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| 2. |
- Holm, Lena, et al.
(författare)
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Histamine is not involved in pentagastrin-induced gastric mucosal vasodilation in the rat.
- 1994
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Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 266:1 Pt 1, s. G55-61
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Tidskriftsartikel (refereegranskat)abstract
- The effects of histamine and its role in the gastric mucosal vascular response to pentagastrin were studied in anesthetized rats. Blood flow was measured with laser-Doppler flowmetry (LDF) and with red blood cell velocity measurements in the superficial mucosal microcirculation. Acid secretion was determined by titration of the saline covering 0.8 cm2 of the fundic mucosa. Pentagastrin (40 micrograms.kg-1 x h-1 i.v. induced a blood flow increase (+40%), which was not significantly altered by ranitidine (H2-receptor antagonist, 2 mg/kg iv bolus), whereas the stimulated acid output was abolished. In experiments in which the H1-receptor antagonist pyrilamine (2.5 mg/kg i.v. bolus) was administered before pentagastrin stimulation, pentagastrin still increased blood flow by approximately 60%. Intravenous histamine (4 mg.kg-1 x h-1) induced a blood flow reduction in parallel with the reduction in blood pressure (vascular resistance unchanged). Even during intra-arterial (thoracic aorta) infusion of histamine (1 or 4 mg.kg-1 x h-1), gastric vascular resistance was unchanged. In animals pretreated with pyrilamine, histamine (4 mg.kg-1 x h-1 i.v.) left the gastric blood flow and blood pressure unchanged. These results indicate that the pentagastrin-induced increase in the rat gastric blood flow is not dependent on histamine.
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| 3. |
- Holm, Lena, et al.
(författare)
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Influence of tactile stimulation of the rat gastric mucosa on blood flow and acid output.
- 1993
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Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 265:2 Pt 1, s. G303-9
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Tidskriftsartikel (refereegranskat)abstract
- The influence of tactile stimulation of the gastric mucosa (mimics the mechanical influence of the food bolus) on the gastric mucosal blood flow and acid output was studied in rats anesthetized with Inactin. Blood flow was measured with laser-Doppler flowmetry (LDF) with the probe positioned above the gastric mucosa, and acid secretion was measured at regular intervals by titration of the saline covering 0.8 cm2 of the mucosa. After gentle tactile stimulation (wiping with cotton tips) of the mucosa for 20 s, blood flow increased to approximately 250% of the control value and then returned to the control level 15 min later, whereas acid output was transiently reduced immediately after tactile stimulation. Pretreatment with lidocaine, methysergide, or hexamethonium did not change the results of tactile stimulation on the blood flow. After indomethacin (3 mg/kg i.v.) LDF was significantly reduced by 33% and the hyperemic response to tactile stimulation was almost abolished. This suggests that endogenously released prostaglandins, not evoked through activation of intramural reflexes that can be blocked by lidocaine, methysergide or hexamethonium, are responsible for the hyperemia seen after tactile stimulation of the gastric mucosa.
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| 4. |
- Holm, Lena, et al.
(författare)
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Role of prostaglandins in regulation of gastric mucosal blood flow and acid secretion.
- 1992
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Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 263:4 Pt 1, s. G446-51
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Tidskriftsartikel (refereegranskat)abstract
- The role of prostaglandins in the rat gastric mucosal vascular response to acid stimulation was studied. Blood flow was measured with laser-Doppler flowmetry (LDF) and with red blood cell velocity measurements in the superficial mucosa; acid secretion was determined by titration. Baseline acid output was calculated to be 0.026 +/- 0.011 mueq/min. Pentagastrin (20 and 40 micrograms.kg-1.h-1 iv) significantly increased acid output to 0.387 +/- 0.104 and 0.546 +/- 0.220 mueq/min and LDF to 119 +/- 10 and 132 +/- 13% of control, respectively. LDF was significantly reduced by 15% after indomethacin (3 mg/kg iv) and was not changed by pentagastrin, whereas acid secretion increased to similar levels as without indomethacin pretreatment. The H2-agonist impromidine (100 and 500 micrograms.kg-1.h-1 iv) induced a dose-dependent increase in acid secretion (0.178 +/- 0.068 and 0.330 +/- 0.072 mueq/min, respectively) while blood flow was unchanged. Despite a substantial blood flow reduction (-38%) by indomethacin, impromidine did not alter blood flow, and acid secretion was dose dependently increased to similar values as without indomethacin pretreatment. These results provide further evidence that there is not necessarily any correlation between blood flow and acid secretion and that the pentagastrin-induced blood flow increase depends on prostaglandin release.
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| 5. |
- Jönson, C, et al.
(författare)
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Effects of hypovolemia on blood flow, arterial [HCO3-], and HCO3- output in the rat duodenum.
- 1990
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Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 259:2 Pt 1, s. G179-83
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Tidskriftsartikel (refereegranskat)abstract
- The effects of bleeding-induced hypovolemia on duodenal blood flow (microsphere technique), arterial [HCO3-], and duodenal HCO3- secretion (in situ titration) were investigated in chloralose-anesthetized rats. A 10% decrease in blood volume reduced duodenal HCO3- secretion by 44%, duodenal blood flow by 31%, and arterial [HCO3-] by 11%. In a group with cervically cut vagal nerves, basal duodenal HCO3- secretion was greater than 50% lower compared with controls. Basal blood flow and arterial [HCO3-] were on similar levels as in nonvagotomized animals. Furthermore, bleeding failed to lower duodenal alkaline output in rats with cut vagal nerves, although blood flow and arterial [HCO3-] were reduced to a similar extent as in the vagally intact controls. In a yohimbine-treated group, a 10% bleeding reduced duodenal blood flow by 28% and arterial [HCO3-] by 7% without influencing duodenal HCO3- secretion. We suggest that the hypovolemia-induced inhibition of duodenal alkaline secretion is not caused by a decrease in blood and/or arterial [HCO3-]. Instead, other factors may be of importance, for example, neural effects on enteric secretomotor neurons or directly on the secreting epithelium.
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| 6. |
- Ljungqvist, Olle, 1954-, et al.
(författare)
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Food deprivation alters liver glycogen metabolism and endocrine responses to hemorrhage
- 1990
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Ingår i: American Journal of Physiology. - : American Physiological Society. - 0002-9513 .- 2163-5773. ; 259:5 Part 1, s. E692-E698
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Tidskriftsartikel (refereegranskat)abstract
- Liver glycogen content, blood glucose, insulin, glucagon, and epinephrine were determined during 1 h hemorrhagic hypotension at 60 mmHg and 23 h thereafter in fed and two groups of 24-h food-deprived rats receiving either no infusion or 30% glucose intravenously during hemorrhage. Liver glycogen content was reduced by greater than 90% after 24-h food deprivation. Fed and food-deprived rats given glucose developed similar and substantial elevations of blood glucose during hemorrhage, whereas changes in blood glucose were modest in food-deprived rats given no infusion. In fed rats, liver glycogen was reduced by 60% during the 1-h bleed, but within 2 h after hemorrhage repletion of liver glycogen content commenced. By 6 h, approximately 75% of the glycogen lost during hemorrhage had been restored, and 23 h after hemorrhage liver glycogen content was six times greater compared with nonbled controls. Although glycogen levels increased after hemorrhage in food-deprived animals, the increase was negligible compared with that found in fed rats. Infusion of glucose during hemorrhage or adrenergic blockade after hemorrhage did not alter glycogen repletion in food-deprived rats. Posthemorrhage fed animals had high levels of insulin, glucagon, and epinephrine during hemorrhage, whereas insulin levels remained low in food-deprived rats despite exogenously induced hyperglycemia. It is concluded that rapid and substantial glycogen repletion can occur even immediately poststress. The conditions seem to be related to the nutritional state at the time of the insult.
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| 7. |
- McNurlan, Margaret A., et al.
(författare)
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Response of protein synthesis in human skeletal muscle to insulin : an investigation with L[2H5]phenylalanine
- 1994
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Ingår i: American Journal of Physiology. - : American Physiological Society. - 0002-9513 .- 2163-5773. ; 67:Part 1, s. E102-E108
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Tidskriftsartikel (refereegranskat)abstract
- The role of insulin in the regulation of muscle protein synthesis in adult humans has been investigated with intravenous infusion of insulin at levels comparable with those observed after normal feeding. Glucose was also infused to maintain euglycemia. Muscle protein synthesis was measured in six healthy subjects before and during insulin and glucose infusion from the incorporation of L-[H-2(5)]phenylalanine into the protein of vastus lateralis sampled by percutaneous biopsy. L-[H-2(5)]phenylalanine was given as a single injection of a flooding amount (45 mg/kg). The relatively low levels of enrichment of phenylalanine in protein (0.005 atom%) were measured by modified gas chromatography-mass spectrometry and verified by comparison with incorporation of L-[2,6-H-3]phenylalanine. Similarity of enrichment in tissue-free and plasma pools (flooding) and linear incorporation over the period of measurement were also verified. The fractional rate of muscle protein synthesis in the group of postabsorptive subjects was 1.65 +/- 0.11% (SE)/day. The rate was unaltered by insulin and glucose infusion, 1.66 +/- 0.16%/day.
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| 8. |
- Nylander, O, et al.
(författare)
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Duodenal mucosal alkaline secretion, permeability, and blood flow.
- 1993
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Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 265:6 Pt 1, s. G1029-38
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Tidskriftsartikel (refereegranskat)abstract
- The relationship between duodenal mucosal alkaline secretion, permeability, and blood flow was examined in anesthetized rats. Duodenum was perfused with saline, and rate of luminal alkalinization (LA), mucosal permeability (clearance of 51Cr-EDTA from blood to lumen), effluent volume, mean arterial blood pressure (MABP), and blood flow (laser-Doppler flowmetry) were determined. Infusion of vasoactive intestinal polypeptide (VIP, 13.5 micrograms.kg-1 x h-1 i.v.) increased LA and fluid secretion but decreased MABP and mucosal permeability. The concentration of base in the secreted fluid was 45 mM. Systemic infusion of VIP (2.5 micrograms.kg-1 x h-1) increased LA and fluid secretion; the HCO3- concentration in secreted fluid was 86 mM. The lower VIP dose affected neither blood flow nor mucosal permeability. Both intravenous (10 mg/kg + 3 mg.kg-1 x h-1) and intraluminal (3 x 10(-3) M) N omega-nitro-L-arginine (L-NNA) increased LA and effluent volume; the HCO3- concentration in the secreted fluid was 38 and 44 mM, respectively. Intravenous, but not intraluminal, L-NNA increased mucosal permeability and decreased blood flow. Reduction of arterial blood pressure by blood withdrawal or by injection of prazosin (50 micrograms/kg i.v.) or hexamethonium (20 mg/kg i.v.) decreased LA and mucosal permeability. Prazosin decreased blood flow, whereas hexamethonium slightly increased blood flow. We conclude that NO may be an inhibitory regulator of LA and that both L-NNA and VIP increase LA via stimulation of active HCO3- transport. VIP probably increases HCO3- and fluid secretion by two separate ion transport mechanisms. No causal relationship exists between LA and blood flow, between LA and mucosal permeability, or between mucosal permeability and blood flow. A positive linear correlation exists between MABP and mucosal permeability, suggesting that marked changes of MABP may influence permeation of small water-soluble solutes across duodenal mucosa.
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| 9. |
- Nylander, O, et al.
(författare)
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Vasoactive intestinal polypeptide reduces hydrochloric acid-induced duodenal mucosal permeability.
- 1993
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Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 264:2 Pt 1, s. G272-9
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Tidskriftsartikel (refereegranskat)abstract
- The duodenum in anesthetized rats was perfused with HCl, and mucosal integrity was assessed by measuring the clearance of 51Cr-labeled EDTA from blood to lumen and/or by morphological examination (lesion score). Duodenal blood flow was determined by laser Doppler flowmetry and luminal alkalinization as well as H+ disappearance by backtitration. Intravenous infusion of vasoactive intestinal polypeptide (VIP; 13.5 micrograms.kg-1.h-1) increased luminal alkalinization threefold and decreased clearance of 51Cr-EDTA by 50%. VIP also decreased arterial blood pressure and induced a small and irregular decrease in duodenal blood flow. Perfusion with 10 mM HCl increased clearance of 51Cr-EDTA 2.1-fold, but the lesion score was not different from that in saline-perfused animals. Perfusion with 20 mM HCl increased clearance of 51Cr-EDTA four-fold and induced a greater lesion score than did 10 mM. Perfusion with either 10 or 20 mM HCl did not affect the duodenal blood flow. VIP reduced the rise in clearance of 51Cr-EDTA in response to 10 mM but not that to 20 mM HCl. Intravenous injection of prazosin (50 micrograms/kg) decreased luminal alkalinization, clearance of 51Cr-EDTA, blood pressure, and duodenal blood flow. In prazosin-pretreated rats, perfusion with 10 mM HCl increased clearance of 51Cr-EDTA 2.6-fold, and the lesion score was greater in this group than in animals infused with VIP. A positive linear correlation was obtained between HCO3- secretion and the mean rate of H+ disappearance.(ABSTRACT TRUNCATED AT 250 WORDS)
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