Histamine is not involved in pentagastrin-induced gastric mucosal vasodilation in the rat

1994 ◽  
Vol 266 (1) ◽  
pp. G55-G61
Author(s):  
L. Holm ◽  
A. Jagare
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Receptor Antagonist ◽  
Vascular Resistance ◽  
Acid Output ◽  
Gastric Blood Flow ◽  
H2 Receptor Antagonist ◽  
Doppler Flowmetry ◽  
Blood Flow Reduction ◽  
H1 Receptor Antagonist

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.

Effect of topical histamine on mucosal microvascular permeability and acid secretion in the rat stomach

1984 ◽  
Vol 246 (6) ◽  
pp. G654-G659
Author(s):  
H. Nagata ◽  
P. H. Guth
Keyword(s):  
Acid Secretion ◽  
Receptor Antagonist ◽  
Acid Output ◽  
Microvascular Permeability ◽  
H2 Receptor Antagonist ◽  
Beta Adrenergic ◽  
Microscopy Technique ◽  
Adrenergic Antagonist ◽  
H1 Receptor Antagonist

The effect of topical histamine on microvascular permeability to macromolecules was studied in the rat gastric mucosa using a fluorescent in vivo microscopy technique. Acid secretion was measured in the pylorus-ligated rat. A topical dose of 10(-2)M histamine increased acid output to a maximum, which was equal to the maximum values attained by intravenous or subcutaneous histamine. Only in rats pretreated with a beta-adrenergic antagonist did 10(-2) to 5 X 10(-2)M histamine cause leak of a fluorescein-albumin conjugate from mucosal microvessels. Leak occurred around collecting venules but not from capillaries. An H1-receptor antagonist, but not an H2-receptor antagonist, significantly decreased histamine-induced leaks. We concluded the following. 1) topically applied histamine penetrates into the mucosa and can increase acid secretion to the same extent as parenteral histamine. 2) Topical histamine increases microvascular permeability to macromolecules only when beta-adrenergic receptors are blocked. Larger doses of histamine are needed for initiating the permeability change than for initiating the acid secretory response. 3) H1-receptors in venules are involved in the histamine-induced increase in permeability.

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.

eNOS involved in colitis-induced mucosal blood flow increase

2007 ◽  
Vol 293 (6) ◽  
pp. G1281-G1287 ◽  
Author(s):  
Joel Petersson ◽  
Olof Schreiber ◽  
Andreas Steege ◽  
Andreas Patzak ◽  
Anna Hellsten ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Control Level ◽  
Mucosal Blood Flow ◽  
Control Group ◽  
Trinitrobenzene Sulfonic Acid ◽  
Doppler Flowmetry ◽  
Arterial Blood

The role of NO in inflammatory bowel disease is controversial. Studies indicate that endothelial nitric oxide synthase (eNOS) might be involved in protecting the mucosa against colonic inflammation. The aim of this study was to investigate the involvement of nitric oxide (NO) in regulating colonic mucosal blood flow in two different colitis models in rats. In anesthetized control and colitic rats, the distal colon was exteriorized and the mucosa visualized. Blood flow (laser-Doppler flowmetry) and arterial blood pressure were continuously monitored throughout the experiments, and vascular resistance was calculated. Trinitrobenzene sulfonic acid (TNBS) or dextran sulfate sodium (DSS) was used to induce colitis. All groups were given the NOS inhibitor Nω-nitro-l-arginine (l-NNA) or the inducible NOS (iNOS) inhibitor l- N6-(1-iminoethyl)-lysine (l-NIL). iNOS, eNOS, and neuronal NOS (nNOS) mRNA in colonic samples were investigated with real-time RT-PCR. Before NOS inhibition, colonic mucosal blood flow, expressed as perfusion units, was higher in both colitis models compared with the controls. The blood flow was reduced in the TNBS- and DSS-treated rats during l-NNA administration but was not altered in the control group. Vascular resistance increased more in the TNBS- and DSS-treated rats than in the control rats, indicating a higher level of vasodilating NO in the colitis models. l-NIL did not alter blood pressure or blood flow in any of the groups. iNOS and eNOS mRNA increased in both colitis models, whereas nNOS remained at the control level. TNBS- and DSS-induced colitis results in increased colonic mucosal blood flow, most probably due to increased eNOS activity.

Role of histamine H1- and H2-receptors in postprandial intestinal hyperemia

1982 ◽  
Vol 243 (4) ◽  
pp. G248-G252 ◽  
Author(s):  
C. C. Chou ◽  
H. Siregar
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
H1 Receptor ◽  
H2 Receptor Antagonist ◽  
Arterial Infusion ◽  
H2 Receptors ◽  
Before And After ◽  
Anesthetized Dogs ◽  
H1 Receptor Antagonist

Studies were conducted in anesthetized dogs to assess whether histamine H1- and/or H2-receptors play a role in post-prandial intestinal hyperemia. The vascular and metabolic responses of jejunal segments to intra-arterial infusion of histamine and luminal placement of food before and after administration of tripelennamine, an H1-receptor antagonist, metiamide, an H2-receptor antagonist, and the combination of both antagonists were compared. Administration of the antagonists had no effect of jejunal blood flow and intestinal oxygen uptake (VO2). Tripelennamine or metiamide alone attenuated while the combination of both blocked the histamine-induced increases in blood flow and VO2. Metamide alone had no effect on the food-induced increases in flow and VO2. Tripelennamine significantly attenuated the food-induced increase in flow and blocked the increase in VO2. A 30% increase in flow was reduced to 15% after tripelennamine. The effects of tripelennamine plus metiamide were statistically the same as those of tripelennamine alone. It is concluded that endogenous histamines may play a role in postprandial intestinal hyperemia, and the effect is primarily mediated by the H1-receptors.

scholarly journals Famotidine prevents canine gastric blood flow reduction by NSAIDs

2005 ◽  
Vol 21 (s2) ◽  
pp. 55-59 ◽  
Author(s):  
J. Hata ◽  
T. Kamada ◽  
N. Manabe ◽  
H. Kusunoki ◽  
D. Kamino ◽  
...  
Keyword(s):  
Blood Flow ◽  
Gastric Blood Flow ◽  
Flow Reduction ◽  
Blood Flow Reduction

Forearm and finger blood flow responses to passive body tilts

1979 ◽  
Vol 46 (2) ◽  
pp. 288-292 ◽  
Author(s):  
Y. A. Mengesha ◽  
G. H. Bell
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Pulse Rate ◽  
Forearm Blood Flow ◽  
Body Tilt ◽  
Finger Blood Flow ◽  
Arterial Blood ◽  
Forearm Vascular Resistance

Ten to fifteen healthy subjects, ages 18--30 yr, were used to assess the correlation of forearm blood flow with graded passive body tilts and vascular resistance and also to discern the relative effects of body tilts on finger blood flow. In the head-up tilts forearm blood flow and arterial blood pressure fell progressively, whereas forearm vascular resistance and pulse rate increased. In the head-down tilts the forearm blood flow and the arterial blood pressure increased, whereas the forearm vascular resistance and pulse rate decreased. These changes were found to be significantly correlated with the different tilt angles and with one another. In a preliminary study it was found that infrared heating of the carpometacarpal region produced finger vasodilatation similar to the forearm vasodilatation observed by Crockford and Hellon (6). However, unlike forearm blood flow, finger blood flow showed no appreciable response to either the head-up or head-down tilts. This indicates that the sympathetic tone and the volume of blood in the finger are not appreciably altered by this test procedure at least 1 min after the body tilt is assumed.

scholarly journals Minimal role for H1 and H2 histamine receptors in cutaneous thermal hyperemia to local heating in humans

2006 ◽  
Vol 100 (2) ◽  
pp. 535-540 ◽  
Author(s):  
Brett J. Wong ◽  
Sarah J. Williams ◽  
Christopher T. Minson
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Histamine Receptor ◽  
Receptor Activation ◽  
Control Site ◽  
Doppler Flowmetry ◽  
Histamine Receptor Antagonist ◽  
And Control

The precise mechanism(s) underlying the thermal hyperemic response to local heating of human skin are not fully understood. The purpose of this study was to investigate a potential role for H1 and H2 histamine-receptor activation in this response. Two groups of six subjects participated in two separate protocols and were instrumented with three microdialysis fibers on the ventral forearm. In both protocols, sites were randomly assigned to receive one of three treatments. In protocol 1, sites received 1) 500 μM pyrilamine maleate (H1-receptor antagonist), 2) 10 mM l-NAME to inhibit nitric oxide synthase, and 3) 500 μM pyrilamine with 10 mM NG-nitro-l-arginine methyl ester (l-NAME). In protocol 2, sites received 1) 2 mM cimetidine (H2 antagonist), 2) 10 mM l-NAME, and 3) 2 mM cimetidine with 10 mM l-NAME. A fourth site served as a control site (no microdialysis fiber). Skin sites were locally heated from a baseline of 33 to 42°C at a rate of 0.5°C/5 s, and skin blood flow was monitored using laser-Doppler flowmetry (LDF). Cutaneous vascular conductance was calculated as LDF/mean arterial pressure. To normalize skin blood flow to maximal vasodilation, microdialysis sites were perfused with 28 mM sodium nitroprusside, and control sites were heated to 43°C. In both H1 and H2 antagonist studies, no differences in initial peak or secondary plateau phase were observed between control and histamine-receptor antagonist only sites or between l-NAME and l-NAME with histamine receptor antagonist. There were no differences in nadir response between l-NAME and l-NAME with histamine-receptor antagonist. However, the nadir response in H1 antagonist sites was significantly reduced compared with control sites, but there was no effect of H2 antagonist on the nadir response. These data suggest only a modest role for H1-receptor activation in the cutaneous response to local heating as evidenced by a diminished nadir response and no role for H2-receptor activation.

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

Vasoactive intestinal polypeptide reduces hydrochloric acid-induced duodenal mucosal permeability

1993 ◽  
Vol 264 (2) ◽  
pp. G272-G279 ◽  
Author(s):  
O. Nylander ◽  
E. Wilander ◽  
G. M. Larson ◽  
L. Holm
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Vasoactive Intestinal Polypeptide ◽  
Lesion Score ◽  
Morphological Examination ◽  
Mucosal Permeability ◽  
Doppler Flowmetry ◽  
Arterial Blood ◽  
51Cr Edta ◽  
Intestinal Polypeptide

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)

Changes in Blood Pressure in the Rainbow Trout During Hypoxia

1967 ◽  
Vol 46 (2) ◽  
pp. 297-305 ◽  
Author(s):  
G. F. HOLETON ◽  
D. J. RANDALL
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Rainbow Trout ◽  
Vascular Resistance ◽  
Ventral Aorta

1. Methods for cannulating the ventral aorta of the trout, which permit the measurement of blood pressure in the unanaesthetized, unrestrained, intact fish are described. 2. Rate and amplitude of breathing and blood pressure in the dorsal and ventral aortae increase during hypoxia. These changes are associated with a marked bradycardia. 3. There are increases in vascular resistance to blood flow in both respiratory and systemic circulations during hypoxia. 4. Post hypoxia is associated with large increases in ventral aortic and dorsal aortic pressures.

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