scholarly journals Electroacupuncture at Zusanli Prevents Severe Scalds-Induced Gut Ischemia and Paralysis by Activating the Cholinergic Pathway

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Huan Wang ◽  
Lei Wang ◽  
Xian Shi ◽  
Song Qi ◽  
Sen Hu ◽  
...  
Keyword(s):  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Protective Role ◽  
Burn Injuries ◽  
Barrier Dysfunction ◽  
Cholinergic Pathway ◽  
Scald Injury ◽  
Cervical Vagotomy ◽  
Severe Burn Injuries

Severe burn injuries may result in gastrointestinal paralysis, and barrier dysfunction due to gut ischemia and lowered vagus excitability. In this study we investigate whether electroacupuncture (EA) at Zusanli (ST36) could prevent severe scalds-induced gut ischemia, paralysis, and barrier dysfunction and whether the protective role of EA at ST36 is related to the vagus nerve. 35% burn area rats were divided into six groups: (a) EAN: EA nonchannel acupoints followed by scald injury; (b) EA: EA at ST36 after scald injury; (c) VGX/EA: vagotomy (VGX) before EA at ST36 and scald injury; (d) VGX/EAN: VGX before EAN and scald injury; (e) atropine/EA: applying atropine before scald injury and then EA at ST36; (f) atropine/EAN: applying atropine before scald injury and then EA at nonchannel acupoints. EA at the Zusanli point significantly promoted the intestinal impelling ratio and increased the amount of mucosal blood flow after scald injury. The plasma diamine oxidase (DAO) and intestinal permeability decreased significantly after scald injury in the EA group compared with others. However, EA after atropine injection or cervical vagotomy failed to improve intestinal motility and mucosa blood flow suggesting that the mechanism of EA may be related to the activation of the cholinergic nerve pathway.

The Role of Mucosal Blood Flow in the Regulation of Sodium Absorption from the Gut

1976 ◽  
Vol 50 (2) ◽  
pp. 28P-28P ◽  
Author(s):  
A. H. G. Love ◽  
L. C. Chen ◽  
J. Reeve ◽  
N. Veall
Keyword(s):  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Sodium Absorption

Protective role of NO in the regional hemodynamic changes during acute endotoxemia in rats

1994 ◽  
Vol 266 (4) ◽  
pp. H1558-H1564 ◽  
Author(s):  
M. F. Mulder ◽  
A. A. van Lambalgen ◽  
E. Huisman ◽  
J. J. Visser ◽  
G. C. van den Bos ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Saline Group ◽  
Protective Role ◽  
Organ Blood Flow ◽  
Organ Perfusion ◽  
Hemodynamic Changes ◽  
Systemic Blood

The role of NO during the first hour of endotoxemia is still controversial. To evaluate whether NO is protective or detrimental to the regulation of systemic blood pressure, cardiac output (CO), and organ perfusion in rats during acute endotoxemia, we have studied the effects of inhibition of NO synthesis. Thirty minutes after 0.1 mg NG-nitro-L-arginine (L-NNA; group L, n = 7, partial inhibition), 1 mg L-NNA (group H, n = 6, complete inhibition), or saline (group E, n = 7) intravenous infusion, anesthetized volume-loaded rats were infused with endotoxin Escherichia coli O127:B8 (8 mg.kg-1 x h-1) from time (t) = 0 to 60 min. Organ blood flow was measured with radioactive microspheres. In group H, at time 0, CO was lower than in group E (by -29%; P < 0.05), and systemic vascular resistance (SVR) was higher than in groups E and L (by 72 and 51%, respectively; P < 0.05). Perfusion of the pancreas, stomach, intestines, and kidney was lower (P < 0.05) and corresponding organ vascular resistance (OVR) higher (P < 0.05) in group H than in groups E and L (except kidney in group L). At t = 60 min, in groups H and L, CO was lower (by -45 and -26%, respectively; P < 0.05) and SVR was higher (by 112 and 54%, respectively; P < 0.05) than in group E. In group L only blood flow to the heart, pancreas, intestines, and kidney was significantly lower than in group E, and corresponding OVR was higher.(ABSTRACT TRUNCATED AT 250 WORDS)

Cholecystokinin secretagogue-induced gastroprotection: role of nitric oxide and blood flow

2003 ◽  
Vol 284 (3) ◽  
pp. G399-G410 ◽  
Author(s):  
Sonlee D. West ◽  
Kenneth S. Helmer ◽  
Lily K. Chang ◽  
Yan Cui ◽  
George H. Greeley ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Gastric Injury ◽  
Protective Mechanism ◽  
Adaptive Cytoprotection ◽  
Mucosal Defense ◽  
Calcium Dependent

This study was done to examine the role of CCK in gastric mucosal defense and to assess the gastroprotective roles of nitric oxide and blood flow. In rats, the CCK secretagogues oleate and soybean trypsin inhibitor augmented gastric mucosal blood flow and prevented gastric injury from luminal irritants. Type A CCK receptor blockade negated CCK secretagogue-induced gastroprotection and exacerbated gastric injury from bile and ethanol but did not block adaptive cytoprotection. CCK secretagogue-induced gastroprotection and hyperemia were negated by nonselective nitric oxide synthase (NOS) inhibition ( N G-nitro-l-arginine methyl ester) but not by selective inducible NOS inhibition (aminoguanidine). Gastric mucosal calcium-dependent NOS activity, but not calcium-independent NOS activity, was increased following CCK and CCK secretagogues. The release of endogenous CCK plays a role in the intrinsic gastric mucosal defense system against injury from luminal irritants. The protective mechanism appears to involve increased production of nitric oxide from primarily the constitutive isoforms of NOS and a resultant increase in blood flow.

Role of Nitric Oxide in Mucosal Blood Flow Response and the Healing of HCI-lnduced Lesions in the Rat Stomach

Digestion ◽  
1997 ◽  
Vol 58 (1) ◽  
pp. 19-27 ◽  
Author(s):  
K. Takeuchi ◽  
S. Kato ◽  
K. Takehara ◽  
Y. Asada ◽  
T. Yasuhiro
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Rat Stomach ◽  
Blood Flow Response ◽  
Flow Response

Central neurotensin affects rat gastric integrity, prostaglandin E2, and blood flow

1989 ◽  
Vol 256 (1) ◽  
pp. G226-G232 ◽  
Author(s):  
L. Zhang ◽  
P. C. Colony ◽  
J. H. Washington ◽  
J. F. Seaton ◽  
G. L. Kauffman
Keyword(s):  
Blood Flow ◽  
Gastric Mucosa ◽  
Prostaglandin E2 ◽  
Cold Water ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Protective Role ◽  
Mucosal Integrity ◽  
Microscopic Damage ◽  
Dose Dependent

The aim of this study is to define the effect(s) of centrally administered neurotensin (NT) on gastric mucosal integrity, prostaglandin E2 (PGE2) generation, and blood flow during stress induced by cold-water restraint (CWR) in rats. Intracerebroventricular (icv) NT reduced macroscopic and microscopic damage. The former effect was dose dependent and was totally blocked by indomethacin pretreatment. Gastric mucosal PGE2 increased 27 and 30% at 30 and 60 min, respectively, in nonrestrained rats given icv NT. PGE2 generation was reduced in control rats during CWR but was maintained in CWR rats treated with icv NT. Gastric mucosal blood flow (GMBF) was significantly reduced in control rats during CWR. Mucosal blood flow was maintained at nonrestraint levels in the presence of icv NT during CWR; however, this effect was abolished by parenteral indomethacin pretreatment. Similarly, intravenous 16,16-dimethyl-PGE2 (200 micrograms.kg-1.h-1) maintained GMBF of non-CWR levels as well as preventing the macroscopic damage normally associated with CWR. These data suggest a protective role for central NT on the gastric mucosa, mediated, at least in part, by PGE2 generation and gastric mucosal blood flow.

Gastric mucosal blood flow response to stress in streptozotocin diabetic rats: Regulatory role of nitric oxide

1997 ◽  
Vol 32 (6) ◽  
pp. 726-733 ◽  
Author(s):  
Hitoshi Suzuki ◽  
Tooru Shimosegawa ◽  
Akihiko Satoh ◽  
Kenji Kimura ◽  
Shuichi Ohara ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Diabetic Rats ◽  
Blood Flow Response ◽  
Flow Response ◽  
Response To Stress ◽  
Streptozotocin Diabetic Rats
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