The effect of pitressin on esophageal blood flow of the dog

1991 ◽  
Vol 69 (12) ◽  
pp. 1810-1813 ◽  
Author(s):  
S. F. White ◽  
P. K. Dinda ◽  
I. T. Beck
Keyword(s):  
Blood Flow ◽  
Lower Esophageal Sphincter ◽  
Intravenous Infusion ◽  
Striated Muscle ◽  
Partial Agonist ◽  
Venous Pressure ◽  
The Body ◽  
Portal Venous Pressure ◽  
Squamous Mucosa ◽  
Esophageal Sphincter

In a previous study on canine esophagus, we reported that intravenous infusion of isoproterenol caused mucosal (i.e., mucosal + submucosal) vasodilation only in the lower esophageal sphincter (but not in the body) and muscularis vasodilation only in the body (not in the lower esophageal sphincter). In the present study, we have investigated in dogs whether these esophageal tissues also exhibit a similar difference in their vasoconstrictory response to intravenous infusion of pitressin. All measurements were made before (basal) and after infusion of 0.02 U pitressin∙min−1∙kg−1 for 15 min. Pitressin significantly decreased portal venous pressure and blood flow, and increased vascular resistance of all tissues of the esophagus. This vasoconstriction of the tissues, however, was higher in the squamous mucosa of the body than in the columnar mucosa of the lower esophageal sphincter. In contrast, it was higher in the smooth muscle of the lower esophageal sphincter than in the striated muscle of the body. These data together with those of our previous report on isoproterenol demonstrate that pitressin causes a pronounced vasoconstriction in those esophageal tissues where isoproterenol had no effect. Conversely, pitressin causes least vasoconstriction in those tissues where isoproterenol produced a significant vasodilation. These differences could be the result of partial agonist actions or differences in receptor density or in receptor-effector coupling mechanism.Key words: microspheres, portal venous pressure, esophageal body, lower esophageal sphincter.

Gastrointestinal blood flow in the opossum with special reference to the esophagus

1990 ◽  
Vol 68 (9) ◽  
pp. 1221-1225 ◽  
Author(s):  
Folkert G. Zijlstra ◽  
Taimi T. Hynna-Liepert ◽  
P. K. Dinda ◽  
Ivan T. Beck ◽  
William G. Paterson
Keyword(s):  
Animal Model ◽  
Blood Flow ◽  
Smooth Muscle ◽  
Gastrointestinal Tract ◽  
Lower Esophageal Sphincter ◽  
Striated Muscle ◽  
Muscularis Propria ◽  
Distal Esophagus ◽  
Muscle Fibres ◽  
Esophageal Sphincter

The opossum esophagus, like that of the human, is composed of striated muscle fibres proximally and smooth muscle fibres distally. Because of this similarity the opossum has been used extensively as an animal model for esophageal studies, but to date no data on esophageal blood flow have been reported in this species. The purpose of this study was to establish the basal blood flow characteristics of different regions of the opossum gastrointestinal tract with particular reference to the esophagus. Intracardiac injection of 15-μm microspheres was used to provide an estimate of blood flow (mL∙min−1∙g−1 dry tissue) to the whole wall, the combined layer of mucosa plus submucosa, and the muscularis propria. Basal blood flow in the whole tissue and mucosa–submucosa was significantly higher in the lower esophageal sphincter than in the proximal or distal esophagus. The muscularis propria blood flow displayed an aborally increasing gradient with flow to proximal esophagus (striated muscle) < distal esophagus (smooth muscle) < lower esophageal sphincter. Regional differences in blood flow to other regions of the gastrointestinal tract were similar to that described in other species. In addition, no changes in basal blood flow occurred despite repeated microsphere injections, suggesting that this species provides a good animal model for the study of gastrointestinal blood flow.Key words: microspheres, blood flow, esophagus, stomach, intestine.

Effect of portal hypertension on splenic blood flow, intrasplenic extravasation and systemic blood pressure

2003 ◽  
Vol 284 (6) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Susan Kaufman ◽  
Jody Levasseur
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Systemic Blood Pressure ◽  
Portal Venous Pressure ◽  
Systemic Blood ◽  
Fluid Extravasation

We have previously shown that intrasplenic fluid extravasation is important in controlling blood volume. We proposed that, because the splenic vein flows in the portal vein, portal hypertension would increase splenic venous pressure and thus increase intrasplenic microvascular pressure and fluid extravasation. Given that the rat spleen has no capacity to store/release blood, intrasplenic fluid extravasation can be estimated by measuring the difference between splenic arterial inflow and venous outflow. In anesthetized rats, partial ligation of the portal vein rostral to the junction with the splenic vein caused portal venous pressure to rise from 4.5 ± 0.5 to 12.0 ± 0.9 mmHg ( n = 6); there was no change in portal venous pressure downstream of the ligation, although blood flow in the liver fell. Splenic arterial flow did not change, but the arteriovenous flow differential increased from 0.8 ± 0.3 to 1.2 ± 0.1 ml/min ( n = 6), and splenic venous hematocrit rose. Mean arterial pressure fell (101 ± 5.5 to 95 ± 4 mmHg). Splenic afferent nerve activity increased (5.6 ± 0.9 to 16.2 ± 0.7 spikes/s, n = 5). Contrary to our hypothesis, partial ligation of the portal vein caudal to the junction with the splenic vein (same increase in portal venous pressure but no increase in splenic venous pressure) also caused the splenic arteriovenous flow differential to increase (0.6 ± 0.1 to 1.0 ± 0.2 ml/min; n = 8). The increase in intrasplenic fluid efflux and the fall in mean arterial pressure after rostral portal vein ligation were abolished by splenic denervation. We propose there to be an intestinal/hepatic/splenic reflex pathway, through which is mediated the changes in intrasplenic extravasation and systemic blood pressure observed during portal hypertension.

The Effect of Intravenous Infusion of Synthetic Human Gastrin-I on Lower Esophageal Sphincter (LES) Pressure in the Dog and its Relation to Gastrin Level

Digestion ◽  
1976 ◽  
Vol 14 (4) ◽  
pp. 376-380 ◽  
Author(s):  
H.M. Jennewein ◽  
H. Hummelt ◽  
R. Siewert ◽  
F. Waldeck
Keyword(s):  
Lower Esophageal Sphincter ◽  
Intravenous Infusion ◽  
Gastrin Level ◽  
Esophageal Sphincter ◽  
Human Gastrin

Effects of Hct and norepinephrine on segmental vascular resistance distribution in isolated perfused rat livers

2004 ◽  
Vol 286 (1) ◽  
pp. H121-H130 ◽  
Author(s):  
Chiaki Kamikado ◽  
Toshishige Shibamoto ◽  
Minoru Hongo ◽  
Shozo Koyama
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Regression Line ◽  
Venous Occlusion ◽  
Portal Venous Pressure ◽  
Venous Resistance ◽  
Four Levels ◽  
Rat Livers ◽  
Line Analysis

We studied the effects of blood hematocrit (Hct), blood flow, or norepinephrine on segmental vascular resistances in isolated portally perfused rat livers. Total portal hepatic venous resistance ( Rt) was assigned to the portal ( Rpv), sinusoidal ( Rsinus), and hepatic venous ( Rhv) resistances using the portal occlusion (Ppo) and the hepatic venous occlusion (Phvo) pressures that were obtained during occlusion of the respective line. Four levels of Hct (30%, 20%, 10%, and 0%) were studied. Rpv comprises 44% of Rt, 37% of Rsinus, and 19% of Rhv in livers perfused at 30% Hct and portal venous pressure of 9.1 cmH2O. As Hct increased at a given blood flow, all three segmental vascular resistances of Rpv, Rsinus, and Rhv increased at flow >15 ml/min. As blood flow increased at a given Hct, only Rsinus increased without changes in Rpv or Rhv. Norepinephrine increased predominantly Rpv, and, to a smaller extent, Rsinus, but it did not affect Rhv. Finally, we estimated Ppo and Phvo from the double occlusion maneuver, which occluded simultaneously both the portal and hepatic venous lines. The regression line analysis revealed that Ppo and Phvo were identical with those measured by double occlusion. In conclusion, changes in blood Hct affect all three segmental vascular resistances, whereas changes in blood flow affect Rsinus, but not Rpv or Rhv. Norepinephrine increases mainly presinusoidal resistance. Ppo and Phvo can be obtained by the double occlusion method in isolated perfused rat livers.

Effect of prostaglandin E2 on esophageal motility in man

1975 ◽  
Vol 39 (3) ◽  
pp. 479-481 ◽  
Author(s):  
A. Mukhopadhyay ◽  
S. Rattan ◽  
R. K. Goyal
Keyword(s):  
Prostaglandin E2 ◽  
Lower Esophageal Sphincter ◽  
Esophageal Motility ◽  
Lower Esophageal Sphincter Pressure ◽  
Upper Esophageal Sphincter ◽  
The Body ◽  
Inhibitory Influence ◽  
Sphincter Pressure ◽  
Esophageal Sphincter ◽  
Peristaltic Contractions

Studies were performed to investigate the effect of prostaglandin E2 on esophageal motility in 12 healthy volunteers. PGE2 infusion caused a dose-dependent reduction in the lower esophageal sphincter pressure. The threshold dose was less than 0.05 mug-kg-1-min-1 and maximal reduction of pressure (60%) occurred with a dose of 0.4 mug-kg-1-min-1. In contrast to its effect on the lower esophageal sphincter, PGE2 did not alter the pressure in the upper esophageal sphincter. PGE2 did not influence resting esophageal pressures; the amplitude of peristaltic contractions was reduced in the lower but not in the upper part of the body of the esophagus. These studies show that in man PGE2 exerts selective inhibitory influence on the activity of the lower part of the esophagus and lower esophageal sphincter which are composed of smooth muscle fibers.

scholarly journals The relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver

Gut ◽  
1998 ◽  
Vol 42 (2) ◽  
pp. 276-282 ◽  
Author(s):  
X Li ◽  
I S Benjamin ◽  
B Alexander
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Steady State ◽  
Portal Vein ◽  
Rat Liver ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Portal Vein Ligation ◽  
The Relationship ◽  
Wedged Hepatic Venous Pressure

Background—Portal hypertension is associated with gross haemodynamic disturbances characterised by high cardiac output, low peripheral vascular resistance, increased splanchnic blood flow, and portal systemic shunting.Aims—To study the relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver.Methods—Different sized microspheres were sequentially injected into the portal vein of male Wistar rats.Results—Steady state portal venous pressure was increased by 102.2 (35.6)% (14.9 (3.6) mm Hg) and 272.3 (78.0)% (24.0 (2.2) mm Hg) above the basal pressure following sequential injections of 15 and 80 μm diameter microspheres, respectively. Sequential injection of 15, 40, and 80 μm diameter microspheres in either ascending or descending order of size did not generate further increases in portal venous pressure. A single injection of 1.8 × 105 80 μm microspheres consistently produced a steady state portal venous pressure of 19.0 (1.3) mm Hg but did not approach the much higher value of 36.6 (43.2) mm Hg measured during clamping of the portal vein. These data indicate that the opening of patent intrahepatic shunts was responsible for the reduced pressures observed during microsphere injections and further evidence for this was provided by the location of microspheres in the pulmonary vascular bed. The elevation in portal venous pressure achieved by microsphere injections was not significantly different to that produced in rats subjected to partial portal vein ligation (20.7 (0.5) mm Hg, p>0.05). Wedged hepatic venous pressure decreased from 6.7 (0.7) to 3.0 (0.6) mm Hg following injection of 80 μm microspheres, suggesting a decrease in total hepatic blood flow. Conversely, injection of 15 μm microspheres induced an increase in wedged hepatic venous pressure from 7.0 (1.0) mm Hg to 12.4 (1.8) mm Hg, indicating a localised redistribution of blood flow at the presinusoidal level of the portal venous vascular network and increased intrahepatic shunt flow.Conclusion—It is suggested that there may be a protective pathophysiological role for these shunts when the liver is subjected to changes which induce acute portal hypertension.

Nifedipine Has No Effect on Liver Blood Flow or Portal Venous Pressure

InPharma ◽  
1988 ◽  
Vol 641 (1) ◽  
pp. 16-16
Keyword(s):  
Blood Flow ◽  
Venous Pressure ◽  
Liver Blood Flow ◽  
Portal Venous Pressure

Calf blood flow and oxygen usage during bradykinin infusions

1963 ◽  
Vol 18 (5) ◽  
pp. 1003-1007 ◽  
Author(s):  
Jay D. Coffman ◽  
Stanley L. Javett
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Intravenous Infusion ◽  
Capillary Blood ◽  
The Body ◽  
Oxygen Utilization ◽  
Arterial Infusion ◽  
Calf Blood Flow ◽  
Arteriovenous Shunts ◽  
Rapid Destruction

The effects of continuous intra-arterial and intravenous infusion of synthetic bradykinin on plethysmographic calf blood flow and radioisotope disappearance rates from skeletal muscle, and on calf oxygen utilization in man were studied. The plethysmographic findings during intra-arterial infusion of bradykinin demonstrated a large increase in the total calf blood flow. The radioisotope disappearance rates indicated that skeletal muscle capillary blood flow was definitely involved and that bradykinin does not act on arteriovenous shunts alone. The response to continuous infusion may be transient, sustained, or intermittent, depending largely upon the dose. During continuous intra-arterial infusions of bradykinin, the oxygen utilization changes were variable but, after 5–10 min, were not statistically significant compared to control values. The lack of effect of intravenous infusion and the rapid return of flow to control levels when intra-arterial injections are discontinued confirm the rapid destruction of the endogenous polypeptide in the body. Submitted on February 7, 1963

Effects of nonshunting operations on portal venous pressure and hepatic blood flow

1987 ◽  
Vol 153 (3) ◽  
pp. 295-298 ◽  
Author(s):  
Seiji Kawasaki ◽  
Akio Kidokoro ◽  
Mitsuo Sugiura ◽  
Kensho Sanjo ◽  
Yasuo Idezuki
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Venous Pressure ◽  
Portal Venous Pressure

PS01.014: DESCRIPTION OF ACHALASIA PATIENTS IN CUBA: NINE-YEAR EXPERIENCE

2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 54-54
Author(s):  
Vivianne Anido ◽  
Rosalba Roque González ◽  
Raul Brizuela ◽  
Tatiana Amable ◽  
Luis Pérez ◽  
...  
Keyword(s):  
High Resolution ◽  
Lower Esophageal Sphincter ◽  
Gold Standard ◽  
Esophageal Manometry ◽  
Conflicts Of Interest ◽  
The Body ◽  
Esophageal Peristalsis ◽  
Loss Of Function ◽  
Esophageal Sphincter ◽  
Over 40 Years

Abstract Background Achalasia is a primary neurodegenerative disease of the esophagus characterized by loss of function of the lower esophageal sphincter (LES) and aperistalsis of the body of the esophagus. Among the diagnostic elements, conventional or high-resolution esophageal manometry is the ‘gold standard’ for diagnosis. In this study, our objective was to investigate the epidemiology and characteristics of patients with Achalasia, seen at the CNCMA, Cuba. Methods A retrospective, descriptive and observational study was performed on patients with Achalasia, diagnosed through conventional esophageal manometry, from January 2006 to December 2015. The database of patients diagnosed with the disease is analyzed at the center's Motility Laboratory. Esophageal manometries were performed by the perfusion method, with Medtronic equipment, 4 register channel catheters, at 5 cm from each other, with Polygram software, from 2005 to 2008 and from then on with catheters Zynetic, Alpine, and Polygram.Net software version 4.1.1322. The consent was asked to performance the test and the scientific use of the results. Results 332 patients were diagnosed with achalasia through manometry. More than half of patients with achalasia in this study were female, over 40 years. Patients had no proved associations with other diseases. By conventional esophageal manometry, the typical features were poor relaxation, normal basal pressure of the lower esophageal sphincter and absence of esophageal peristalsis. Conclusion Conventional esophageal manometry was useful to stablish the diagnostic of Achalasia, showing the typical features of the disease. Disclosure All authors have declared no conflicts of interest.

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