A novel in vitro model of Brunner's gland secretion in the guinea pig duodenum

2000 ◽  
Vol 278 (3) ◽  
pp. G477-G485 ◽  
Author(s):  
Beverley A. Moore ◽  
Gerald P. Morris ◽  
Stephen Vanner
Keyword(s):  
Guinea Pig ◽  
In Vitro Model ◽  
Gland Secretion ◽  
Luminal Diameter ◽  
Brunner's Glands ◽  
Brunner’S Glands ◽  
Brunner’S Gland ◽  
Vitro Model ◽  
Brunner's Gland

A novel in vitro model that combined functional and morphological techniques was employed to directly examine pathways regulating Brunner's gland secretion in isolation from epithelium. In vitro submucosal preparations were dissected from guinea pig duodenum. A videomicroscopy technique was used to measure changes in luminal diameter of glandular acini as an index of activation of secretion. Carbachol elicited concentration-dependent dilations of the lumen (EC50= 2 μM) by activating muscarinic receptors on acinar cells. Ultrastructural and histological analyses demonstrated that dilation was accompanied by single and compound exocytosis of mucin-containing granules and the accumulation of mucoid material within the lumen. Inflammatory mediators (histamine, PGE1, PGE2) and intestinal hormones (CCK, gastrin, vasoactive intestinal polypeptide, secretin) also stimulated glandular secretion, whereas activation of submucosal secretomotor neurons by 5-hydroxytryptamine did not. This study directly demonstrates that multiple hormonal, inflammatory, and neurocrine agents activate Brunner's glands, whereas many have dissimilar effects on the epithelium. This suggests that Brunner's glands are regulated by pathways that act both in parallel to and in isolation from those controlling epithelial secretion.

A pharmacodynamic study on clenbuterol-induced toxicity: β1- and β2-adrenoceptors involvement in guinea-pig tachycardia in an in vitro model

2007 ◽  
Vol 45 (9) ◽  
pp. 1694-1699 ◽  
Author(s):  
Gabriela Mazzanti ◽  
Antonella Di Sotto ◽  
Claudia Daniele ◽  
Lucia Battinelli ◽  
Gianfranco Brambilla ◽  
...  
Keyword(s):  
Guinea Pig ◽  
In Vitro Model ◽  
Pharmacodynamic Study ◽  
Vitro Model

Antiarrhythmic Effects of Ranolazine in a Guinea Pig in Vitro Model of Long-QT Syndrome

2004 ◽  
Vol 310 (2) ◽  
pp. 599-605 ◽  
Author(s):  
Lin Wu ◽  
John C. Shryock ◽  
Yejia Song ◽  
Yuan Li ◽  
Charles Antzelevitch ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Long Qt Syndrome ◽  
In Vitro Model ◽  
Long Qt ◽  
Qt Syndrome ◽  
Vitro Model ◽  
Antiarrhythmic Effects

Potassium currents regulating secretion from Brunner's glands in guinea pig duodenum

2004 ◽  
Vol 286 (3) ◽  
pp. G377-G384 ◽  
Author(s):  
Jason Kovac ◽  
Beverley Moore ◽  
Stephen Vanner
Keyword(s):  
Guinea Pig ◽  
Basolateral Membrane ◽  
Acinar Cells ◽  
Resting Membrane Potential ◽  
Channel Blockers ◽  
Membrane Hyperpolarization ◽  
Brunner's Glands ◽  
Brunner’S Glands ◽  
External K

This study examined the role of outward K+ currents in the acinar cells underlying secretion from Brunner's glands in guinea pig duodenum. Intracellular recordings were made from single acinar cells in intact acini in in vitro submucosal preparations, and videomicroscopy was employed in the same preparation to correlate these measures with secretion. Mean resting membrane potential was -74 mV and was depolarized by high external K+ (20 mM) and the K+ channel blockers 4-aminopyridine (4-AP), quinine, and clotrimazole. The cholinergic agonist carbachol (60–2,000 nM; EC50 = 200 nM) caused a concentration-dependent initial hyperpolarization of the membrane and an associated decrease in input resistance. This hyperpolarization was significantly decreased by 20 mM external K+ or membrane hyperpolarization and increased by 1 mM external K+ or membrane depolarization. It was blocked by the K+ channel blockers tetraethylammonium (TEA), 4-AP, quinine, and clotrimazole but not iberiotoxin. When videomicroscopy was employed to measure dilation of acinar lumen in the same preparation, carbachol-evoked dilations were altered in a parallel fashion when external K+ was altered. The dilations were also blocked by the K+ channel blockers TEA, 4-AP, quinine, and clotrimazole but not iberiotoxin. These findings suggest that activation of outward K+ currents is fundamental to the initiation of secretion from these glands, consistent with the model of K+ efflux from the basolateral membrane providing the driving force for secretion. The pharmacological profile suggests that these K+ channels belong to the intermediate conductance group.

scholarly journals P640New in vitro model for proarrhythmia screening: iks inhibition potentiates the qtc prolonging effect of ikr inhibitors in isolated guinea pig hearts

2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S116.4-S116
Author(s):  
P Kui ◽  
SZ Orosz ◽  
A Sarusi ◽  
CS Cseko ◽  
T Forster ◽  
...  
Keyword(s):  
Guinea Pig ◽  
In Vitro Model ◽  
Vitro Model

An indomethacin-sensitive contraction induced by β-antagonists in guinea pig airways

2004 ◽  
Vol 82 (6) ◽  
pp. 393-401
Author(s):  
Fredrik Johansson ◽  
Rolf G.G Andersson ◽  
Eva Lindström ◽  
Samuel S Svensson
Keyword(s):  
Guinea Pig ◽  
Adrenergic Receptor ◽  
In Vitro Model ◽  
Smooth Muscle Contraction ◽  
Lipoxygenase Inhibitor ◽  
Airway Reactivity ◽  
Contractile Effect ◽  
Vitro Model ◽  
Additional Explanation

β-adrenergic receptor (β-AR) antagonists have been associated with increased airway reactivity in asthmatics and potentiation of contractile stimuli in animal models. In the present study, using an in vitro model of tracheal preparations from guinea pigs, we show that the β-AR antagonists propranolol and pindolol induce a smooth muscle contraction. A prerequisite for this contraction is that the airway preparations have been pre-treated with an β-AR agonist. Our data show that the contractile effect of β-AR antagonists is not a simple consequence of reversing the agonist-induced relaxation. Furthermore, the effect seems to be mediated through interaction with β2-ARs since the response is stereo-selective, and the selective β1-AR receptor antagonist atenolol did not induce any contractile response. SQ 29,546, a thromboxane A2 antagonist; MK 886, a lipoxygenase inhibitor; and indomethacin, a cyclooxygenase inhibitor significantly inhibited the contractions of the tracheal preparations induced with propranolol or pindolol. We put forward the hypothesis that the contractile effect of the β-AR antagonist is a consequence of their inverse agonist activity, which is only evident when the receptor population have a higher basal activity. Our results indicate a novel additional explanation for the known side effect, bronchoconstriction, of β-AR antagonist.Key words: beta antagonist, guinea pig trachea, propranolol, formoterol, pindolol, indomethacin.

scholarly journals Large Brunner’s gland adenoma of the duodenum for almost 10 years

2020 ◽  
Vol 15 (1) ◽  
pp. 237-240
Author(s):  
Bo Yang ◽  
Ke Li ◽  
Runlan Luo ◽  
Zuming Xiong ◽  
Lianwei Wang ◽  
...  
Keyword(s):  
Benign Tumor ◽  
Accurate Diagnosis ◽  
Case Presentation ◽  
Brunner's Glands ◽  
Gastrointestinal Obstruction ◽  
Brunner’S Glands ◽  
Rare Benign Tumor ◽  
Brunner’S Gland ◽  
Brunner's Gland ◽  
Upper Gastrointestinal

AbstractBackgroundBrunner’s gland adenoma is a rare benign tumor arising from Brunner’s glands. It is mostly small in size, and patients with this tumor are asymptomatic.Case presentationWe report the case of a 63-year-old woman with upper gastrointestinal obstruction for almost 10 years, who was pathologically diagnosed with large Brunner’s gland adenoma of the duodenum. Postoperatively, no sign of recurrence has been noted until now.ConclusionThis study may help clinicians to understand and provide a more accurate diagnosis of Brunner’s gland adenoma.

Proarrhythmic and Antiarrhythmic Effects of Bupivacaine in an In Vitro Model of Myocardial Ischemia and Reperfusion 

1998 ◽  
Vol 88 (5) ◽  
pp. 1318-1329 ◽  
Author(s):  
Sandra Picard ◽  
Rene Rouet ◽  
Frederic Flais ◽  
Pierre Ducouret ◽  
Gerard Babatasi ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Guinea Pig ◽  
In Vitro Model ◽  
Cardiovascular Effects ◽  
Control Group ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion ◽  
Simulated Ischemia ◽  
Vitro Model

Background Bupivacaine may have toxic cardiovascular effects when accidentally administered by intravascular injection. However, its electrophysiologic effects in the presence of myocardial ischemia remain unknown. The authors evaluated the electrophysiologic and anti- and proarrhythmic effects of bupivacaine in an in vitro model of the ischemic and reperfused myocardium. Methods In a double-chamber bath, a guinea pig right ventricular muscle strip was subjected partly to normal conditions and partly to simulated ischemia followed by reperfusion. The electrophysiologic effects of bupivacaine were studied at 1, 5, and 10 microM concentrations. Results Bupivacaine (5 and 10 microM) decreased the maximal upstroke velocity of the action potential (Vmax) in normoxic conditions and further decreased (10 microM) the Vmax decrease induced by ischemic conditions. Bupivacaine reduced the mean occurrence time to the onset of myocardial conduction blocks (9 +/- 3 min; mean +/- SD; P < 0.005 with 5 and 10 microM, compared with 17 +/- 6 min during simulated ischemia with no drug or control), and it increased the number of preparations that became inexcitable to pacing (55% of preparations, with 1 microM and 100% with 5 and 10 microM, compared with 17% for the control group). The incidence of spontaneous arrhythmias was reduced by 5 and 10 microM bupivacaine during ischemia and reperfusion and was enhanced by 1 microM bupivacaine during the ischemic phase. Conclusions In guinea pig myocardium under ischemic conditions, bupivacaine induced a loss of excitability at concentrations of 5 and 10 microM. Proarrhythmic effects observed at 1 microM were considered as lower than the cardiotoxic range in normoxic conditions. The incidence of reperfusion arrhythmias was decreased at all concentrations.

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