative study of human intestinal blood flow.

Adolescent↗
PubMed1986

Effects of naloxone in intestinal shock in the rat.

The contribution of endogenous opioid peptides to the development of circulatory derangement in severe shock was studied using naloxone. A standardized intestinal shock was induced in rats by applying a pressure of 120 cm water on the mesenteric vessels for 60 min. The rats were then given either saline or naloxone. Mean arterial blood pressure improved and a less severe acidosis resulted in naloxone-treated animals compared to saline-treated. No differences were found in hematocrit, the degree of small intestinal mucosal lesions, or survival rates after 7 days comparing naloxone and saline treatment. Survival time increased after naloxone but not after saline treatment. The results support the hypothesis that endogenous opioid peptides contribute to cardiovascular collapse in intestinal shock.

Acid-Base Equilibrium↗
PubMed1985

Mechanisms underlying the intestinal fluid secretion evoked by nociceptive serosal stimulation of the rat.

Intestinal net fluid transport was measured in vivo continuously with a gravimetric method. Chemical stimulation of the jejunal serosa with hydrochloric acid (0.1 M), ethanol (20%), cat bile or 7-deoxycholic acid (10 mM) evoked an intestinal fluid secretion. Hexamethonium (10 mg/kg b.wt.i.v.) or serosal application of lidocaine (1% solution) partially blocked this secretory response. Bradykinin and prostaglandin E1, two important inflammatory mediators, elicited fluid secretion when applied to the serosal surface at a concentration of 10(-4) M. This secretion was also partly inhibited by hexamethonium. Furthermore indomethacin (10 mg/kg b.wt. i.v.) or pyrilamine (10 mg/kg b.wt. i.v.), a H1-receptor blocker, partly inhibited the secretory response caused by chemical stimulation of the serosa while cimetidine (1 mg/kg b.wt. i.v.), a H2-receptor blocker, had no effect. Freeze sectioned samples from chemically stimulated intestines were examined by fluorescence microscopy. A leakage of i.v. administrated Evans blue labelled albumin into the interstitial space of the serosa and the outer layer of the muscularis was found. It is concluded: The intestinal fluid secretion studied is mainly elicited by nociceptive stimulation of nerves in the serosa or the outer muscularis. The reflex may be activated by the local release of histamine, kinins and prostaglandins. The reflex studied is part of an inflammatory response.

Animals↗
PubMed1985

The enteric nervous system participates in the secretory response to the heat stable enterotoxins of Escherichia coli in rats and cats.

Intestinal secretion was evoked in periarterially denervated jejunal segments of anesthetized rats and cats by exposing the intestines to the heat stable (ST) toxins from a strain of Escherichia coli producing both STa and STb toxins. The secretion was significantly inhibited and to about the same relative extent by the addition of each one of the three following drugs: hexamethonium (i.v., rats), lidocaine (applied on the serosal surface, rats) and tetrodotoxin (intra-arterial, cats). Atropine inhibited fluid secretion in some experiments. It is proposed that a nervous mechanism is mediating part of the secretory response to Escherichia coli heat stable toxins, since three different drugs, which influence nervous activity in different ways, significantly diminished the secretory response. A model for the secretory nervous reflex(es) within the enteric nervous system is proposed; Escherichia coli heat stable toxins activate a "receptor cell" in the epithelium, which then stimulates surrounding dendritic nerve endings via the release of unknown substance(s). A nicotinic receptor is involved but further characteristics of the nervous reflex(es) remain to be elucidated.

Animals↗
PubMed1985

Evaluation of laser Doppler flowmetry in the assessment of intestinal blood flow in cat.

Laser Doppler flowmetry with a differential detector system has been used in the assessment of blood flow in the feline small intestine. Simultaneous mucosal and serosal laser Doppler flowmeter recordings were compared with total blood flow of a bowel segment measured by an optical drop-recorder unit in 6 cats. Blood flow through the muscularis layer was estimated using the 85Kr washout technique. A correlation coefficient of r = 0.96 (mucosal recordings = 90, serosal recordings = 80, p less than 0.001) was obtained between laser Doppler flowmeter output signals and total blood flow at different levels of vascular tone, regardless of whether the flowmeter recordings were made from the mucosal or the serosal side of the bowel wall. At intense vasodilation, the flowmeters showed a tendency to underestimate blood flow. The flowmeter signals were at variance with the muscularis blood flow but were clearly correlated to the calculated mucosal-submucosal blood flow. The uneven blood flow distribution in the intestinal wall did not affect the ability of the flowmeters to reflect total blood flow from either side of the bowel wall. A calibration curve could be constructed for approximate interpretation of the laser Doppler signals in absolute flow units. However, further experiments in humans and further development of the technique must be performed to elucidate clinical applications of the method.

Animals↗
PubMed1985

Effects of intra-arterially infused adenosine triphosphate (ATP) on release of vasoactive intestinal polypeptide (VIP) from the gastrointestinal tract of the cat.

Close i.a. infusions of ATP were made to the stomach, the small intestine or the colon in the cat. The vascular reactions were followed by recording arterial pressure and total venous outflow continuously and the release of VIP was estimated intermittently from arterio-venous concentration differences and blood flow. In all experiments ATP caused a vasodilatation and an increased release of VIP into blood. In control experiments it was shown that evoking a vasodilatation of the same magnitude by close i.a. infusions of isoprenaline or papaverine did not evoke any similar release of VIP. It is concluded that the infused ATP released VIP from the different parts of the gastrointestinal tract. Possible mechanisms underlying this effect are tentatively discussed.

Adenosine Triphosphate↗