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

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

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

Role of Sensory Neurons in the Control of Gastric Mucosal Blood Flow and Protection

1995 ◽  
pp. 1-14
Author(s):  
P. Holzer ◽  
I. Th. Lippe ◽  
M. Jocič ◽  
Ch. Wachter ◽  
R. Amann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sensory Neurons ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow

Role of prostaglandins in regulation of gastric mucosal blood flow and acid secretion

1992 ◽  
Vol 263 (4) ◽  
pp. G446-G451 ◽  
Author(s):  
L. Holm ◽  
A. Jagare
Keyword(s):  
Blood Flow ◽  
Acid Secretion ◽  
Acid Output ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Doppler Flowmetry ◽  
Blood Flow Reduction ◽  
Red Blood Cell Velocity ◽  
Blood Flow Increase

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.

Sign in / Sign up

Export Citation Format

Share Document