Treatment of gastric ulcers and diarrhea with the Amazonian herbal medicine sangre de grado

2000 ◽  
Vol 279 (1) ◽  
pp. G192-G200 ◽  
Author(s):  
Mark J. S. Miller ◽  
Wallace K. MacNaughton ◽  
Xiao-Jing Zhang ◽  
Jane H. Thompson ◽  
Randi M. Charbonnet ◽  
...  
Keyword(s):  
Herbal Medicine ◽  
Cost Effective ◽  
Electrical Field Stimulation ◽  
Skin Lesions ◽  
Gastric Ulcers ◽  
Myeloperoxidase Activity ◽  
Field Stimulation ◽  
Electrical Field ◽  
Ussing Chambers ◽  
Cost Effective Treatment

Sangre de grado is an Amazonian herbal medicine used to facilitate the healing of gastric ulcers and to treat gastritis, diarrhea, skin lesions, and insect stings. This study was designed to evaluate the gastrointestinal applications. Gastric ulcers were induced in rats by brief serosal exposure of the fundus to acetic acid (80%). Sangre de grado was administered in drinking water at 1:1,000 and 1:10,000 dilutions from the postoperative period to day 7. Guinea pig ileum secretory responses to capsaicin, electrical field stimulation, and the neurokinin-1 (NK-1) agonist [Sar9,Met(O2)11]substance P were examined in Ussing chambers. Sangre de grado facilitated the healing of experimental gastric ulcer, reducing myeloperoxidase activity, ulcer size, and bacterial content of the ulcer. The expression of proinflammatory genes tumor necrosis factor-α, inducible nitric oxide synthase (iNOS), interleukin (IL)-1β, IL-6, and cyclooxygenase-2 was upregulated by ulcer induction but reduced by sangre de grado treatment, particularly iNOS and IL-6. In Ussing chambers, sangre de grado impaired the secretory response to capsaicin but not to electrical field stimulation or the NK-1 agonist. We conclude that sangre de grado is a potent, cost-effective treatment for gastrointestinal ulcers and distress via antimicrobial, anti-inflammatory, and sensory afferent-dependent actions.

Regulation of intestinal goblet cell secretion. IV. Electrical field stimulation in vitro

1984 ◽  
Vol 247 (6) ◽  
pp. G682-G687 ◽  
Author(s):  
T. E. Phillips ◽  
T. H. Phillips ◽  
M. R. Neutra
Keyword(s):  
Cholinergic Neurons ◽  
Electrical Field Stimulation ◽  
Goblet Cells ◽  
Mucus Secretion ◽  
Enteric Neurons ◽  
Field Stimulation ◽  
Cell Secretion ◽  
Electrical Field ◽  
Ussing Chambers

To determine whether transmitters released from enteric neurons can elicit secretion from goblet cells, full-thickness sheets of adult rat distal ileum or descending colon were mounted in modified Ussing chambers, and mucus secretion was assessed morphologically after electrical field stimulation (EFS). Square-wave pulses (56 V, 2 ms duration) were delivered at 10 Hz for 5 min. Goblet cells in colonic crypts, but not those on the mucosal surface, secreted mucus in response to EFS. This secretion was at least in part atropine insensitive, indicating a noncholinergic mechanism. In the ileum goblet cells located in the crypts, but not on villi, secreted mucus when tissue was mounted in the chamber, even in the absence of EFS. This “unelicited” secretion did not occur in unmounted control tissue in vitro, and it could be prevented by preincubating ileal tissue in 1 microM tetrodotoxin (TTX) or 10 microM atropine for 15 min before mounting. Furthermore, following preincubation with either TTX or atropine, EFS' failed to elicit secretion. Incubation of unmounted tissue with TTX, however, did not block the secretory response of crypt goblet cells to 20 microM carbachol. Thus, intrinsic cholinergic neurons may be sxtimulated during the mounting of the ileum in the chamber. Taken together, these data demonstrate that mucus secretion from crypt goblet cells may be regulated by cholinergic (in ileum and perhaps colon) and noncholinergic (in colon) elements of the enteric nervous system.

Further studies on the motor response of the human isolated urinary bladder to tachykinins, capsaicin and electrical field stimulation

1989 ◽  
Vol 20 (5) ◽  
pp. 663-669 ◽  
Author(s):  
Carlo Alberto Maggi ◽  
Riccardo Patacchini ◽  
Paolo Santicioli ◽  
Damiano Turini ◽  
Gabriele Barbanti ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Motor Response ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Electrical Field

Pharmacologic responses of the mouse urinary bladder

Open Medicine ◽  
2009 ◽  
Vol 4 (2) ◽  
pp. 192-197 ◽  
Author(s):  
A. Canda ◽  
Christopher Chapple ◽  
Russ Chess-Williams
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Minor Role ◽  
Detrusor Muscle ◽  
Field Stimulation ◽  
Muscarinic Agonists ◽  
Electrical Field ◽  
M3 Receptor

AbstractThe aim of the study was to determine pathways involved in contraction and relaxation of the mouse urinary bladder. Mouse bladder strips were set up in gassed Krebs-bicarbonate solution and responses to various drugs and electrical field stimulation were obtained. Isoprenaline (b-receptor agonist) caused a 63% inhibition of carbachol precontracted detrusor (EC50=2nM). Carbachol caused contraction (EC50=0.3µM), responses were antagonised more potently by 4-DAMP (M3-antagonist) than methoctramine (M2-antagonist). Electrical field stimulation caused contraction, which was inhibited by atropine (60%) and less by guanethidine and α,β-methylene-ATP. The neurogenic responses were not potentiated by inhibition of nitric oxide synthase. Presence of an intact urothelium significantly depressed responses to carbachol (p=0.02) and addition of indomethacin and L-NNA to remove prostaglandin and nitric oxide production respectively did not prevent the inhibitory effect of the urothelium. In conclusion, b-receptor agonists cause relaxation and muscarinic agonists cause contraction via the M3-receptor. Acetylcholine is the main neurotransmitter causing contraction while nitric oxide has a minor role. The mouse and human urothelium are similar in releasing a factor that inhibits contraction of the detrusor muscle which is unidentified but is not nitric oxide or a prostaglandin. Therefore, the mouse may be used as a model to study the lower urinary tract.

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